What is pulmonary rehabilitation?

Pulmonary rehabilitation is a medically-supervised exercise and education program designed to help with difficulty breathing or if you are increasingly limited in your everyday activities due to COPD, emphysema, chronic bronchitis and other lung diseases.

Pulmonary rehabilitation is offered at the following locations:

MercyOne Des Moines Medical Center

MercyOne Dubuque Medical Center

MercyOne Elkader Medical Center

MercyOne Waterloo Medical Center

MercyOne Oelwein Medical Center

MercyOne Siouxland Medical Center

Our pulmonary rehabilitation experts understand the life-changing difficulties breathing problems can cause for you. We will help you improve your quality of life through emotional support, exercise and education.

How does pulmonary rehabilitation work?

Pulmonary rehabilitation incorporates physical reconditioning, self-care education, breathing exercises and techniques to improve your ability to carry out your daily activities. The program will also help you reduce the risks and complications of lung irritation and/or infection and promote social interaction and emotional well-being.

By attending classes, you will learn many things about your lungs. The exercise classes will help you be more active with less shortness of breath. Usually, you will be exercising both your arms and legs. The exercise classes will help you feel better and become stronger by helping you get into better shape.

Pulmonary rehabilitation will help you:

  • Alleviate shortness of breath with activity
  • Cope with feelings of fear or apprehension
  • Improve your quality of life
  • Increase exercise tolerance and strengthen breathing muscles
  • Increase your ability to function independently
  • Learn more about your disease, treatment options, coping strategies and breathing techniques
  • Maintain health behaviors
  • Recognize, treat and resist respiratory infection and flare-ups
  • Reduce and control breathing difficulties
  • Reduce exacerbations and hospitalizations

Who could benefit from pulmonary rehabilitation?

You can benefit from pulmonary rehabilitation if you have had:

  • chronic obstructive pulmonary disease (COPD)
    • emphysema
    • chronic bronchitis
  • cystic fibrosis (CF)
  • interstitial lung disease
    • sarcoidosis
    • pulmonary fibrosis
  • lung surgery
  • muscular dystrophy
  • and other lung diseases

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Respiratory distress, also called acute respiratory distress syndrome (ARDS), is respiratory failure caused by rapid onset of widespread inflammation in the lungs

It can occur in patients who are critically ill or significantly injured.

Symptoms can include shortness of breath, rapid breathing, and bluish skin coloration.

Respiratory distress can be a serious, even fatal, condition.

Anyone who experiences these symptoms should seek emergency medical care immediately.

Diagnosing the cause of respiratory distress is not easy and requires clinical knowledge, a careful physical examination, and attention to detail.

STRETCHERS, LUNG VENTILATORS, EVACUATION CHAIRS: SPENCER PRODUCTS ON THE DOUBLE BOOTH AT EMERGENCY EXPO

What is Respiratory Distress?

Respiratory distress, also called acute respiratory distress syndrome (ARDS), is respiratory failure caused by rapid onset of widespread inflammation in the lungs.

Patients with ARDS have severe shortness of breath and often are unable to breath without the support of a ventilator.

Symptoms can include shortness of breath (dyspnea), rapid breathing (tachypnea), and bluish skin coloration (cyanosis). Respiratory distress is a critical, often fatal condition, especially among the elderly and severely ill. If not properly treated, some extreme cases of respiratory distress can lead to a decreased quality of life.

THE IMPORTANCE OF TRAINING IN RESCUE: VISIT THE SQUICCIARINI RESCUE BOOTH AND FIND OUT HOW TO BE PREPARED FOR AN EMERGENCY

Respiratory distress can be primary or secondary:

  • Primary respiratory distress means the problem is in the lungs.
  • Secondary respiratory distress means the problem is somewhere else in the body and the lungs are compensating.

Possible primary respiratory distress problems include:

  • Anaphylaxis
  • Asthma
  • COPD
  • Pleural effusion
  • Pneumonia
  • Pneumothorax
  • Pulmonary edema

Possible secondary respiratory distress problems can include:

  • Diabetic ketoacidosis
  • Head trauma
  • Metabolic acidosis
  • Stroke
  • Sepsis
  • Toxicological overdose

Causes of Respiratory Distress and Treatment

Respiratory distress has a range of causes that can affect treatment, so EMTs must start by carefully considering the source of the condition.

For respiratory distress, the focus is usually on the lungs and auscultation (listening for sounds from the lungs, heart, and other organs).

An EMS provider’s assessment may include a physical exam, incident history, and vital signs before deciding the next step in treatment and transport of their patient.

The following are some of the most common types of respiratory distress and a brief overview of the appropriate treatment for each one.

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Airway Obstruction

There are many ways that a foreign object can lodge in an airway causing an obstruction.

For example, a stroke can damage swallowing reflexes, making the person more prone to choking.

Consumption of alcohol and some drugs can also suppress the gag reflex, which could also lead to choking.

Treatment: If the airway obstruction is mild and the patient is coughing forcefully, EMS providers may not interfere with the patient’s efforts to clear the obstruction.

If the patient has signs of severe airway obstruction, as indicated by a silent cough, cyanosis, or the inability to speak or breathe, you should intervene.

If in some cases a patient becomes unresponsive, you can perform a finger sweep to clear the airway obstruction, but only if you can see solid material blocking their airway.

Asthma

Asthma is a chronic, inflammatory disease of the airways.

Asthma attacks can be induced by many different causes including allergens, infections, exercise, and smoke.

Patients with asthma are very sensitive to things such as dust, pollen, drugs, air pollutants, and physical stimuli.

During an asthma attack, the muscles around the bronchioles tighten, the lining of the inside the bronchioles swells, and the inside of the bronchioles fills with thick mucus.

This severely restricts expiration of air from the lungs. Patients will often describe a history of asthma and have a prescription for a metered-dose inhaler.

TreatmentBasic Life Support treatment considerations include:

  • Calming the patient
  • Airway management
  • Oxygen therapy
  • Assisting with a prescribed inhaler

COPD

Chronic obstructive pulmonary disease (COPD) is a group of diseases that includes asthma, emphysema, and chronic bronchitis.

COPD causes a slow process of dilation and disruption of the airways and alveoli, and it includes several related irreversible conditions that limit the ability to exhale.

Symptoms of COPD include shortness of breath, fever, and increased sputum production.

The patient’s medical history can include conditions such as upper-respiratory infection, chronic bronchitis, emphysema, smoking, or working with hazardous substances such as chemicals, smoke, dust, or other substances.

Treatment. Common medications for COPD include:

  • Prednisone
  • Proventil
  • Ventolin
  • Atrovent
  • Azmacort

EMS treatment for a COPD patient with respiratory distress should include high flow oxygen.

Congestive Heart Failure

Congestive heart failure (CHF) results from too much fluid in the lungs, making it difficult to get air in.

This is in contrast to COPD patients, who typically experience difficulty getting the air out.

CHF occurs when the ventricles are weakened by a heart attack, underlying coronary artery disease, hypertension, or valve disease.

This impairs the heart’s ability to contract and empty during systole and blood backs up in the lungs and tissues of the body.

CHF is usually chronic with acute exacerbations.

During an acute episode, the patient will typically present sitting up, short of breath, diaphoretic, and pale, or cyanotic in color.

Breathing sounds can include rales or wheezes.

The medical history can include increased salt ingestion, respiratory infection, non-compliance with medications, angina, or symptoms of acute coronary syndrome.

Treatment. Common medications include:

  • ACE inhibitors
  • Furosemide (Lasix)
  • HCTZ (hydrochlorthiazide)
  • Beta-blockers
  • Angiotensin II receptor blockers
  • Digoxin (Lanoxin)

When treating patients who are suffering from congestive heart failure, seat the patient upright and administer high flow oxygen.

You may also consider positive pressure ventilation with a bag-valve-mask (BVM) if the patient is experiencing severe respiratory difficulty.

Inhalation Injuries

Inhalation injuries are caused by inhaling chemicals, smoke, or other substances.

Common symptoms include shortness of breath, coughing, hoarseness, chest pain due to bronchial irritation, and nausea.

Individuals with decreased respiratory reserve, including a history of COPD or CHF, are likely to experience an exacerbation of the disease.

Treatment: If a patient is in respiratory distress, treat immediately with high flow oxygen.

Assist breathing with a bag-valve-mask (BVM) if the respiratory effort is insufficient as indicated by a slow rate and poor air exchange.

Pneumonia

Symptoms of pneumonia include fever, chills, cough (often with yellowish sputum), shortness of breath, general discomfort, fatigue, loss of appetite and headache.

There can be chest pain associated with breathing (usually sharp and stabbing in nature) and worsened by coughing or deep inspirations.

Other signs that sometimes present are rales, clammy skin, upper abdominal pain, and blood-tinged sputum.

Treatment: Emergency care for pneumonia depends on the severity of the patient’s breathing difficulty but may include oxygen therapy.

Pneumothorax

A pneumothorax is the presence of air between the two layers of the pleura—which are the membranes lining the thorax and enveloping the lungs.

It is caused when an internal or external wound allows air to enter the space between these pleural tissues, which can cause the lungs to collapse.

A pneumothorax can occur spontaneously (e.g., a rupture caused by disease or localized weakness of the lung lining) or as a result of trauma (e.g., gunshot or stab wound).

People who have a prior history of pneumothorax or COPD may be more at higher risk of experience this medical condition.

In some rare instances, even forceful coughing can cause a pneumothorax.

A pneumothorax can cause sharp chest pain and shortness of breath.

The patient’s breathing will sound diminished and you may be able to feel air coming from under the patient’s skin.

Treatment:  EMS treatment of a pneumothorax includes high-flow oxygen. Be judicious with your use of positive-pressure ventilation. It can turn a spontaneous pneumothorax into a life-threatening tension pneumothorax.

Tension Pneumothorax

A tension pneumothorax is a progressively worsening pneumothorax that begins to impinge on the function of the lungs and the circulatory system.

It is caused when a lung injury acts like a one-way valve that allows free air to move into the pleural space but prevents the free exit of that air.

Pressure builds inside the pleural space and compresses the lungs and other organs.

Early signs of a tension pneumothorax include:

  • Increased dyspnea
  • Cyanosis
  • Signs of shock
  • Distended neck veins
  • Shift in PMI (Point of maximum intensity, where the heart is the loudest through auscultation)
  • Tracheal displacement
  • Tracheal deviation

Treatment: If the patient is hypotensive or showing signs of hypoperfusion, then EMS providers should initiate temporizing treatment for tension pneumothorax.

Open chest wounds should have a sealable dressing placed over them with a one-way air valve to prevent air build up.

This one-way valve can be created by applying an occlusive dressing and taping on three sides.

The EMS provider should perform needle decompression on the chest wall to release encased air.

Pulmonary Embolism

A pulmonary embolism (PE) can occur when a particle (such as a blood clot, fat embolus, amniotic fluid embolus, or air bubble) gets loose in the blood stream and travels to the lungs.

If the particle lodges in a major branch of the pulmonary artery, this can interrupt blood circulation to the lungs.

If blood cannot reach the alveoli, then it cannot be oxygenated.

This condition can be caused by immobility of the lower extremities, prolonged bed rest, or recent surgery.

Signs of PE are a sudden onset of shortness of breath, rapid breathing, chest pain worsened by breathing, and coughing up blood.

Treatment: Pulmonary embolism is a life-threatening condition and should be treated with high flow oxygen and rapid transport. Move the patient gently to avoid dislodging additional emboli (particles).

When to Call Emergency Number for Respiratory Distress

Breathing is something most of us do instinctively, day and night. We don’t even think about it.

So, if you experience shortness of breath or difficulty breathing it can be quite alarming.

If you experience shortness of breath that interferes with your daily routine or body functions, you should call Emergency Number or have someone drive you to the nearest Emergency Room immediately.

You should call Emergency Number immediately if you experience shortness of breath together with any of the following  symptoms:

  • Chest pain
  • Dizziness
  • Pain that spreads to your arms, neck, jaw or back
  • Sweating
  • Trouble breathing
  • How to Treat Respiratory Distress

If you experience shortness of breath, or shortness of breath together with any of the symptoms listed above, you need to call Emergency Number or get to an ER immediately.

Treatment of respiratory distress requires a doctor.

The first goal in treating respiratory distress will be to improve the oxygen levels in your blood.

Without sufficient oxygen, your organs can fail. Increasing your blood oxygen levels can be achieved through supplemental oxygen or a mechanical ventilator that pushes air into your lungs.

Careful management of any intravenous fluids will also be critical.

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People with respiratory distress are usually given medication to:

  • Prevent and treat infections
  • Relieve pain and discomfort
  • Prevent blood clots in the legs and lungs
  • Minimize gastric reflux
  • Sedate

USA: How Do EMTs & Paramedics Treat Respiratory Distress

For all clinical emergencies, the first step is rapid and systematic assessment of the patient.

For this assessment, in the USA most EMS providers will use the ABCDE approach.

The ABCDE (Airway, Breathing, Circulation, Disability, Exposure) approach is applicable in all clinical emergencies for immediate assessment and treatment.

It can be used in the street with or without any equipment.

It can also be used in a more advanced form where emergency medical services are available, including emergency rooms, hospitals or intensive care units.

Treatment Guidelines & Resources for Medical First Responders

Treatment guidelines for respiratory distress can be found on page 163 of the National Model EMS Clinical Guidelines by the National Association of State EMT Officials (NASEMSO).

These guidelines are maintained by NASEMSO to facilitate the creation of state and local EMS system clinical guidelines, protocols, and operating procedures.

These guidelines are either evidence-based or consensus-based and have been formatted for use by EMS professionals.

TRAINING: VISIT THE BOOTH OF DMC DINAS MEDICAL CONSULTANTS IN EMERGENCY EXPO

The guidelines include a rapid assessment of the patient for symptoms of respiratory distress, which may include:

  • Shortness of breath
  • Abnormal respiratory rate or effort
  • Use of accessory muscles
  • Quality of air exchange, including depth and equality of breath sounds
  • Wheezing, rhonchi, rales, or stridor
  • Cough
  • Abnormal color (cyanosis or pallor)
  • Abnormal mental status
  • Evidence of hypoxemia
  • Signs of a difficult airway

Pre-hospital treatments and interventions might include:

  • Non-invasive ventilation techniques
  • Oropharyngeal airways (OPA) and nasopharyngeal airways (NPA)
  • Supraglottic airways (SGA) ort extraglottic devices (EGD)
  • Endotracheal intubation
  • Post-intubation management
  • Gastric decompression
  • Cricothyroidotomy
  • Transport to closest hospital for airway stabilization

EMS providers should reference the CDC Field Triage Guidelines for decisions regarding transport destination for injured patients.

Read Also

Emergency Live Even More…Live: Download The New Free App Of Your Newspaper For IOS And Android

Basic Airway Assessment: An Overview

Three Everyday Practices To Keep Your Ventilator Patients Safe

Benefits And Risks Of Prehospital Drug Assisted Airway Management (DAAM)

Respiratory Distress Syndrome (ARDS): Therapy, Mechanical Ventilation, Monitoring

Chest Pain, Emergency Patient Management

Ambulance: What Is An Emergency Aspirator And When Should It Be Used?

Notions Of First Aid: The 3 Symptoms Of A Pulmonary Embolism

Quick And Dirty Guide To Chest Trauma

Neonatal Respiratory Distress: Factors To Take Into Account

Resuscitation Manoeuvres: Cardiac Massage On Children

Emergency-Urgency Interventions: Management Of Labor Complications

What Is Transient Tachypnoea Of The Newborn, Or Neonatal Wet Lung Syndrome?

Tachypnoea: Meaning And Pathologies Associated With Increased Frequency Of Respiratory Acts

Postpartum Depression: How To Recognise The First Symptoms And Overcome It

Postpartum Psychosis: Knowing It To Know How To Deal With It

Clinical Review: Acute Respiratory Distress Syndrome

Seizures In The Neonate: An Emergency That Needs To Be Addressed

Stress And Distress During Pregnancy: How To Protect Both Mother And Child

Respiratory Distress: What Are The Signs Of Respiratory Distress In Newborns?

Emergency Paediatrics / Neonatal Respiratory Distress Syndrome (NRDS): Causes, Risk Factors, Pathophysiology

Respiratory Distress Syndrome (ARDS): Therapy, Mechanical Ventilation, Monitoring

Childbirth And Emergency: Postpartum Complications

Signs Of Respiratory Distress In Children: Basics For Parents, Nannies And Teachers

Three Everyday Practices To Keep Your Ventilator Patients Safe

Ambulance: What Is An Emergency Aspirator And When Should It Be Used?

The Purpose Of Suctioning Patients During Sedation

Supplemental Oxygen: Cylinders And Ventilation Supports In The USA

Behavioural And Psychiatric Disorders: How To Intervene In First Aid And Emergencies

Fainting, How To Manage The Emergency Related To Loss Of Consciousness

Altered Level Of Consciousness Emergencies (ALOC): What To Do?

Source

Unitek EMT



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Asia Pacific Digital Respiratory Device Market to soar at CAGR

The Asia-Pacific Digital Respiratory Device Market Analysis, 2023, by MarkNtel Advisors, presents a well-researched, detail-driven, and accurate study for the stakeholders. This analysis entails prominent aspects like trends, & recent developments, drivers, opportunities, challenges, & restraints, among other parameters, influencing the overall industry expansion across different locations.

According to Asia-Pacific Digital Respiratory Device Market Research Report: Forecast (2023-2028), "The market is projected to grow at a CAGR of around 36.2% during the forecast period, i.e., 2023-28. The market growth is aided by the region's increasing number of respiratory diseases, including asthma, sleep apnea, chronic bronchitis, and more.

However, emerging economies, coupled with bolstering public awareness, are adopting new technologically advanced devices with government-increased healthcare expenditure. Furthermore, the increasing geriatric population and obesity presents chances for the market to expand more in coming years."

Request A Free PDF of The Study's Report (To Completely Understand This Report's [Summary + TOC]] Structure) - www.marknteladvisors.com/query/request-sample/asia-pacific-digital-respiratory-device-market.html

Segmentation Analysis

The Asia-Pacific Digital Respiratory Device Market is highly fragmented and comprises various bifurcations & geographies. These sections cover information on opportunities & challenges faced by the players, fluctuations in the demand, supply, revenue generation, size, sales, profits, volume, & price, among other parameters for the investors.

The stakeholders can also attain an overview of the external factors influencing the industry expansion over the years. The Asia-Pacific Digital Respiratory Device Market bifurcates into the following segmentations:

By Device Type

-Therapeutic Devices

--CPAP Devices

--BI-PAP Devices

--Humidifiers

--Nebulizers

--Ventilators

--Inhalers

--Oxygen Concentrates

--Resuscitators

-Diagnostics Monitoring Devices

--Spirometers

--Pulse Oximeters

-Consumables and Accessories

-Respiratory Therapy Wearable Medical Device

--Watch and Wristband

-Disposables

--Nasal Cannulas

--Filters

--Breathing Circuits

By End-User

-Homecare

-Hospitals and Clinics

-Ambulatory Care Centers

By Application

-Chronic Obstructive Pulmonary Disease

-Sleep Apnea

-Asthma

-Infectious Disease

Check Out the Complete Research Study's Comprehensive Benchmark, Click Here - www.marknteladvisors.com/research-library/asia-pacific-digital-respiratory-device-market.html

Growing Prevalence of Asthma Stimulates Demands for Digital Respiratory Devices

"Asthma as most prominent in APAC region instigate demand for related treatment methods in the forecasting period. Healthcare professionals facing continuous blocks in managing respiratory diseases despite the presence of novel therapies propel the demand for smart inhalers with advanced features. Moreover, the features of tracking dosage, supervising schedules, recording data, and more, further accelerate the market demand and growth.", states the research report.

Rapid Adoption of Digital Respiratory Devices Grants China the Lion's Market Share

"Country-wise, China procures the largest share with its rapid adoption of digital respiratory devices after the outbreak of Covid-19 and to cope with increasing asthma and respiratory problems with the ever-increasing aging population. Besides, China's initiative, Healthy China 2030, further propels the market to seek and improve the national health system.

However, the increasing cases of respiratory diseases among the growing population of India has resulted in the rapid adoption of new health-related technologies, promising lucrative growth to the market.", states the research report by Markntel Advisors.

Competitive Projection & Analysis

The researchers at Markntel Advisors have rigorously profiled each company operating in the industry, offering insights to the stakeholders about the competition and allowing them to strategize their tactics using the data put together in the report.

This information comprises the recent developments, mergers & acquisitions, product/service launches, expansion plans, & opportunities utilized to attain revenue, alongside the role & participation of the governments and more.

The prominent players profiled in the report include Philips, 3M Healthcare, Astra Zenca Plc., Novartis AG, GE Healthcare, Masimo Corporation, Cipla Ltd., Resmed Ltd., Teva Pharmaceuticals Industries Ltd., and Acorda Therapeutics.

For Any Additional Information or Questions About This Report, Please Contact Us @ - www.marknteladvisors.com/query/talk-to-our-consultant/asia-pacific-digital-respiratory-device-market.html

Customization Available

To avail of exciting offers & customization services on the report, reach out to MarkNtel Advisors and get a personalized analysis of the Asia-Pacific Digital Respiratory Device Market. Out researchers compile data for the stakeholders, incorporating all the prominent aspects influencing the industry expansion alongside the particular chapters requested. This detail-driven, unbiased, and accurate data on grounds curating the fundamentals underlying the market potential & lucrative opportunities shall benefit the investors in numerous ways in the future.

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DUBLIN--()--The "Chronic Obstructive Pulmonary Disease (COPD) Market, Global Forecast 2023-2028, Industry Trends, Growth, Insight, Impact of Inflation, Company Analysis" report has been added to ResearchAndMarkets.com's offering.

The Global Chronic Obstructive Pulmonary Disease (COPD) Market will increase to around USD 22.91 Billion by 2028 according to the publisher. Chronic inflammatory lung disease causes breathing difficulties.

Companies Mentioned

  • AstraZeneca
  • Pfizer, Inc
  • GlaxoSmithKline plc
  • Novartis AG
  • AstellasPharma Inc.
  • Abbott Laboratories
  • BoehringerIngelheim International GmbH
  • Almirall

It is a group of progressive lung diseases. The most common diseases are emphysema and chronic bronchitis. COPD, if left untreated, can lead to worsening respiratory infection, heart problems, and the progression of various other diseases.

COPD is commonly caused due to smoking tobacco-related products. The longer and more tobacco products an individual smokes, the greater risk of having COPD.

Cigarette smoking, cigar smoke, pipe smoke, and second-hand smoke can also cause COPD. According to World Health Organization (WHO), COPD is considered the third leading cause of death worldwide, and nearly 90% of Global Chronic Obstructive Pulmonary Disease deaths in those under 70 years of age occur in low and medium income countries (LMIC).

Worldwide Chronic Obstructive Pulmonary Disease Market will grow at a CAGR of 5.73% from 2022 to 2028

The rise in the incidence of COPD is the major contributor to the market's growth. In addition, people's lifestyle change is responsible for increasing habits like smoking and drinking.

The other factors that influence the growth of the COPD market are a rise in demand for medications for the treatment of COPD symptoms, an increase in funding for R&D and drug production by government and pharmaceutical companies, growing awareness among people across developing and underdeveloped countries, are boosting the growth of the market companies.

Nevertheless, the high cost of COPD treatment and lack of knowledge about COPD is anticipated to hinder the market's growth. Also, factors like patent expiry for medical devices will restrict the development of the market.

Chronic Bronchitis will lead in Chronic Obstructive Pulmonary Disease Market

Based on type, the global COPD market is categorized into; chronic bronchitis and emphysema. The chronic bronchitis category dominates the market share of the worldwide COPD market. The reason for its dominance is the growing incidence and prevalence of chronic bronchitis worldwide, due to the rise in the consumption of cigarettes and the increase in industrialization, which results in air pollution and the release of harmful gases into the environment.

Drug remain the most important segment in Treatment Type

Based on treatment, the global COPD market is divided into; drugs, oxygen therapy, surgery, and others. The drugs segment has a higher market share in the market, owing to the increasing use of drugs as the first line of treatment for COPD to make breathing easier by widening airways.

The oxygen therapy market is also expected to surge at a significant CAGR rate in the forecast period. The growth can be attributed to factors like the rapid growth of the geriatric population, the rising prevalence of tobacco smoking, the development of respiratory disorders, the increase in the usage of home-based oxygen therapy, and technological advancements.

Rise in Number of COPD Therapeutics Dispensed to boost the hospital Segment

The distribution channels can be segmented into; hospital pharmacies, retail pharmacies, and online pharmacies. The hospital pharmacies segment has a high market share. The dominance due to the rising number of patients suffering from chronic respiratory diseases and rising awareness about these diseases. Furthermore, the availability of various diagnostics and treatment facilities and higher purchasing power has contributed to the segment's growth.

North American area dominates the COPD Industry

The report divides the region into; North America, Europe, Asia-Pacific, Latin America, and Middle-East & Africa. The North American area dominates the market share. This can be attributed to increased investment in R&D activities to develop innovative drugs for treating diseases. Also, the rise in an older population, rising incidence and prevalence of chronic respiratory diseases, technological advancement, growing healthcare sectors, and massive presence of leading market players are some of the major factors that boost the COPD Market in the region.

The Asia-Pacific region is forecasted to have significant growth, owing to increasing focus on the development of healthcare infrastructure, rising prevalence of various chronic respiratory diseases along with lifestyle diseases, rise in industrialization, changes in the lifestyle, and increase in the patient population suffering from COPD in the developing nations such as China, and India. According to our research report, Worldwide Chronic Obstructive Pulmonary Disease (COPD) Market was at US$ 16.40 Billion in 2022.

For more information about this report visit www.researchandmarkets.com/r/f0ka08

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The 2023 report from the Global Initiative for Chronic Obstructive Lung Disease (GOLD) — “Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease” (COPD)1 — details “an expanded range of therapies for COPD that now can be considered to improve mortality,” according to Gerard J. Criner, MD, FACP, FACCP, an author of the 2023 GOLD Report and director of the 2022 GOLD COPD Day conference, held in November, where the updated 5th version of the GOLD report was released and the scientific underpinnings of the updates were discussed.

The expanded range of COPD therapies discussed in the 2023 report includes “an expanded role of triple inhaled therapy in select patient populations, as well as noninvasive ventilation, which also may have a role in improving exacerbation in select patient groups with COPD,” said Dr Criner, who is Chair and Professor of Thoracic Medicine and Surgery at the Lewis Katz School of Medicine at Temple University in Philadelphia, which hosts the annual GOLD COPD Day conference.

The 2023 GOLD report contains numerous other important updates as well. Among these are a reconsideration of the definitions and taxonomy of COPD and symptomatic exacerbations; new material on chronic bronchitis; and an increased focus on genetic and environmental causal factors in COPD aside from tobacco smoking.

Definitions, Heterogeneity, and Exacerbations

An important change in the 2023 GOLD report involves “clarifications and suggestions on the definition of COPD,” said Dr Criner. Related to this, the updated report also has expanded the discussion of how an exacerbation is defined, he added. “We’ve integrated newer work on codifying the onset of an exacerbation and defining the severity of an exacerbation by using not only symptoms but also physiologic criteria in grading the exacerbation as mild, moderate, or severe. Now that’s more a hypothesis than something with data wrapped around it, but is meant to fuel thought into how we can do a better job of assessing exacerbations.”

The revised definition of COPD in the 2023 report “now describes symptoms clearly and underscores the heterogeneity of COPD,” said Fernando J. Martinez, MD, MS, another coauthor of the 2023 GOLD Report. “GOLD has now embraced the concept of both early COPD and pre-COPD, and this now is incorporated into the GOLD document,” explained Dr Martinez, who is also Chief of the Pulmonary and Critical Care Medicine Division at Weill Cornell Medicine in New York City.

“There’s a lot of interest right now regarding the heterogeneity of COPD,” added Dr Martinez. “Two very relevant articles recently advocated for highlighting that heterogeneity in the definition of COPD.2,3 Exactly what implication that’s going to have for patient management and therapeutics, no one yet knows. But that level of heterogeneity is now something that’s very clearly seen as an important component of COPD in general,” he stressed.

With regard to defining exacerbations and their severity, Dr Martinez added, “the science committee recommended adopting the ’Rome Proposal,4 which suggested that the definition of severity should evolve away from what therapies are used, and rather toward a series of objective parameters: how bad the symptoms are, whether there’s evidence of inflammation or an oxygen saturation problem, and so on. So that is a recommendation that was made for consideration only at this time, because it is not yet clear whether it has any therapeutic implications,” said Dr Martinez.

Assessment Schema and Pharmacotherapy

The evolution of GOLD’s approach to pharmacotherapeutic assessment for COPD — one of the topics “of greatest interest” at the 2022 COPD Day conference, according to Dr Martinez — is covered at length in the 2023 GOLD report.

Until the release of the 2023 report, it was recommended that clinicians determine a patient’s initial COPD pharmacologic regimen using the “ABCD Assessment Tool,” said Dr Criner, who described the tool as “a sort of ‘four squared’ algorithm…based on symptoms and exacerbation history.” First presented in the 2011 GOLD report and later refined in the 2017 GOLD report, the ABCD Assessment Tool was “based on the patient’s level of symptoms, future risk of exacerbations, the extent of airflow limitation, the spirometric abnormality, and the identification of comorbidities” and was “a major advance from the simple spirometric grading system” used previously, the 2018 GOLD report stated.5

Based on recent evidence, however, the 2023 GOLD report has further revised this tool, which is now called the “ABE Assessment Tool.”1 According to the 2023 report, this change recognizes the clinical relevance of exacerbations, independent of the level of symptoms, in making assessments. As Dr Martinez explains it, “This year we got rid of the ‘C’ [ie, less symptomatic, high-exacerbation-risk] and ‘D’ [ie, more symptomatic, high-risk] groups in the ABCD tool, and merged them into one ‘E’ group, representing exacerbation-prone patients. This was partly because the ‘C’ group was so uncommon in large population studies, and partly because the exacerbation component is such a crucial issue to address.”

The 2023 GOLD report also included significant changes in COPD pharmacotherapeutic strategy, said Dr Martinez. The first change is in line with the American Thoracic Society/European Respiratory Society (ATS/ERS) statement that combination bronchodilator therapy — a long-acting beta agonist (LABA) and a long-acting muscarinic antagonist (LAMA) together — is better than LABA or LAMA as monotherapy,6,7 he explained. “We now recommend dual bronchodilator therapy up front for symptomatic patients. There was advocacy for this for many years, and we finally made that change.”

“There is increasing awareness that dual bronchodilator therapy is initially indicated in people who are symptomatic or have exacerbations,” said Dr Criner. “This includes people who have COPD exacerbations and have peripheral blood eosinophilia.”

Yet more discussion on this topic seems inevitable; as Dr Martinez noted, “implementation of dual bronchodilator therapy and quantitative cutoff values for eosinophilia in treatment selection” were the subject of “spirited debates,” at the recent COPD Day Conference.

Another significant change in COPD pharmacotherapeutic strategy in the 2023 GOLD report is the recommendation to use inhaled triple therapy rather than inhaled corticosteroid (ICS)-plus-LABA for higher-risk patients who are more symptomatic and exacerbation prone. After much debate, the GOLD science committee concluded that for these patients, “triple therapy beats ICS/LABA in every category,” said Dr Martinez, who was involved with 2 or 3 major studies of these therapies. 8,9  As a result, said Dr Martinez, “ICS/LABA has been dropped from the therapeutic recommendations in GOLD. That is a major change. ICS/LABA remains one of those commonly used regimens globally. There are various generic formulations, and payers love it, because it’s cheap; but now it’s dropped off the GOLD therapeutic strategy. So it will be interesting to see how payers interpret that.”

To support this change, the 2023 report highlights “very convincing data that triple therapy, in a particular population of patients, can improve all-cause mortality.10,11 We included a tabular representation of all of the studies that have shown improvements in mortality, for pharmacotherapy and nonpharmacotherapy, and we recommend that be incorporated into therapeutic decision-making for individual patients,” Dr Martinez noted. “So the management recommendations for stable COPD have now changed to emphasize dual bronchodilators and triple therapy, and also with a strong emphasis on the eosinophil as a circulating biomarker that can be used to guide response.”

Chronic Bronchitis and Mucus Hypersecretion

The burden of mucus hypersecretion in patients with COPD is also covered in the 2023 report, said Dr Criner. In particular, chronic bronchitis is discussed at greater length, with a review of some of its pathobiology and epidemiology, as well as a discussion of new medical and interventional treatments.

“There is a lot of interest in particular symptoms such as cough and sputum production. But it’s only recently that the clinical implications of those symptoms have become evident,” said Dr Martinez. He added that “the effort to target a particular symptomatic expression of COPD, such as cough and sputum production, is now a very active area, with practical implications for patients. Interventional studies are ongoing; and oral pharmacotherapeutic approaches, including cystic fibrosis transmembrane conductance regulator (CFTR) potentiators,12 are under evaluation right now.”

Vascular Disease and Other Updates

The 2023 report also discusses pulmonary vascular diseases, both secondary pulmonary hypertension and pulmonary embolism. The latter has been the focus of more recent studies, including a large French study published in JAMA.13 As Dr Criner explained, “In that study, about 6% of patients who presented with an acute exacerbation of COPD were found to have a pulmonary embolism at the time of presentation.” This study “highlights the fact that some people with COPD exacerbations actually have COPD with exacerbation of symptoms that are due to another cause, such as pulmonary embolism, heart failure, or ischemic heart disease” — a topic of interest that was discussed during the conference, said Dr Criner. Accordingly, he noted, the importance of screening patients with COPD for comorbid conditions like pulmonary embolism and other diseases is reflected in the 2023 GOLD report.

Certain sections of the new report have some degree of updated information but were not exhaustively revised, said Dr Criner. “We discuss imaging more than previously, particularly the role of computed tomography (CT) scanning — both its current role and the role we think it will have in the future. We have also expanded and revised the discussion of surgical and interventional treatments for COPD. This includes indications for bullectomy or lung reduction surgery; bronchoscopic treatments for lung reduction, an evolving field both in and outside the US; and interventional treatments that are currently being studied for chronic bronchitis. There is also a more comprehensive discussion of the role, benefits, and complications of lung transplantation. Finally, we revised and updated chapters on comorbidities and on COVID-19.”

Interstitial Lung Abnormalities: A Future Topic

Interstitial lung abnormalities in patients with COPD was a topic of interest at the GOLD conference that was not exhaustively covered in the 2023 GOLD report, said Dr Criner. Interstitial lung abnormalities “have been reported in several epidemiologic studies, mainly imaging studies characterizing patients who have been exposed to smoke, and also studies of lung cancer screening data. These studies demonstrate that patients with COPD have some interstitial changes that could be related to smoke exposure, or occupational exposure, or smoking in people who also are predisposed to interstitial lung diseases,” said Dr Criner. This topic is likely to be a focus in the future, he added.

Disclosures:Dr Criner reports receiving grants from AstraZeneca, Boehringer Ingelheim, Broncus, Chiesi, Corvus, Genentech, Gilead, GlaxoSmithKline, Fisher-Paykel Healthcare, Lilly, NIH-NHLBI, Novartis, Olympus, PA-DOH, Pfizer, Pearl, PneumRx, Pulmonx, Regeneron, Roche and Spiration; consultant fees from Almirall, AstraZeneca, Broncus, BTG, CSA Medical, GlaxoSmithKline, EOLO, Intuitive, Ion, Mereo, Nuvaira, PneumRx, Pulmonx, Regeneron and Sanofi; and an equity interest in Free Flow Medical and Pleural Dynamics. Dr Martinez reports receiving fees for consulting and/or speaker roles with AstraZeneca, Boehringer Ingelheim, Chiesi, Sanofi/Regeneron, CSL, Behring, GlaxoSmithKline, Medtronic, Novartis, Polarean, Pulmatrix, Pulmonx, and Theravance/Viatris.

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According to the research. Chronic inflammatory lung disease causes breathing difficulties. It is a group of progressive lung diseases. The most common diseases are emphysema and chronic bronchitis. COPD, if left untreated, can lead to worsening respiratory infection, heart problems, and the progression of various other diseases.

New York, Jan. 18, 2023 (GLOBE NEWSWIRE) -- Reportlinker.com announces the release of the report "Chronic Obstructive Pulmonary Disease (COPD) Market, Global Forecast 2023-2028, Industry Trends, Growth, Insight, Impact of Inflation, Company Analysis" - www.reportlinker.com/p06381980/?utm_source=GNW

COPD is commonly caused due to smoking tobacco-related products. The longer and more tobacco products an individual smokes, the greater risk of having COPD. Cigarette smoking, cigar smoke, pipe smoke, and second-hand smoke can also cause COPD. According to World Health Organization (WHO), COPD is considered the third leading cause of death worldwide, and nearly 90% of Global Chronic Obstructive Pulmonary Disease deaths in those under 70 years of age occur in low and medium income countries (LMIC).

Worldwide Chronic Obstructive Pulmonary Disease Market will grow at a CAGR of 5.73% from 2022 to 2028

The rise in the incidence of COPD is the major contributor to the market’s growth. In addition, people’s lifestyle change is responsible for increasing habits like smoking and drinking. The other factors that influence the growth of the COPD market are a rise in demand for medications for the treatment of COPD symptoms, an increase in funding for R&D and drug production by government and pharmaceutical companies, growing awareness among people across developing and underdeveloped countries, are boosting the growth of the market companies. Nevertheless, the high cost of COPD treatment and lack of knowledge about COPD is anticipated to hinder the market’s growth. Also, factors like patent expiry for medical devices will restrict the development of the market.

Chronic Bronchitis will lead in Chronic Obstructive Pulmonary Disease Market
Based on type, the global COPD market is categorized into; chronic bronchitis and emphysema. The chronic bronchitis category dominates the market share of the worldwide COPD market. The reason for its dominance is the growing incidence and prevalence of chronic bronchitis worldwide, due to the rise in the consumption of cigarettes and the increase in industrialization, which results in air pollution and the release of harmful gases into the environment.

Drug remain the most important segment in Treatment Type
Based on treatment, the global COPD market is divided into; drugs, oxygen therapy, surgery, and others. The drugs segment has a higher market share in the market, owing to the increasing use of drugs as the first line of treatment for COPD to make breathing easier by widening airways.

The oxygen therapy market is also expected to surge at a significant CAGR rate in the forecast period. The growth can be attributed to factors like the rapid growth of the geriatric population, the rising prevalence of tobacco smoking, the development of respiratory disorders, the increase in the usage of home-based oxygen therapy, and technological advancements.

Rise in Number of COPD Therapeutics Dispensed to boost the hospital Segment
The distribution channels can be segmented into; hospital pharmacies, retail pharmacies, and online pharmacies. The hospital pharmacies segment has a high market share. The dominance due to the rising number of patients suffering from chronic respiratory diseases and rising awareness about these diseases. Furthermore, the availability of various diagnostics and treatment facilities and higher purchasing power has contributed to the segment’s growth.

North American area dominates the COPD Industry
The report divides the region into; North America, Europe, Asia-Pacific, Latin America, and Middle-East & Africa. The North American area dominates the market share. This can be attributed to increased investment in R&D activities to develop innovative drugs for treating diseases. Also, the rise in an older population, rising incidence and prevalence of chronic respiratory diseases, technological advancement, growing healthcare sectors, and massive presence of leading market players are some of the major factors that boost the COPD Market in the region.

The Asia-Pacific region is forecasted to have significant growth, owing to increasing focus on the development of healthcare infrastructure, rising prevalence of various chronic respiratory diseases along with lifestyle diseases, rise in industrialization, changes in the lifestyle, and increase in the patient population suffering from COPD in the developing nations such as China, and India. According to our research report, Worldwide Chronic Obstructive Pulmonary Disease (COPD) Market was at US$ 16.40 Billion in 2022.

Key Players in Chronic Obstructive Pulmonary Disease Market
COPD market is consolidated with the presence of a small number of key players. Also, the key players are constantly involved in product innovation and development, technological advancements, agreements, mergers, and acquisitions to procure a higher market share. The key players in the market are; AstraZeneca, Pfizer Inc., GlaxoSmithKline Plc, Novartis AG, Astellas Pharma, Abbott Laboratories, Boehringer Ingelheim International GmbH, and Almirall.

For instance, In Nov 2021, AstraZeneca announced that sold rights to sell Tudorza, also known as Eklira abroad, and Duaklir to the Switzerland-based pharmaceutical company CovisPharma Group for US$ 270 Mn. These products are indicated for treating chronic obstructive pulmonary disease (COPD).

The report titled “Chronic Obstructive Pulmonary Disease Market, Global Forecast by Product Type (Chronic Bronchitis and Emphysema), Treatment (Drugs, Oxygen Therapy, Surgery & Others), Distribution Channels (Hospital Pharmacies, Retail Pharmacies and Online Pharmacies), Regions (North America, Europe, Asia Pacific, Latin America, Middle East & Africa), Company Analysis (AstraZeneca, Pfizer, Inc, GlaxoSmithKline plc., Novartis AG, AstellasPharmaInc, Abbott Laboratories, BoehringerIngelheim International GmbH&Almirall)” Provides a detailed analysis of Chronic Obstructive Pulmonary Disease Market.

Product Types - Market has been covered from 2 viewpoints
1. Chronic Bronchitis
2. Emphysema

Treatment- Market has been covered from 4 viewpoints
1. Drugs
2. Oxygen Therapy
3. Surgery
4. Others

Distribution Channels - Market has been covered from 3 viewpoints
1. Hospital Pharmacies
2. Retail Pharmacies
3. Online Pharmacies

Distribution Channels - Market has been covered from 5 viewpoints
1. North America
2. Europe
3. Asia Pacific
4. Latin America
5. Middle East & Africa

All the companies have been studied from 3 points
• Overview
• Recent Developments
• Sales Analysis

Company Analysis
1. AstraZeneca
2. Pfizer, Inc
3. GlaxoSmithKline plc
4. Novartis AG
5. AstellasPharma Inc.
6. Abbott Laboratories
7. BoehringerIngelheim International GmbH
8. Almirall
Read the full report: www.reportlinker.com/p06381980/?utm_source=GNW

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By Steven Reinberg HealthDay Reporter

(HealthDay)

TUESDAY, Jan. 17, 2023 (HealthDay News) -- Major surgery is a challenge for people with chronic obstructive pulmonary disease (COPD), raising their odds of death within a year by 61%, new research shows.

The researchers also found these patients incurred 13% higher health care costs in the year after their operation, compared to patients without the respiratory condition.

"These increased risks and costs were evident long after the immediate 30-day postoperative period," said lead researcher Dr. Ashwin Sankar, a clinician investigator in anesthesiology at the University of Toronto, in Canada.

The study quantifies the additional risks COPD patients face, which doctors should discuss before surgery, he said.

"Informing patients of the risk of surgery is an important component of the informed-consent process prior to surgery. We suggest that clinicians and patients weigh these risks when deciding to proceed with surgery," Sankar explained.

This study can't prove that COPD caused the deaths after surgery as most of the COPD patients had other chronic health conditions, which could have contributed to the outcomes.

"What we suggest to clinicians is to use COPD as a flag for other conditions, and to ensure that modifiable risk factors are optimized prior to surgery," Sankar said.

Also, because patients with COPD are at risk beyond 30 days after surgery, it may be worthwhile to support these patients' recovery beyond the first month after surgery, he added.

In the United States, about 16 million people have COPD, according to the U.S. Centers for Disease Control and Prevention. COPD includes a group of diseases, emphysema and chronic bronchitis among them, that block airflow and restrict breathing.

For the study, Sankar and his colleagues collected data on nearly 933,000 patients who had major surgery, including total hip or knee replacement, gastrointestinal surgery, vascular surgery or other elective operations. More than 170,000 of these patients suffered from COPD.

The COPD patients were older, more likely to be male, frail, have lower income and have pre-existing conditions, such as heart disease, diabetes and lung cancer, the researchers noted.

Dr. Mangala Narasimhan is senior vice president of critical care services at Northwell Health in New Hyde Park, N.Y. "It does make sense that after surgery these patients would have more complications," she said.

"The advice to physicians is to consider the need for surgery and to counsel patients that there is more risk of complications, and that patients at least know that going into it so they can make informed decisions," she added.

Narasimhan's advice to anyone with COPD is, number one, do not smoke. "Smoking leads to increased risks of a lot of other things in the future," she said. "If you are smoking, quit as soon as you possibly can. Even if you quit later in life, there is definitely some benefit."

Also, she said that patients should consider whether surgery is necessary.

"No surgery is without its risk," Narasimhan said. "For these patients, it's significantly riskier and they should consider that before jumping into a procedure." Of course, some surgeries can't be avoided, she acknowledged.

If you must have major surgery, Narasimhan advises getting any health issues under control beforehand. This includes COPD, diabetes, lung cancer or heart disease.

"The one piece of advice is not to ignore the underlying risks. They will catch up with you, so optimize your medical condition prior to going into surgery," she said.

Narasimhan said your doctor may even withhold surgery until your health is the best it can be.

SOURCES: Ashwin Sankar, MD, clinician investigator, anesthesiology, University of Toronto, Canada; Mangala Narasimhan, DO, senior vice president, critical care services, Northwell Health, New Hyde Park, N.Y.; CMAJ (Canadian Medical Association Journal), Jan. 17, 2023

Copyright © 2023 HealthDay. All rights reserved.

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TUESDAY, Jan. 17, 2023 (HealthDay News) -- Major surgery is a challenge for people with chronic obstructive pulmonary disease (COPD), raising their odds of death within a year by 61%, new research shows.

The researchers also found these patients incurred 13% higher health care costs in the year after their operation, compared to patients without the respiratory condition.

"These increased risks and costs were evident long after the immediate 30-day postoperative period," said lead researcher Dr. Ashwin Sankar, a clinician investigator in anesthesiology at the University of Toronto, in Canada.

The study quantifies the additional risks COPD patients face, which doctors should discuss before surgery, he said.

"Informing patients of the risk of surgery is an important component of the informed-consent process prior to surgery. We suggest that clinicians and patients weigh these risks when deciding to proceed with surgery," Sankar explained.

This study can't prove that COPD caused the deaths after surgery as most of the COPD patients had other chronic health conditions, which could have contributed to the outcomes.

"What we suggest to clinicians is to use COPD as a flag for other conditions, and to ensure that modifiable risk factors are optimized prior to surgery," Sankar said.

Also, because patients with COPD are at risk beyond 30 days after surgery, it may be worthwhile to support these patients' recovery beyond the first month after surgery, he added.

In the United States, about 16 million people have COPD, according to the U.S. Centers for Disease Control and Prevention. COPD includes a group of diseases, emphysema and chronic bronchitis among them, that block airflow and restrict breathing.

For the study, Sankar and his colleagues collected data on nearly 933,000 patients who had major surgery, including total hip or knee replacement, gastrointestinal surgery, vascular surgery or other elective operations. More than 170,000 of these patients suffered from COPD.

The COPD patients were older, more likely to be male, frail, have lower income and have pre-existing conditions, such as heart disease, diabetes and lung cancer, the researchers noted.

Dr. Mangala Narasimhan is senior vice president of critical care services at Northwell Health in New Hyde Park, N.Y. "It does make sense that after surgery these patients would have more complications," she said.

"The advice to physicians is to consider the need for surgery and to counsel patients that there is more risk of complications, and that patients at least know that going into it so they can make informed decisions," she added.

Narasimhan's advice to anyone with COPD is, number one, do not smoke. "Smoking leads to increased risks of a lot of other things in the future," she said. "If you are smoking, quit as soon as you possibly can. Even if you quit later in life, there is definitely some benefit."

Also, she said that patients should consider whether surgery is necessary.

"No surgery is without its risk," Narasimhan said. "For these patients, it's significantly riskier and they should consider that before jumping into a procedure." Of course, some surgeries can't be avoided, she acknowledged.

If you must have major surgery, Narasimhan advises getting any health issues under control beforehand. This includes COPD, diabetes, lung cancer or heart disease.

"The one piece of advice is not to ignore the underlying risks. They will catch up with you, so optimize your medical condition prior to going into surgery," she said.

Narasimhan said your doctor may even withhold surgery until your health is the best it can be.

The report was published Jan. 17 in the CMAJ (Canadian Medical Association Journal)Canadian Medical Association Journal).

More information

For more on COPD, head to the U.S. Centers for Disease Control and Prevention.

SOURCES: Ashwin Sankar, MD, clinician investigator, anesthesiology, University of Toronto, Canada; Mangala Narasimhan, DO, senior vice president, critical care services, Northwell Health, New Hyde Park, N.Y.; CMAJ (Canadian Medical Association Journal), Jan. 17, 2023

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Chronic obstructive pulmonary disease, or COPD, refers to a group of disease that cause airflow obstruction and breathing-related problems. It includes emphysema and chronic bronchitis and has become a major burden to people’s health and economy. COPD is a silent killer in low- and middle-income countries (LMICs): an estimated 328 million people have COPD worldwide , and in 15 years, COPD is expected to become the leading cause of death and the economic impact of COPD among LMICs is expected to increase to £1.7 trillion by 2030

The Month of November Is COPD Awareness Month and 16th November is World COPD Day. The 2022 theme for World COPD Day is “Your Lungs for Life” . This year’s theme aims to highlight the importance of lifelong lung health. Everyone is born with a healthy lung (except congenital cases)but in due course of time smoking, air pollution takes a toll in our lungs and leads to various respiratory disease. In This article we are discussing the preventions and things we should follow to prevent and control COPD other than the medicine part.

Smoking is the leading cause of COPD. Smoking and secondhand smoke exposure during childhood and teenage years can slow lung growth and development and can increase the risk of developing COPD later in life. Secondhand smoke is smoke from burning tobacco products, such as cigarettes,hookah or smoke that has been exhaled, or breathed out, by a person .Quitting to smoke is the easiest way to prevent COPD and those already suffering from COPD ,quitting cigarette smoking helps to prevent Disease Progression.

Air pollution is a known factor which contributes in both causing and exacerbating the symptoms of COPD. Outdoor air pollution from industrial production, garbage burning, secondhand smoke, cigarette smoking and indoor air pollution from biomass fuel are some of the potential sources of air pollution. Common adverse health effects of air pollution are increased irritation of the respiratory tract, chronic cough, chest tightness, decreased pulmonary function and increased vulnerability to allergens and other immune system challenges. Many cities and regions in the developed nations keep a check on their air pollution levels so that people who are suffering from COPD avoid the outdoors when pollution levels are high. In developing nations and underdeveloped regions, there should be implementation of COPD awareness programmes for understanding the disease and being conscious of it. Biomass Fuel exposure is a leading cause of COPD in women hence women should avoid biomass fuel exposure to cook food.

Changes in lifestyle are possible and may be beneficial in preventing COPD. Chest Physiotherapy like Deep Diaphragmatic exercise and purse lip Breathing, Nutritional counselling, education on lung disease help us succeed to curb progression of the disease. The progressive course of COPD is connected with the development of extra pulmonary complications such as cardiovascular diseases, skeletal muscle dysfunction, osteoporosis, cachexia, anxiety and depression. Respiratory rehabilitation is a multidisciplinary program for treating patients with chronic pulmonary diseases and its principal goal is to improve both a person’s quality of life and also how well they function during daily activities.. Physiotherapy is the cornerstone in the structure of respiratory rehabilitation. Physiotherapy includes strength and endurance exercises and breathing exercises to optimize exercise tolerance ,add vigour in daily activities, reduces breathlessness, improves quality of life by applying various therapeutic exercises and breathing techniques.

Next comes the role of Vaccine in Controlling COPD. Patient Suffering From COPD should take their Influenza Vaccine and Pneumococcal Vaccines timely as they help in reducing COPD exacerbation

Lastly before concluding I would emphasize that in COPD ,inhalers are the mainstay of treatment and right inhalers with proper inhalation technique should be taught to COPD patients and COPD patients should never stop their medicine themselves without consulting their doctor. If we follow these simple things, not only COPD can be controlled to a great extent but can also reduce the economic burden which is having a great toll in the developing countries.

Disclaimer: This article is a paid publication and does not have journalistic/editorial involvement of Hindustan Times. Hindustan Times does not endorse/subscribe to the content(s) of the article/advertisement and/or view(s) expressed herein. Hindustan Times shall not in any manner, be responsible and/or liable in any manner whatsoever for all that is stated in the article and/or also with regard to the view(s), opinion(s), announcement(s), declaration(s), affirmation(s) etc., stated/featured in the same.

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Global Asthma And COPD Devices Market

Global Asthma And COPD Devices Market

Market Overview
The asthma and COPD devices market is projected to register a CAGR of 5.2% during the forecast period (2023-2032). A collection of lung conditions known as chronic obstructive pulmonary disease (COPD) make breathing challenging. Emphysema and chronic bronchitis can be a part of COPD. An inflammation of the airways results in a temporary narrowing of the airways that supply oxygen to the lungs, and asthma is a chronic illness that makes breathing difficult.

Scope of the Report
According to the report's intended audience, asthma is a chronic respiratory condition marked by mucus production, inflammation, and muscle tension that restricts the lungs' airways. Similarly, the fundamental cause of Chronic Obstructive Pulmonary Disease (COPD), which is tobacco smoking, is the obstruction of the airways, which further results in difficulties breathing. The devices that are utilised to treat these aforementioned respiratory disorders include those for treating asthma and COPD. The market for asthma and chronic obstructive pulmonary disease (COPD) devices is divided into segments based on product (inhaler and nebulizer), indication (asthma and COPD), and geography (North America, Europe, Asia-pacific, Middle East and Africa, and South America). The market research also includes projected market estimates and trends for 17 various nations worldwide.

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Global Asthma and COPD Devices Market: Segmentations

Global Asthma and COPD Devices Market: By Key Players
AstraZeneca
Boehringer Ingelheim
Drive DeVilbiss Healthcare
GF Health Products
Glaxosmithcline
Invacare
Merck
Omron Healthcare
PARI Pharma
Philips Healthcare

Global Asthma and COPD Devices Market: By Types
Inhaler
Nebulizer

Global Asthma and COPD Devices Market: By Applications
Hospital
Online Store
Medical Machinery Sales Center

Global Asthma and COPD Devices Market: Regional Analysis
The countries covered in the regional analysis of the Global Asthma and COPD Devices market report are U.S., Canada, and Mexico in North America, Germany, France, U.K., Russia, Italy, Spain, Turkey, Netherlands, Switzerland, Belgium, and Rest of Europe in Europe, Singapore, Malaysia, Australia, Thailand, Indonesia, Philippines, China, Japan, India, South Korea, Rest of Asia-Pacific (APAC) in the Asia-Pacific (APAC), Saudi Arabia, U.A.E, South Africa, Egypt, Israel, Rest of Middle East and Africa (MEA) as a part of Middle East and Africa (MEA), and Argentina, Brazil, and Rest of South America as part of South America.

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Competitive Landscape
Due to the presence of significant market participants, the market for devices for COPD and asthma is very competitive. AstraZeneca PLC, Boehringer Ingelheim GmbH, GlaxoSmithKline PLC, Novartis AG, Hoffmann-La Roche Ltd, Boehringer Ingelheim International GmbH, Merck & Co., Inc, Baxter International, Cipla Ltd, OMRON Healthcare Europe B.V, Teva Pharmaceutical Industries Ltd, PARI Medical Holding, Koninklijke Philips N.V., and Beximco Pharmaceuticals Ltd are some of the leading players.

Table Of Contents:
1 Report Overview

 1.1 Study Scope
 1.2 Key Market Segments
 1.3 Players Covered: Ranking by Asthma and COPD Devices Revenue
 1.4 Market Analysis by Type
 1.4.1 Global Asthma and COPD Devices Market Size Growth Rate by Type: 2023 VS 2032
 1.4.2 Inhaler
 1.4.3 Nebulizer
 1.5 Market by Application
 1.5.1 Global Asthma and COPD Devices Market Share by Application: 2023-2032
 1.5.2 Hospital
 1.5.3 Online Store
 1.5.4 Medical Machinery Sales Center
 1.6 Study Objectives
 1.7 Years Considered
 1.8 Overview of Global Asthma and COPD Devices Market
 1.8.1 Global Asthma and COPD Devices Market Status and Outlook (2017-2032)
 1.8.2 North America
 1.8.3 East Asia
 1.8.4 Europe
 1.8.5 South Asia
 1.8.6 Southeast Asia
 1.8.7 Middle East
 1.8.8 Africa
 1.8.9 Oceania
 1.8.10 South America
 1.8.11 Rest of the World
2 Market Competition by Manufacturers
 2.1 Global Asthma and COPD Devices Production Capacity Market Share by Manufacturers (2017-2022)
 2.2 Global Asthma and COPD Devices Revenue Market Share by Manufacturers (2017-2022)
 2.3 Global Asthma and COPD Devices Average Price by Manufacturers (2017-2022)
 2.4 Manufacturers Asthma and COPD Devices Production Sites, Area Served, Product Type
3 Sales by Region
 3.1 Global Asthma and COPD Devices Sales Volume Market Share by Region (2017-2022)
 3.2 Global Asthma and COPD Devices Sales Revenue Market Share by Region (2017-2022)
 3.3 North America Asthma and COPD Devices Sales Volume
 3.3.1 North America Asthma and COPD Devices Sales Volume Growth Rate (2017-2022)
 3.3.2 North America Asthma and COPD Devices Sales Volume Capacity, Revenue, Price and Gross Margin (2017-2022)
 3.4 East Asia Asthma and COPD Devices Sales Volume
 3.4.1 East Asia Asthma and COPD Devices Sales Volume Growth Rate (2017-2022)
 3.4.2 East Asia Asthma and COPD Devices Sales Volume Capacity, Revenue, Price and Gross Margin (2017-2022)

Acute COVID-19 appears to have a complex effect on asthmatics, being tempered by a number of interrelated disease-specific, demographic, and environmental factors. According to a study done in October 2020 titled "Impact of COVID-19 on people with asthma: a mixed-methods analysis from a United Kingdom-wide survey," those who reported having COVID-19 used their inhalers more frequently and had worse asthma management than those who did not. Additionally, according to a November 2021 article titled "Influence of the First Wave of COVID-19 on Asthma Inhaler Prescriptions," there were significant worries about the enormous demand for asthma inhalers during the start of the COVID-19 pandemic. It was discovered that there was a significant increase in inhalers just in March 2020 using the primary-care medical records of 614,700 asthma patients between January and June 2020.

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• Provision of market value (USD Billion) data for each segment and sub-segment
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• Analysis by geography highlighting the consumption of the product/service in the region as well as indicating the factors that are affecting the market within each region
• Competitive landscape which incorporates the market ranking of the major players, along with new service/product launches, partnerships, business expansions, and acquisitions in the past five years of companies profiled
• Extensive company profiles comprising of company overview, company insights, product benchmarking, and SWOT analysis for the major market players
• The current as well as the future market outlook of the industry with respect to recent developments which involve growth opportunities and drivers as well as challenges and restraints of both emerging as well as developed regions
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The Respiratory Device Accessories market reports provide a detailed analysis of area market expansion, competitiveness, global and regional market size and growth analysis. It also offers recent developments such as market share, opportunity analysis, product launch and sales analysis, segmentation growth, market innovation and value chain optimization and SWOT analysis. The latest reports on the market cover the current impact of COVID-19 on the market. This has brought about some changes in market conditions. Early and future assessments of rapidly changing Respiratory Device Accessories market scenarios and impacts are covered in the report.

Contrive Datum Insights analyses that the global Respiratory Device Accessories market to be growing at a CAGR of 9.5% in the forecast period of 2023-2030.

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Top Companies in the Global Respiratory Device Accessories Market:

Smiths Medical, Inc. (ICU Medical, Inc.), ResMed, Philips Healthcare, Mindray, Medtronic, Lowenstein Medical Technology, Hamilton Medical, Getinge, GE Healthcare, Fisher & Paykel Healthcare, Drager, BD, Armstrong Medical (Eakin Healthcare Group), Ambu A/

Recent Development:

Dragerwerk AG & CO. KGAA unveiled the Oxylog VE300, a newly developed emergency and transport ventilator that is especially well suited for use outside of the hospital environment, in May 2017.

Philips will release the PHILIPS RESPIRONICS E30 VENTILATOR in April 2020. As a result, the company will be able to assist healthcare professionals by offering high-quality ventilators.

Masimo Corporation purchased NantHealth’s Connected Care Business in January 2020. Through connectivity, automation, and breakthrough noninvasive monitoring technologies, Masimo will be able to aid hospitals in providing constant care.

This report segments the global market based on Types are:

Breathing Circuit

Filter

This report segments the global market based on Applications are:

Hospital

Household

Clinic

Regional Outlook: Regions covered in the market report is:

North America is anticipated to account for the largest market share due to the early adoption of advanced medical technologies, the rise in awareness, the rise in growth of the healthcare sector, and due to favorable compensation setting for many surgical procedures. According to the Centers for Disease Control and Prevention, in 2015, the number of deaths due to chronic lower respiratory diseases (including asthma) in the US were 155,041 and the number of adults diagnosed with chronic bronchitis was 8.9 million.

The European market is expected to hold the second largest market share. The market growth in this region can be attributed to the rising frequency of diabetic patients, an increasing number of surgeries, and the increasing demand for advanced treatment procedures. According to Eurostat statistics in 2014, there were nearly 382 thousand deaths in the European Union due to respiratory diseases. According to the Global Status Report on Non-Communicable Diseases, 2010 by the World Health Organization (WHO), smoking is predicted to cause about 71% of all lung cancer deaths and 42% of chronic respiratory diseases worldwide.

North America (U.S., Canada)

Europe (Germany, U.K., France, Italy, Russia, Spain, Rest of Europe)

Asia-Pacific (China, India, Japan, Australia, Southeast Asia, Rest of Asia Pacific)

South America (Mexico, Brazil, Argentina, Columbia, Rest of South America)

Middle East & Africa (GCC, Egypt, Nigeria, South Africa, Rest of Middle East and Africa)

Year Considered Estimating the Market Size:

  • Historical Years: 2017-2022
  • Base Year: 2023
  • Forecast Period: 2023-2030

 Significance of the report which makes it worth buying:

– A broad and precise understanding of Respiratory Device Accessories Industry is offered in the segmented form based on product types, applications, and regions.

– Respiratory Device Accessories Industry Drivers and challenges affecting the industry growth are presented in this report.

– Evaluating the market competition and planning the business strategies accordingly

– Understanding Respiratory Device Accessories Industry business plans, policies, technological advancements, and company profiles of top players.

Table of Contents:

Part 01: Executive Summary

Part 02: Scope of the Respiratory Device Accessories Market Report

Part 03: Global Market Landscape

Part 04: Global Respiratory Device Accessories Market Sizing

Part 05: Global Market Segmentation by Product

Part 06: Five Forces Analysis

Part 07: Customer Landscape

Part 08: Geographic Landscape

Part 09: Decision Framework

Part 10: Drivers and Challenges

Part 11: Market Trends

Part 12: Vendor Landscape

Part 13: Vendor Analysis

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Some of the key questions answered in this report:

Which are the key factors driving the Respiratory Device Accessories market?

What was and what will be the size of the emerging market in 2030?

Which region is expected to hold the highest market share in the market?

What trends, challenges, and barriers will impact the development and sizing of the global market?

What is the sales volume, revenue, and price analysis of top manufacturers of the market?

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In the course of our busy days, a bothersome cough or a faint wheeze may hardly be noticed but it is crucial to pay attention to even minor symptoms. Some individuals mistakenly believe that breathing difficulties are a natural part of ageing and these symptoms should be closely monitored since they may be the initial indications of lung diseases such COPD, asthma or lung cancer.

Understanding the early indicators of lung illness can help us be treated before the condition worsens or even becomes life-threatening. The moment you see any of the warning signals listed below, schedule a visit with your doctor very away as your life might be saved by early detection.

In an interview with HT Lifestyle, Dr Arvind Kate, Pulmonologist at Zen Multispecialty Hospital, talked about the different types of lung disease and said, “Numerous illnesses that affect the lungs are referred to as lung disease. Your body may not receive enough oxygen when you have lung illness.” According to him, the most typical pulmonary conditions affecting women are:

1. Asthma affects the bronchial tubes, which are the airways that move air into and out of the lungs. The airways become exceedingly sensitive, irritated, or swollen when you have asthma. Smoke, smog, mould, chemical sprays, and other irritants cause them to respond.

2. Emphysema and chronic bronchitis are two illnesses referred to as chronic obstructive pulmonary disease (COPD). They frequently occur in tandem. Both make breathing challenging and typically get worse with time.

3. Malignant lung cells proliferate abnormally and develop out of control in patients with lung cancer. These malignant cells have the capacity to spread across the body, infiltrate neighbouring tissues, or do both. Small cell and non-small cell lung cancer are the two main types. Non-small cell lung cancer is more common than small cell lung cancer and spreads more slowly.

Agreeing that lung disease's early warning symptoms are simple to ignore, he insisted that understanding the warning signals can enable you to get treatment before the problem worsens so, make an appointment with your healthcare professional if you have any of the following symptoms:

  • A change in an existing chronic cough, a new cough that persists or gets worse or both
  • Blood-producing cough
  • Coughing, laughing, or heavy breathing might cause chest, back, or shoulder pain that becomes worse
  • Sudden, unexpected shortness of breath that happens while doing ordinary tasks
  • Loss of weight without cause
  • Having a fatigued or weak feeling
  • Appetite loss
  • Persistent lung infections like pneumonia or bronchitis
  • Wheezing or a hoarse voice
  • Chronic Mucus Production: Much like a cough, mucus, also known as phlegm or sputum, is a physiological process that the body uses to defend itself against irritants or diseases. However, persistent mucus formation in the lungs is a symptom that the body is battling an infection and may be a sign of a more serious problem. Long-lasting coughs that produce mucus and continue for a month or more may indicate lung illness.
  • Blood in a cough: The upper respiratory tract or the lungs may be the source of blood in a cough. A bloody cough, regardless of where it originates, is an indication of a health issue, maybe a serious one.

There is no better moment than the present to begin paying attention to your lung health. Don't neglect regular health examinations or tests. Any issue with the respiratory system, including a lung injury or illness, can cause these symptoms. It's crucial to consult a lung expert if these symptoms don't go away so they can be diagnosed, treated, and any additional harm can be stopped.

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Introduction

Chronic obstructive pulmonary disease (COPD) is generally characterized by the presence of chronic bronchitis or emphysema that can lead to airway obstruction.1 It is a disease of the airways and lungs that is characterized by a progressive airflow limitation, which is not fully reversible and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases.2 This leads to poor airflow, cough, shortness of breath, and frequent exacerbations, which are often due to infections. In severe cases, it would progress into respiratory failure and pulmonary heart disease, which can have a significant impact on patient’s quality of life.3 COPD is a major cause of morbidity and mortality worldwide.4 Currently, it is the third leading cause of death5,6 and reported as the fifth-largest economic burden worldwide.7 The development of COPD is multifactorial and the risk factors of COPD include both genetic and environmental factors. Some important environmental factors are outdoor air pollution, cigarette smoking, occupational exposure to dust and fumes, biomass smoke inhalation, exposure to second-hand smoke, and previous tuberculosis.8 Interestingly, passive smoking and exposure to smoke from biomass fuel combustion for heating have also been involved in the development of COPD in women.9,10

The global prevalence of COPD is increasing with an estimated mean prevalence of 13% among the general population aged 40 years and above.11,12 Data on COPD prevalence from regions such as the Middle East are virtually absent or often based on inadequate definitions. One population-based` study observed a COPD prevalence of 3.5% in Middle Eastern populations based on reported symptoms of COPD or diagnosed COPD and smoking history. In a study among Saudi smokers aged more than 40 years in primary care clinics, the prevalence of spirometry-confirmed COPD was 14.2%. These regional studies suggest that individuals who are asymptomatic or who have never smoked are unlikely to receive an early diagnosis of COPD, and the true prevalence of the disease is thus underestimated.13–15 There is a low level of awareness of COPD reported among smokers in Saudi Arabia.16 This lack of awareness probably contributes to the marked underdiagnosis of the disease, which is apparent virtually everywhere in the world, although to various degrees. Studies have shown that health education regarding COPD is insufficient not only in general population but also among disease sufferers17 and even the family members of patients who have COPD.18,19

The high prevalence of smoking in Saudi Arabia, the low number of chest physicians, and poor compliance with the COPD guidelines increase the burden of respiratory diseases such as COPD.12,13 The prevalence of COPD will increase even further, unless broad and effective preventive measures are implemented. Hence, awareness is crucial to promote prevention by smoking cessation, enable early diagnosis, and tailor treatment accordingly.12 The increase in awareness of the disease, treatment, and management in the populations shall result in better COPD care and management.13 In fact, lack of knowledge about COPD is one of the major barriers regarding combating against COPD.20 There is a need to conduct more epidemiological studies regarding COPD.21 Decreasing the incidence of COPD would substantially benefit the overall health of the individuals.7 Many individuals can prevent themselves from the disease or get the right treatment at the right time if they know about the disease. To the best of our knowledge, there is no published data or study about the knowledge of COPD and its risk factors among the general population of Saudi Arabia, especially in the Aseer region. Epidemiological studies are urgently needed22 to assess the prevalence of COPD in the region to determine the baseline, against which the future trends in the risk factor levels can be assessed and preventive strategies be planned to promote health among the populations. Therefore, this study was undertaken to assess the awareness of COPD and its risk factors among the adult population in the region.

Materials and Methods

Study Area and Population

The descriptive cross-sectional study was conducted in the Aseer Region, the southern of the Kingdom of Saudi Arabia. The general adult population aged 18 years and above living in the Aseer region during the study period from 1st August 2021 to 31st May 2022 was included.

Sample Size and Technique

All conveniently accessible populations who are fulfilling the eligibility criteria were invited to participate in the study. A minimum sample of 385 was targeted, using the formula.

n = (z)2 p (1 – p)/d2

where Sample size = n, p = 50%, the confidence level 95%, so Z score = 1.96, margin of error (E)=5% and Population 100,000.

The necessary calculated sample was 385 individuals.

Non-probability sampling technique, ie convenience sampling, was used. Patients were included based on their easy availability and willingness to participate in our research project.

Inclusion and Exclusion Criteria

All adult patients aged 18 years and above currently living in the Aseer region were included. Those below 18 years of age and not willing to participate in the study were excluded.

Ethical Approval and Data Collection

Approval was obtained from the Research Ethics Committee of King Khalid University, Aseer, KSA. Data was not disclosed for patient confidentiality. The use of these confidential data in this research project was reviewed and approved by the research ethics committee. The collected data was kept safely in a password-protected cloud.

An anonymous, self-explanatory, questionnaire was designed to assess the knowledge of COPD among the participants. The online questionnaire was prepared in both English and Arabic language using Google forms and distributed among participants through social media and E-mail as face-to-face interviews had to be avoided following the social distancing norms enforced by the government. Electronic voluntary informed consent was attached before the questionnaire in the provided links, and the participants had approved before filling the questionnaire. A pilot study was conducted on 20 participants, to increase the credibility of the questionnaire. The pilot responses were excluded from the final responses of the study. The questionnaire was categorized into the following parts: (1) Demographics and general characteristics were obtained. (2) Awareness of COPD: information was obtained through closed-ended questions that should be answered only in “Yes”, “No” or “Don’t know”.

Data Management and Analysis Plan

The collected data were coded and entered into an Excel software (Microsoft office Excel 2010) database. Data were analyzed using Statistical Package for Social Sciences, version 16.0 (SPSS, Inc., Chicago, IL, USA). Data were presented in descriptive statistics like, frequency and percentage as appropriate.

Tests of significance like the Chi-square test are applied to find out the statistical significance of the difference in percentages. Univariate analysis was done using respondent awareness about COPD as the dependent variable and the sociodemographic and behavioral factors were identified as independent variables. A p-value of <0.05 was taken as statistically significant for the calculations of variables.

Results

Out of 385 respondents, 10.9% were cigarette smokers, 9.9% were electronic smokers and 9.1% were shisha smokers. Majority

(36.4%) of respondents usually spent time or sat with their smoker friends. Dust exposure (26.2%) was the second most common form of risk among the respondents. A higher proportion of the respondents used heating devices based on coal (19.0%), followed by those who spent time in a shisha cafe (11.7%) (Figure 1).

Figure 1 Distribution of study population based on their type of exposure to smoke/dust.

In the present study, it was observed that less than one-third (116, 30.12%) of the study population had ever heard about COPD. Among all, 223 (57.3%) respondents had never heard and 46 (11.9%) respondents did not know anything about COPD. Figure 2 also shows the percentage of respondents who knew about the primary organ affected by COPD (116, 30.12%). Among those who had heard about COPD (n = 116), when queried “Which organ is affected by COPD?”, 92 (79.3%) correctly responded lungs, 12 (10.3%) responded heart, nine (7.7%) responded trachea, one (0.8%) responded throat, and two (1.7%) did not know (Figure 2).

Figure 2 Distribution of the respondents based on their awareness about COPD and their knowledge of the primary organ affected by COPD.

Only 1.3% of respondents self reported that they had been diagnosed with COPD. All those diagnosed with COPD were Saudi males, were aged between 18 and 39 years and the majority of them were smokers (80%) (Figure 3).

Figure 3 Percent distribution of respondents ever diagnosed with COPD.

Table 1 illustrates the association of respondents who had ever heard of COPD with their sociodemographic status. Almost 99% were Saudi nationals. The majority of respondents were aged between 18 and 29 years out of which 41.9% had ever heard of COPD. A higher proportion of male (41.1%) respondents had heard of COPD as compared to the female respondents (17.4%). A higher proportion of the respondents were unmarried (n = 211) followed by married (n = 170), out of which 89 (42.2%) unmarried and 25 (14.7%) married respondents had ever heard of COPD. More than fifty percent of respondents had an income of less than 5000 SAR. Nearly 37.8% of them had heard of COPD. Almost more than three-fourth of respondents were having a higher university degree. However, only 31.9% of respondents from the university level had ever heard of COPD. Most of the respondents were students (41.03%) and officers (39.2%). Sociodemographic variables such as age group, sex, marital status, income, and occupation showed a significant association with awareness of COPD.

Table 1 Association Between Socio-Demographic Variables and Awareness of COPD Among Respondents

Table 2 illustrates the association between respondents smoking behaviours (cigarette smoker, shisha smoker, electronic smoker, spending time or sit with smokers, spending time in shisha cafes), heating devices based on coal and exposure to dust with awareness of COPD. The study outcome reported that smoking behaviours were not found to be statistically significant, whereas only respondents having exposure to dust were found statistically significant among those who had ever heard of COPD. Among smokers, cigarette smoking was more common among respondents. The majority of respondents (140/385, 36.3%) spent time or sitting with smokers, out of which 35.7% had heard about COPD. Out of 385 respondents, only 101 (26.2%) were exposed to dust. Among those who were exposed to dust, one-fifth of respondents had ever heard of COPD.

Table 2 Association Between Smoke and Dust Exposure and Awareness of COPD

Table 3 represents awareness of the respondents pertaining to COPD. Among those who were aware of COPD (n = 116), the most common symptom known was cough (52.17%) followed by shortness of breath (39.6%). Out of a total of 116 respondents who had heard of COPD, nearly 41.4% knew that COPD is exclusive because of progress in age, COPD is expensive for society more than lung cancer (49.0%), cigarette smoking affects COPD (34.5%), COPD is fully recoverable with short-term use of antibiotics (35.0%), COPD is rare (18.8%), COPD lasts more than 18 months (48.1%), COPD can get worse with smoke exposure (37.4%), COPD can lead to disability (46.7%), and quitting smoking has an important role in preventing COPD (34.0%).

Table 3 Respondents Answers Pertaining to Awareness of COPD

Discussion

Chronic obstructive pulmonary disease is one of the commonest diseases among smokers and passive smokers as well. It affects the lungs and causes breathing difficulties hence having an impact on the daily adjusted life years (DALYs) of patients. StigHagstad et al reported the prevalence of COPD in Sweden, which showed that among non-smokers prevalence was found to be 7.7%, whereas among smokers it was 18.3%.23

DD Ghorpade et al reported that 99.1% of the Indian population never heard of the word COPD, whereas only 0.9% heard about COPD. Out of the population who heard about COPD 72% think that the lungs, 6% think that the heart is affected by COPD, whereas 22% do not know which organ is affected by COPD.24 While our study reported that 30% had heard the term COPD, about 57.9% of the population never heard, and 11.9% did not know about COPD. Out of 30% of the population who heard had about COPD, 79.3% thought that it affects the lungs, 7.7% thought that it affects the heart, 10.34% thought that it affects the throat, 1.72% thought trachea, and 0.86% did not know about the organ affected by COPD.

Awareness of COPD in our study is almost similar to the study conducted by MasaharuAsai et al which showed 21.3% awareness in the Japanese population.25 A population-based study in north-eastern Italy had a prevalence of COPD at about 6.8% according to self-reported physician diagnosis.26

Data obtained from the National Health and Nutrition Examination Survey (NHANES) reported an age-standardized prevalence of self-reported COPD of about 3.47%,27 whereas in our study we found that only 1.30% of respondents were ever diagnosed with COPD. About 14.33% have mineral dust exposure and 5.2% have exhaust fumes exposure. However, more than half of our respondents also believe that COPD is not a rare disease. The difference might be associated with the awareness, exposure to the risk factors, or even correct diagnosis by the physicians. Cigarette smokers are thought to be the most at risk of developing COPD. However, recent studies have shown that people with life-long exposure to biomass smoke are also at high risk of developing COPD. Most common in developing countries, biomass fuels such as wood and coal are used for cooking and heating indoors daily. Women and children have the highest amounts of exposure and are therefore more likely to develop the disease. Despite epidemiological studies providing evidence of the causative relationship between biomass smoke and COPD, there are still limited mechanistic studies on how biomass smoke causes, and contributes to the progression of COPD.28 Among nonsmokers, there is 10.2% environmental tobacco exposure (ETS) at home and 12.6% have ETS in public places and 20.3% have exposure in dedicated spaces.29

According to our study awareness of COPD was more among the Saudi population than the non-Saudis. This can be attributed to the fact that the newly arrived expatriates might not be aware of the health care programs available in the Kingdom. In our study, about 41.9% of the population who were aware of COPD belonged to the 18–29 years of age group, and those who have university education 31.9% were also more aware than higher education 24%, which is showing the direct relationship of educational status with awareness regarding COPD. The majority of our respondents also believe that COPD is an age-related disease in this study. This reflects that they also think that as age progresses COPD worsens. In Saudi Arabia, the prevalence of smoking (cigarettes and waterpipes) is estimated to be 20%, compared with 16.2% in Canada, 16.8% in the United States, 14.7% in Australia, and 12.1% in Qatar.30 Majority of Saudi smokers are of young age as well and its prevalence keeps on rising among young adolescents, which is quite alarming.31 Household air pollution is generated from cooking and heating using biomass and coal, collectively known as solid fuels. Exposure to household air pollution, including dust, heating devices, wood, coal, and fuel burning, is associated with increased prevalence and mortality of COPD.32

Household air pollution is considered one of the primary risk factors for non-smoking-related COPD especially in low- and middle-income countries.33 In our study, we found that 19% of our respondents have exposure to heating devices and 26.2% have exposure to dust. This is alarming in terms of the development of COPD in the future, and suitable preventive measures should be taken for such people. According to the 2018 National Health Interview Survey (NHIS), 27.6% of the population were smokers, 12.0% of females, and 15.6% of males were current cigarette smokers in adults aged ≥18 years in the United States.34

Among our study population, about 29.9% of total respondents were having tobacco smoke exposure, 10.9% were cigarette smokers, 9.9% were electronic smokers, and 9.1% were shisha smokers. These exposures keep them at high risk to the development of respiratory diseases including COPD, whereas 19.4% of Spanish general population was smoker.35

Electronic cigarettes (e-cigarettes) are battery-operated electronic nicotine devices, which consist of a mouthpiece (to inhale), a power source, a heating element (atomizer), and a disposable cartridge or refillable tank with liquid solution (e-liquid). The e-liquid contains propylene glycol, glycerin, nicotine, and flavor chemicals. Upon puffing-activated heating, the e-liquid is atomized, and the smoker inhales the resulting aerosol or vapor. These chemicals are well-known causative agents for the development of not only respiratory diseases but also cancers.36 Cai et al reported that in August 2018, the FDA declared e-cigarette use in youth an epidemic thereafter several immediate actions were taken to establish new policies aimed at preventing youth access to e-cigarettes. These actions and their implementations should be conducted by the Ministry of the health of Saudi Arabia as well to prevent youth from using e-cigarettes and their health hazards.37 Not only active smoking, shisha, and e-cigarettes, passive smoking also causes COPD. StigHagstad et al reported that passive smoking through environmental exposure to smoke (ETS) ever at home was associated with a higher prevalence of COPD compared with non-exposed subjects (8.0% vs 4.2%, P 5 0.004).29

A large percentage 36.4% of our study population usually spend time or sit with his/her smoker friends, 19.0% were in habit of using heating devices based on coal and 11.7% spend time in shisha cafes. So a total of 67.1% of our study population have exposure to passive smoking. This is proven to be as dangerous as smoking itself and imposes bad health outcomes in the future. The majority of our respondents who were aware of COPD think that it affects the throat (50%), heart (42.9%), and trachea (40%), whereas in another study by Ghorpade et al respondent’s knowledge was more about the lung (71.4%) as an affected organ for COPD. About 34.5% think that it is caused by smoking.24

Mohigefer et al reported that medical student’s knowledge regarding commonest symptom was dyspnea (80.3%) and giving up smoking prevented worsening of COPD (96.6%), whereas in our general population of respondents they think cough was 52% as the commonest symptom of COPD and dyspnea thereafter (39.66%).38 About 30% of people think that quitting smoking can prevent COPD in our study. The difference in knowledge regarding common symptoms is obvious because among the general population idea about COPD is not much understood as compared to medical students. This imposes great responsibility on health care professionals about public health education regarding COPD and quitting smoking.

Nearly half of our respondents think that COPD lasts a maximum of 18 months, 37.4% think that further smoke exposure worsens the COPD and 46.7% think that it can cause disabilities. Almost half of our respondents also think that the treatment of COPD is very expensive even more than the treatment of cancer. This is comparable to another study where majority of respondents (80%) believe that life expectancy is about 14 years among patients with COPD, 85% believe that it causes arrhythmias and 88% think it can cause lung cancer as well.39 In the previous study, it is been shown that severity of COPD increases with progressive age.40 Age is one of the concomitant factors regarding worsening COPD.41

In 2015, COPD caused 2.6% of global disability-adjusted life years (DALYs) and ranked eighth globally, and recently, it is reported as the fifth-largest economic burden worldwide.7,42 These figures reflect that there is a need to provide correct information to the people about the disease itself and lifelong consequences including the impact on disability-adjusted life years as well which a patient might face in their life if having COPD. It increases the importance of avoidance of risk factors for COPD for prevention and control of the disease.

Almost half of our respondents also think that the treatment of COPD is very expensive even more than the treatment of cancer. More than half of the respondents also believe that it cannot be cured with the use of antibiotics. Trends were observed in multiple studies of direct and healthcare costs for European countries measured by patient and year, where the higher costs were associated with more severe COPD and a frequent history of exacerbations. The highest costs reported corresponded to hospitalizations and the associated pharmacological treatment. The importance of the loss of productivity and premature retirement within the profile of the COPD patient was also highlighted as the main generator of indirect costs of the disease.43 However, we can also enumerate in future studies that web-based interventions might be beneficial for the health education regarding COPD.44

Our study has a few limitations. The cross-sectional nature of this study and convenience sampling used cannot confirm the causality association between the compared variables. The self-reported responses could over or underestimate the results. Also, the subjects for the study were chosen from a particular region, and thus they may not have been the representatives of the entire Kingdom. Considering that patients were included through social media, there could be a high risk of selection bias toward younger people and from a high social class. However, our study area had a representative mix of subjects, with all the different age groups and socioeconomic classes. A larger nationwide study can be conducted involving different regions to know the trends of the increasing blood COPD among the general population. However, making an attempt to assess the awareness of COPD in the general population in Saudi Arabia is the strength of our study. Most of the previous studies have been conducted in health professionals before.45,46

Conclusion

In the present study, we found that less than one-third of the study population had ever heard about COPD. Nearly one-third spent time or sat with smokers. A higher percentage of population was cigarette smokers (10.9%), followed by electronic smokers (9.9%) and shisha smokers (9.1%). The awareness regarding the disease was low among the respondents. Only 34.0% correctly knew that quitting smoking has an important role in preventing COPD. This study projects an urgent need of improving awareness of COPD and its risk factors in the general population. This subject should be strengthened in the curriculum and discussed in public campaigns and seminars. Further nationwide study is required to help the policymakers for implementing suitable preventive and curative strategies to promote the pulmonary health of the population.

Funding

The authors extend their appreciation to the Deanship of Scientific Research at King Khalid University, Saudi Arabia for funding this work through Small Groups Project under grant number RGP.1/62/43.

Disclosure

The authors report no conflicts of interest in this work.

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9. Beeh KM, Kornmann O, Beier J, et al. Clinical application of a simple questionnaire for the differentiation of asthma and chronic obstructive pulmonary disease. Respir Med. 2004;98(7):591–597. doi:10.1016/j.rmed.2004.01.004

10. Sana A, Somda SMA, Meda N, Bouland C. Chronic obstructive pulmonary disease associated with biomass fuel use in women: a systematic review and meta-analysis. BMJ Open Respir Res. 2018;5(1):e000246. PMID: 29387422; PMCID: PMC5786909. doi:10.1136/bmjresp-2017-000246

11. Seo JY, Hwang YI, Mun SY, et al. Awareness of COPD in a high risk Korean population. Yonsei Med J. 2015;56(2):362–367. doi:10.3349/ymj.2015.56.2.362

12. Tinkelman DG, Price D, Nordyke RJ, et al. COPD screening efforts in primary care: what is the yield? Prim Care Respir J. 2007;16:41–48. doi:10.3132/pcrj.2007.00009

13. Kögler H, Metzdorf N, Glaab T, et al. Preselection of patients at risk for COPD by two simple screening questions. Respir Med. 2010;104(7):1012–1019. doi:10.1016/j.rmed.2010.01.005

14. Pinkerton M, Chinchilli V, Banta E, et al. Differential expression of microRNAs in exhaled breath condensates of patients with asthma, patients with chronic obstructive pulmonary disease, and healthy adults. J Allergy Clin Immunol. 2013;132(1):217–219. doi:10.1016/j.jaci.2013.03.006

15. Tan WC, Sin DD, Bourbeau J, et al.; Can COLD collaborative research group. Characteristics of COPD in never-smokers and ever-smokers in the general population: results from the CanCOLD study. Thorax. 2015;70(9):822–829. doi:10.1136/thoraxjnl-2015-206938.

16. Alhomayani FKH, Almalki SH, Alqahtani M, Almalki AH. Awareness of Chronic Obstructive Pulmonary Disease (COPD) among smokers in Saudi Arabia: a cross-sectional study. Am J Med Sci Med. 2019;7(5):184–189.

17. Raptis DG, Rapti GG, Papathanasiou IV, Papagiannis D, Gourgoulianis KI, Malli F. Level of knowledge about COPD among patients and caregivers. In: GeNeDis 2020. Cham: Springer; 2021:299–305).

18. Lee SH, Lee H, Kim YS, Park HK, Lee MK, Kim KU. Predictors of low-level disease-specific knowledge in patients with chronic obstructive pulmonary disease. Int J Chron Obstruct Pulmon Dis. 2020;15:1103. doi:10.2147/COPD.S244925

19. Robinson SA, Cooper JA, Goldstein RL, et al. A randomised trial of a web-based physical activity self-management intervention in COPD. ERJ Open Res. 2021;7(3):00158–2021. doi:10.1183/23120541.00158-2021

20. O’Toole J, Krishnan M, Riekert K, Eakin MN. Understanding barriers to and strategies for medication adherence in COPD: a qualitative study. BMC Pulm Med. 2022;22(1):1–8. doi:10.1186/s12890-022-01892-5

21. Golpe R, Dacal-Rivas D, Blanco-Cid N, Castro-Añón O. Need for epidemiological studies on chronic obstructive pulmonary disease in Rural Spain. Arch Bronconeumol. 2021;1:S0300–2896.

22. Price DB, Yawn BP, Jones RCM. Improving the differential diagnosis of chronic obstructive pulmonary disease in primary care. Mayo Clin Proc. 2010;85(12):1122–1129. doi:10.4065/mcp.2010.0389

23. StigHagstad H, Backman AB, Ekerljung L, et al. Prevalence and risk factors of COPD among never-smokers in two areas of Sweden e Occupational exposure to gas, dust or fumes is an important risk factor. Respir Med. 2015;109(11):1439–1445. doi:10.1016/j.rmed.2015.09.012

24. Ghorpade DD, Raghupathy A, Londhe JD, et al. COPD awareness in the urban slums and rural areas around Pune city in India. NPJ Prim Care Respir Med. 2021;31(1):6. doi:10.1038/s41533-021-00220-4

25. Asai M, Tanaka T, Kozu R, et al. Effect of a Chronic Obstructive Pulmonary Disease (COPD) intervention on COPD awareness in a regional city in Japan. Intern Med. 2015;54(2):163–169. doi:10.2169/internalmedicine.54.2916

26. Guerriero M, Caminati M, Viegi G, et al. COPD prevalence in a north-eastern Italian general population. Respir Med. 2015;109(8):1040–1047. doi:10.1016/j.rmed.2015.05.009

27. Doney B, Kurth L, Halldin C, et al. Occupational exposure and airflow obstruction and self-reported COPD among ever-employed US adults using a COPD-job exposure matrix. Am J Ind Med. 2019;62(5):393–403. doi:10.1002/ajim.22958

28. Capistrano SJ, van Reyk D, Chen H, et al. Evidence of biomass smoke exposure as a causative factor for the development of COPD. Toxics. 2017;5(4):36. doi:10.3390/toxics5040036

29. Hagstad S, Bjerg A, Ekerljung L, et al. Passive smoking exposure is associated with increased risk of COPD in never smokers. Chest. 2014;145(6):1298–1304. doi:10.1378/chest.13-1349

30. Alsubaiei ME, Cafarella PA, Frith PA, et al. Factors influencing management of chronic respiratory diseases in general and chronic obstructive pulmonary disease in particular in Saudi Arabia: an overview. Ann Thorac Med. 2018;13(3):144–149. doi:10.4103/atm.ATM_293_17

31. Moradi-Lakeh M, El Bcheraoui C, Tuffaha M, et al. Tobacco consumption in the Kingdom of Saudi Arabia, 2013: findings from a national survey. BMC Public Health. 2015;15(1):611. doi:10.1186/s12889-015-1902-3

32. Siddharthan T, Grigsby MR, Goodman D, et al. Association between household air pollution exposure and chronic obstructive pulmonary disease outcomes in 13 Low- and middle-income country settings. Am J Respir Critic Care Med. 2018;197(5):611–620. doi:10.1164/rccm.201709-1861OC

33. Gut-Gobert C, Cavailles A, Dixmier A, et al. Women and COPD: do we need more evidence? Eur. Respir. Rev. 2019;28(151):180055. doi:10.1183/16000617.0055-2018

34. Creamer MR, Wang TW, Babb S, et al. Tobacco product use and cessation indicators among adults — United States, 2018. MMWR Morb Mortal Wkly Rep. 2019;68:1013–1019. doi:10.15585/mmwr.mm6845a2

35. Rubio MC, Hermosa JL, Miravitlles M, López-Campos JL. Knowledge of chronic obstructive pulmonary disease, presence of chronic respiratory symptoms and use of spirometry among the Spanish population: CONOCEPOC 2019 study. Arch Bronconeumol. 2021;57(12):741–749. doi:10.1016/j.arbr.2021.10.003

36. Centers for Disease Control and Prevention [CDC] (2019b). Outbreak of lung injury associated with the use of E-cigarette, or vaping, products. Available from: www.cdc.gov/tobacco/basic_information/e-cigarettes/severe-lung-disease.html. Accessed November 5, 2019.

37. Cai H, Garcia JGN, Wang C. More to add to E-cigarette regulations: unified approaches. Chest. 2020;157(4):771–773. doi:10.1016/j.chest.2019.11.024

38. Mohigefer J, Calero-Acuña C, Marquez-Martin E, et al. Understanding of COPD among final-year medical students. Int J Chron Obstruct Pulmon Dis. 2017;13:131–139. doi:10.2147/COPD.S138539

39. Akshaya A, Priya VV, Don KR, et al. Awareness on risk factors of Chronic Obstructive Pulmonary Disease (COPD) among college students. Eur J Mol Clin Med. 2020;7(1):2681–2699.

40. Fathima M, Bawa Z, Mitchell B, Foster J, Armour C, Saini B. COPD management in community pharmacy results in improved inhaler use, immunization rate, COPD action plan ownership, COPD knowledge, and reductions in exacerbation rates. Int J Chron Obstruct Pulmon Dis. 2021;83:519. doi:10.2147/COPD.S288792

41. Elsa LP, Justo G, Blanca L. Patient’s awareness on COPD is the strongest predictor of persistence and adherence in treatment-naïve patients in real life: a prospective cohort study. BMC Pulm Med. 2021;21(1):1. doi:10.1186/s12890-020-01377-3

42. GBD 2015 Chronic Respiratory Disease Collaborators. Global, regional, and national deaths, prevalence, disability-adjusted life years, and years lived with disability for chronic obstructive pulmonary disease and asthma, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet Respir Med. 2017;5(9):691–706. Erratum in: Lancet Respir Med. 2017 Oct;5(10): e30.PMID: 28822787; PMCID: PMC5573769. doi:10.1016/S2213-2600(17)30293-X

43. Gutiérrez Villegas C, Paz-Zulueta M, Herrero-Montes M, et al. Cost analysis of chronic obstructive pulmonary disease (COPD): a systematic review. Health Econ Rev. 2021;11(1):31. PMID: 34403023; PMCID: PMC8369716. doi:10.1186/s13561-021-00329-9

44. Mongiardo MA, Robinson SA, Finer EB, Rivera PN, Goldstein RL, Moy ML. The Effect of a web-based physical activity intervention on COPD knowledge: a secondary cohort study. Respir Med. 2021;190(190):106677. doi:10.1016/j.rmed.2021.106677

45. Alshahrani A, Gautam AP, Aseeri F, et al. Knowledge, attitude, and practice among physical therapists toward COVID-19 in the Kingdom of Saudi Arabia—A cross-sectional study. Healthcare. 2022;10(1):105. doi:10.3390/healthcare10010105

46. Asdaq SMB, Alshrari AS, Imran M, Sreeharsha N, Sultana R. Knowledge, attitude and practices of healthcare professionals of Riyadh, Saudi Arabia towards covid-19: a cross-sectional study. Saudi J Biol Sci. 2021;28(9):5275–5282. doi:10.1016/j.sjbs.2021.05.036

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False Facebook adverts with millions of views have been touting a "lung cleansing syrup" for a host of diseases from asthma to pneumonia, claiming the product has been approved by the Philippine Food and Drug Administration (FDA). However, the FDA had earlier warned against consuming the product as it has not been tested for safety and efficacy. A pulmonologist told AFP no single medication can cure the diseases mentioned in the false posts.

"GOODBYE TO ASTHMA - PNEUMONIA - BRONCHITIS - C.O.P.D. AT HOME AFTER SEVEN DAYS," reads the text overlay on a video shared on Facebook on November 25, 2022.

The text "FDA approved" can be seen at the bottom of the video, which has been viewed more than a million times.

It shows a man in a lab coat touting a syrup called "BO PHOI TRITYDO". He claims the product can "clean the lungs".

The post's caption makes similar claims about "BO PHOI TRITYDO".

Asthma is a condition caused by the swelling of breathing tubes. It has no cure but its symptoms can be treated with inhalers or other medication.

Pneumonia is an infection of the lungs caused by bacteria, viruses or fungi. Treatment depends on the cause.

Bronchitis is the inflammation of the lung's main air passages. Acute bronchitis is treated with medication, while chronic bronchitis has no cure although symptoms could be reduced through treatment.

Chronic obstructive pulmonary disease (COPD) refers to a group of diseases that occur when the lungs become inflamed and damaged. There is no cure but treatment helps manage symptoms.

Screenshot of the false post taken on January 4, 2023

Similar posts advertising the syrup for these diseases have been viewed over three million times on Facebook here, here, here and here.

Comments on the posts suggest some users believed the claim and wanted to buy the product.

"Can it be taken by a 1-and-a-half-year-old baby with primary complex?" one user asked.

"I have pneumonia, is this a good replacement for maintenance drugs? I'll try this," another wrote.

The posts, however, are false.

Not FDA-approved

In an advisory issued on April 11, 2022, the FDA warned against purchasing and consuming "BO PHOI TRITYDO Herbal Supplement".

It said the product had "not gone through evaluation process of the FDA".

"The agency cannot assure its quality and safety," the advisory reads.

Keyword searches on the FDA's food and drug databases have not found results for the product as of January 6, 2023.

'No cure-all medication'

Dr Mithi Zamora, a Manila-based doctor, told AFP on January 4 there is no "one-size-fits-all solution or medication" that can cure the diseases mentioned in the false posts.

"We definitely do not recommend this. There is no evidence to support its recommendation for the general public's consumption," Zamora said.

"Because we don't know this medication, we cannot tell if they also have potential side effects that can be detrimental to the consumer or the patient."

AFP has previously debunked social media posts promoting unregistered products here, here, here, here and here.

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Report Highlights:

  • Every year, over 150,000 Americans die of chronic obstructive pulmonary disease (COPD), which equals one death every 4 minutes [9].
  • Smoking tobacco causes 75% of COPD deaths, while 25% of the people diagnosed with this condition have never smoked [9].
  • People who have never smoked cigarettes in the last 30 days have a 67% lower COPD prevalence, while former users and cigar users have a 43% and 54% lower prevalence of COPD, respectively [37].
  • In 2019, COPD was the third principal cause of death globally at 5.8%, right behind stroke and ischaemic heart disease [13].
  • The average age at death from COPD between 2000 and 2005 was 76.6 years compared to 72.9 years in 1980-85 [4].
  • 7.3% of COPD patients will live 15 years after admission for worsening COPD compared to 40.6% of the general population of the same age and sex [46].
  • Hospitalized COPD patients have an 82% lower survival rate in the next 15 years after admission for worsening COPD than people in the general population [46].
  • COPD is more prevalent in females at 7.1% than in males at 5.7% because women smokers have a 50% greater likelihood of developing COPD than men [2, 3].
  • According to a Danish study, it takes 25 years of smoking to develop COPD. The data shows that at least 25% of smokers who had no COPD symptoms will develop clinically significant COPD [23].
  • On average, it takes three to five months for the patient to learn whether they qualify for COPD disability and an additional five months to receive the first payment [7].

Chronic obstructive pulmonary disease (short: COPD) encompasses several chronic respiratory diseases characterized by airflow blockage and difficulty breathing [28].

The two main conditions that fall under the term COPD are chronic bronchitis and emphysema. Together with asthma, all these conditions (including COPD) are known as chronic lower respiratory diseases (CLRD) [20].

We’ve gathered the most interesting and helpful statistics about COPD to shed light on this condition.

COPD Prevalence & Mortality Demographics and Statistics

In the United States, every 46.3 deaths out of 100,000 people are attributed to COPD [5].

 

Call out text box saying 43.6 deaths in 100,000 people come from COPD.

According to the World Health Organization, 3.23 million people died of COPD in 2019 — making this condition the third leading cause of death globally [8].

Millions of people around the globe die from COPD every year, as this disease remains a significant global burden. It’s alarming that this condition remains undiagnosed and untreated in millions more.

How Many Deaths Does COPD Cause?

More than 150,000 Americans lose their lives from COPD within a year, which equals one death every 4 minutes [9].

The total number of deaths from chronic lower respiratory diseases (CLRD) was higher in 2018 than in 2020. In 2020, 152,657 people died of CLRD compared to 2018 at 159,486, making these conditions the sixth and fourth main cause of death in the US, respectively [5].

Call out text box saying 139,585 people died every year due to COPD between 1999 and 2020.

In 2017, 160,201 people died of COPD, making it the year with the most deaths from 1999 through 2020. This year is followed by 2018 with 159,486 deaths and 2019 with 156,979 deaths. Among the top five years of death from COPD are 2015, with 155,041 people, and 2016 with 154,596 people [5].

In 2004, 121,987 people died of COPD, making it the year with the lowest number of deaths between 1999 and 2020. With 122,009 and 123, 013 COPD deaths, 2000 and 2001 follow suit, respectively [5].

Compared to 1999, 28,476 more people died of COPD in 2020, which shows the increase in the number of deaths within this period [5].

8,924 more people have died of COPD in 2005 than in 2000, while 7,147 more died in 2010 than 2005. In 2015, 16,961 more people lost their lives to COPD than in 2010, while fewer people (2,384) died of COPD in 2020 than in 2015 [5].

Most (85.58%) COPD deaths occur among those aged 65 years or older with a total of 2.6 million deaths from 1999 through 2020 [5].

COPD Mortality Statistics In the United States

COPD is a principal cause of mortality and morbidity in the United States. The average age at death from COPD in the period between 2000-05 was 76.6 years [4]. The main cause of COPD and COPD deaths is tobacco smoking [40].

What’s the Average Age At Death from COPD?

Between the 1980-85 period, the average age at death from COPD was 72.9 years, while between 2000-05, it rose to 76.6 years. The 3.7 age increase indicates that COPD patients don’t die as young as four decades ago. This may be connected to early diagnosis, prompt treatment, and a decline in tobacco smoking [4].

Scatter plot showing an increase in the average age at death in COPD patients for 3.7 years between the 80s and 00s.

This data comes from the Journal of Chronic Obstructive Pulmonary Disease, which states that there was an increase in the average age at COPD death for three to four years between 1980 and 2005 [4].

What Is the Most Common Cause of Death in COPD Patients?

Studies show that 75% of COPD deaths are attributed to cigarette smoking [9]. This is unsurprising as one in five smokers will develop COPD throughout their lives [33].

Despite the danger COPD presents, data shows that 38% of the nearly 16 million U.S. adults with a COPD diagnosis are current smokers [31].

The fact that puzzles researchers is that 25% of the people who die of COPD have never smoked in their life [9].

Stacked bar showing COPD deaths in smokers (75%) and never smokers (25%).

People who have never smoked have a 67% lower COPD prevalence. The prevalence of COPD is also lower in former cigarette users at 43% and in cigar users at 54% [37].

Former cigarette users have a 72% higher prevalence of COPD compared to people who have never smoked cigarettes [37].

A study published in BM Pulmonary Medicine investigated the exclusive use of cigarettes within the past 30 days. It revealed that tobacco smoke is fundamental for the development and progression of COPD [37].

COPD Deaths Demographics

Of the 152,657 COPD deaths in 2020, women make up the most with 79,715 people. COPD deaths are also the highest among older people aged 75-79 with 25,311 and Whites with 130,947 [5].

COPD Deaths Statistics: Male vs. Female

More women died of COPD (79,715) than men (72,942) in 2020, says data from the Centers for Disease Control and Prevention [5].

The percentage of COPD deaths is higher in females at 52.22% than in males at 47.78%, but men have 9.3 lower percentage points of survival than women. Studies show that male COPD patients who are intubated are more likely to die in the long run than female patients [45].

The crude death rate per 100,000 people is 47.7 for females compared to 45.0 for males [5].

The crude death rate indicates the number of COPD deaths during the year per 100,000 midyear population.

USA map showing that of all states, West Virginia has the highest rate of COPD deaths (90.1), while California has the highest number of deaths (12,907).

Females with severe COPD have a 50% increased risk of hospitalization and a greater risk of death from respiratory complications than males. Females’ lung anatomy, low estrogen levels, and late diagnosis may be important risk factors for these, says a study published in the American Journal of Respiratory and Critical Care Medicine [2].

But, males have a historically higher exposure to smoke from cigarettes and occupational lung irritants as potential COPD risk factors for worse long-term survival [45]. Occupational exposure to lung irritants for COPD causes higher proportional mortality in males than females at a population attributable fraction of 10.6% and 6.1%, respectively [16].

COPD Deaths by Age Statistics

In 2020, most (84.31%) COPD deaths occurred among adults aged 65 years or older at a total of 128,712 [5].

25,311 older adults aged 75 through 79 years died of COPD in 2020. This age group also holds the highest percentage of deaths among all age groups at 16.58%. Older adults aged 80 through 84 follow with 24,052 deaths or 15.76% [5].

14.61% of older adults aged 70 to 74 years died of COPD in 2020, which equals 22,307 deaths. Older adults 85 through 89 are also in the top five age groups for COPD deaths at 13.60% or 20,766 deaths, followed by 65 through 69 year olds at 16,252 deaths or 10.65% [5].

Both the number of COPD deaths and the percentage fall proportionally in younger adults [5].

8.02% or 12,237 of COPD deaths in 2020 happened in adults 60 through 64 years, which is a difference of 4,015 deaths from the 65 through 69 age group. From there, the number of deaths notices nearly a double decline at 6,579 deaths (4.31%) in adults aged 55 through 59 years [5].

The lowest number of deaths in adults over 45 was in COPD patients aged 45 through 49 at 1,038 (0.68%). The 50 through 54 age group follows with 2,500 deaths or 1.64% [5].

In 2020, older adults aged 80 through 84 years had the highest death rate at 372.1 per 100,000. For comparison, only 180 people aged 25 through 29 died of COPD in 2020 at a 0.8 rate per 100,000 [5].

This indicates that both the number and the rate of COPD deaths are closely related to age and are the highest in older adults.

COPD Deaths by Race Statistics

At 130,947 out of 152,657 COPD deaths in 2020, White Americans have the highest number of deaths, percentage of deaths (85.78%), and death rates (65.3 per 100,000). Black Americans come in second with 12,361 deaths or 8.10% of all COPD deaths in 2020 [5].

The number of deaths is lowest in American Indian and Alaska Natives (AIANs) at 861 or 0.56%. Asian Americans at 2,176 (1.43%), and Hispanics at 5,949 or 3.90% follow [5].

Out of all races, Hispanics have the lowest death rate at 9.7 per 100,000, while White Americans have the highest at 65.3. Despite the low number of deaths, AIANs also have a high death rate at 31.1 [5].

Whites are 4.1 times more likely to develop COPD than Hispanics. COPD’s prevalence in Hispanics is lower by both spirometry and clinical diagnosis at 41.6% compared to Whites at 54.2% [1].

The exact reason for this is largely unknown, but a London study suggests that it may be due to ethnic differences in cigarette consumption and potential ethnic susceptibility to this disease [15].

COPD Deaths by State Statistics

At 90.1 per 100,000, West Virginia had the highest COPD death rate, while Hawaii had the lowest at 26.7, shows 2020 data from the CDC [5].

West Virginia is the state with the highest percentage of tobacco use in the nation, with 23.8% of adult West Virginians being current smokers in 2022 [41].

Even though West Virginia had the highest COPD death rate and California is among the five states with lowest COPD death rate (32.8 per 100,000), California had the highest number of deaths at 12,907 or 8.45% out of all US states [5].

California is among the ten states with the lowest tobacco use rates, but it has the top four most polluted cities in the United States [27].

Second and third in line in the number of deaths were Florida (11,791) and Texas (10,402), respectively [5].

USA map showing that of all states, West Virginia has the highest rate of COPD deaths (90.1), while California has the highest number of deaths (12,907).

COPD Prevalence in the United States

COPD affects more than 15 million American adults, but the real number is greater because many people don’t know they have this condition [35].

In 2021, 4.6% of adults aged 18 and over suffered from emphysema or chronic bronchitis [32].

Data shows that more than half of the diagnosed adults are women [35].

COPD Prevalence Statistics: Male vs. Female 

COPD is more prevalent in females at 7.1% than in males at 5.7%. Based on CDC sample data, women also have a higher number of COPD cases (19,989 out of 233,922) compared to men (14,180 out of 202,664) [3].

Biologically, women smokers are more susceptible to this disease because of the faster decline in FEV1 even if smoking fewer cigarettes than men. Studies show that females develop more severe COPD and at an earlier age compared to males (younger than 60) [2].

Evidence shows that the 1960s propaganda by the tobacco industry that targeted women (and resulted in increased smoking rates) is partly to blame [18].

Another reason why women suffer from COPD more than men is that they are commonly misdiagnosed. COPD has been known for decades as a man’s disease, so female smokers are more than 33% less likely to be diagnosed with COPD compared to male smokers [18].

Cumulatively, women consume less tobacco than men but are more susceptible to it, resulting in a more severe, earlier-onset COPD and a faster FEV1 decline. The numbers show that women represent 80% of the nonsmoker COPD patient group, likely due to biomass fuel exposure or indoor air pollution created by poorly ventilated areas for cooking [18].

Note: The FEV1 measures how quickly the lungs are emptied after taking a maximal inhale. An excessive decline of this parameter over the course of 5 or more years is tightly correlated to the level of lung function and a predictor of morbidity and mortality. At a normal rate, the FEV1 decline should be 30 ml/y [44].

COPD Prevalence by Age Statistics

With 5,381 cases, the 70 to 74 age group has the highest number of people with COPD. It’s followed by the 65 to 69 group at 4,998 cases and the 60 to 64 age group at 4,826 cases [3].

The highest prevalence rate of COPD cases by age is in adults aged 75 to 79 at 13.8%. Adults aged 70 to 74 follow at 13.2%, and older than 80 at 12.6% [3]. The prevalence rate of COPD significantly increases with age.

Only 1.7%, or 410 people aged 18 to 24, have ever been told they had COPD, which remains the age group with the lowest prevalence and lowest number of cases. The 25 to 29 age group and the 30 to 34 age group follow with 464 (2.3%) and 632 (3.0%) cases, respectively [3].

Smokers are most likely to suffer from COPD, but this condition is most common in people older than 40 who are smokers or have smoked earlier in life [34].

While young adults can, but rarely, develop COPD, the first symptoms appear in adults who are at least in their forties [10].

COPD Prevalence by Race Statistics

COPD affects American Indian and Alaskan Natives (AIAN) the most at 10.6% or 720 cases out of 7,214 people. At 7.9% or 901 and 7.6% or 27,865 cases, Multiracial Americans and White Americans, respectively, follow [3].

Black Americans are the fourth most commonly affected race from COPD based on CDC’s sample size at 6.3% [3].

White Americans have the highest number of COPD cases at 27,865 out of 330,730 people. Black Americans come in second at 2,386 COPD cases out of 32,946 people. Hispanics are third with 1,566 cases out of 38,230 people [3].

This may be connected to high smoking rates among AIANs at 27.1% compared to Asians and Hispanics at 8.0% each, and the overall US population at 12.5% or 30.8 million people [30].

In 2020, American Indians and Alaska Natives (AIANs) had the highest smoking prevalence compared to other races in the US [30].

This group tends to hold sacred tobacco ceremonials, and use tobacco for religious and medical uses. Also, tobacco sold in their lands is not taxed, so that’s another contributor to increased tobacco smoking rates [30].

COPD Prevalence by State Statistics

Based on CDC’s sample size, New York has the highest number of COPD cases at 3,364. Ohio and Kansas follow at 1,500 and 1,310 cases, respectively [3]. 

The states with the lowest number of COPD cases are Illinois with 211, Nevada with 255, and Delaware with 277 [3].

West Virginia has the highest prevalence rate by state. Out of 6,711 West Virginians, 13.1% or 951 have been told they had COPD at any time of their lives, followed by 10.9% or 699 out of 5,395 Kentuckians [3]. 

Tennessee and Arkansas are also among the top five states with the highest COPD prevalence by state. 10.4% or 529 people out of 4,763 Tennesseans and 9.6% or 646 people out of 5,349 Arkansans have been told they had COPD at any time in their lives [3].

The state with the lowest COPD prevalence by cases is Hawaii, with 3.5% or 346 cases out of 7,768 people, followed by Utah at 4.3% or 543 cases out of 10,546 [3].

USA map showing COPD rates and number of cases (based on sample size) per state.

COPD Statistics Deaths Worldwide

In 2019, 3.23 million people, or 5.8% of global deaths were attributed to COPD. This disease was the third leading cause of death worldwide after ischaemic heart disease with 8.89 million deaths (16.0%) and stroke with 6.19 million (11.2%) [12] [13].

Global and regional estimates show that lower respiratory infections, neonatal conditions, and Alzheimer's were among the ten leading causes of death globally in that year [13].

Diabetes mellitus (1.5 million) and kidney disease (1.33 million) were at the bottom of the list of leading causes of global deaths [12].

Table showing that COPD is the third leading cause of death worldwide, affecting 5.8% of the population or 3.23 million people.

Most Common Causes of COPD in Non-Smokers

53.9% out of 200 non-smoking COPD patients developed this condition due to exposure to biomass smoke, says an Indian study. Treated pulmonary tuberculosis was a significant risk factor in 32.7% of the non-smoking patients and long-standing asthma in 14.2% of the patients [38].

Ten percent (10%) of the non-smoking patients developed COPD due to several risk factors, including occupational exposure, outdoor air pollution exposure, and lower respiratory tract infection in childhood [38].

Up to 30% of people with COPD are non-smokers and have never smoked in their lives [35]. Here are a few more answers to why non-smokers develop COPD.

Call out text box saying that 30% of people who develop COPD don’t smoke and have never smoked.

Poor Lung Development

Out of 200 non-smoking COPD patients, 28.9% suffered more respiratory infections during childhood compared to 18.7% of smokers, shows data from a Korean multicenter cohort [6].

According to researchers, the reason why people who never smoked develop COPD may be improper lung development [24]. Research has shown that even at an early age, older adults with COPD appear to have experienced low lung function. Although unconfirmed, frequent respiratory infections during childhood may explain why non-smokers have experienced low function at an early age [6].

At 57.5% out of 2,477 patients, females comprise a higher proportion of non-smoking COPD patients compared to smoking COPD patients at 3.3% [6]. A strong risk factor for COPD in non-smokers is small airways relative to lung size, says a 2020 JAMA study [24].

Females have relatively smaller airways than males, but the reasons why females with small airways have a greater susceptibility to COPD is unknown. One theory is that the concentration of tobacco smoke may be greater per unit area in a smaller airway surface, but this remains to be investigated [2].

Secondhand Smoke (SHS)

Among 334 COPD patients who don’t actively smoke, 66.65% were exposed to short-term and 34.91% to medium-term secondhand smoke, showed a five-year survey by the US National Health and Nutrition [14].

The short term SHS exposure in COPD patients who don’t actively smoke was 3.73 times higher compared to the general population of adult nonsmokers older than 40 [14].

Call out text box saying nonsmokers have been 3.73 times more exposed to secondhand smoke compared to the general population of nonsmokers.

A significant contributor to COPD in people who don’t smoke and have never smoked is long-term exposure to secondhand smoke [31].

In addition, people who have been exposed to secondhand smoke during childhood and teenage years are at a greater risk of developing COPD in their adult years. This is because exposure to secondhand smoke in children and teens can slow the process of lung growth and development [31].

AATD Deficiency 

One to four percent of COPD patients have a rare, hereditary genetic condition known as alpha-1-antitrypsin deficiency (A1AD) [26]. According to the British Lung Foundation, having AATD increases the likelihood of the patient developing COPD [48].

Research shows that AATD remains underdiagnosed in COPD patients, despite recommendations to check for it in these patients [25].

COPD patients 40 years of age or older have an adjusted rate of AATD of 0.83% [25].

What Are the Stages of COPD?

The stages of COPD are based on the Global Initiative for Chronic Obstructive Lung Disease (GOLD) Guidelines. The GOLD guidelines put COPD development in four stages, including mild, moderate, severe, and very severe [43].

At Stage I of the disease (mild), the person may experience no symptoms but typically has difficulty breathing when walking the stairs. Their airflow is 80% of the normal airflow [42].

At Stage II, or the moderate stage, the person experiences symptoms like chronic cough, breathlessness, or wheezing and needs breaks to catch their breath. Their airflow is within the 50% to 79% range compared to normal levels [42].

At Stage III or the severe stage, the person experiences worsening symptoms. The shortness of breath is greater, and further exacerbations affect the person’s quality of life and may lead to hospitalization. Their airflow remains within the 30% to 50% range of normal levels [42].

At Stage IV, or the very severe stage, the situation becomes alarming because the person’s airflow is less than 30% compared to normal levels. The person experiences severe airflow limitation, and further exacerbations can be life-threatening [42].

Table showing the connection between the FEV1/FVC ratio and the four stages of COPD.

Physicians use these four stages to determine the severity of COPD in the patient and help pair them with the right treatment for their stage [43].

The entire classification is based on two parameters: Forced vital capacity (FVC) and Forced expiratory volume (FEV1) [43].

The FVC parameter measures the largest amount of air the patient can breathe out after taking the deepest breath. The FEV1 parameter measures how much air the patient can exhale from the lungs in 1 second [43].

Every patient has an individual predicted FEV1 value. Once calculated, the doctor compares the predicted value to the actual FEV1 score and its ratio to FVC [43].

How Many Years of Smoking Does It Take to Develop COPD?

After 25 years, 30-40% of smokers will develop any COPD, while at least 25% of completely healthy smokers will develop COPD described as clinically significant [23].

Call out text box saying the percentage of smokers that will develop any COPD is 30-40%.

Call out text box saying the percentage of healthy smokers that will develop clinically significant COPD is 25%.

The data came from a Dutch study that followed men and women who smoked (but had normal lung function) for 25 years that concluded that the longer people smoked, the greater the risk of developing COPD [23].

What’s The Average Life Expectancy for People Diagnosed with COPD?

The average life expectancy in relatively healthy 65-year-old Caucasian males with COPD is 17.4 years at Stage 1 of the disease and 12.5 years at Stage 3 or 4 [39].

Relatively healthy 65-year-old Caucasian females with COPD have an average life expectancy of 19.9 years at Stage 1 of the disease and 14.5 years at Stage 3 or 4 [39].

In conclusion, females diagnosed with COPD have a higher average life expectancy than males [39].

Data shows that people diagnosed with COPD who continue to smoke have the lowest average life expectancy [39].

Current male smokers have the lowest average life expectancy of 8.5 years at Stage 3 or 4 of the disease, while current female smokers have an average life expectancy of 11.3 years at the same stage [39].

Life Expectancy Highest in Never Smokers

In never smokers, there’s a tiny drop in average life expectancy by 0.7 and 1.3 years at stages 2 and 3 of COPD, respectively [39].

Compared to smokers, people who have never smoked but were diagnosed with COPD noticed a moderate decline in life expectancy. Current and former smokers experience a significant reduction in life expectancy from COPD [39].

COPD Average Life Expectancy Chart 

The average life expectancy in people who never smoke is higher than in people diagnosed with COPD who are current and former smokers [39].

  • Compared to never smokers, 65-year old current male and female smokers diagnosed with COPD have a reduced life expectancy of 0.3 and 0.2 years at stage 1, respectively. At stage 2, life expectancy is reduced by 2.2 years in both male and female current smokers. At stage 3 or 4, the life expectancy is greatly reduced compared to never smokers at 5.8 years in current male smokers and 6.1 years in current female smokers.
  • Former male smokers have a reduced life expectancy of 1.4 years and 5.6 years for Stages 2, and 3 or 4, respectively.
  • Former female smokers have a reduced life expectancy of 2 and 6.3 years for stages 2, and 3 or 4, respectively.

In addition to the reduction in life expectancy of COPD, current smokers also lose an additional 3.5 years of their lives due to smoking [39].

What’s The Survival Rate of COPD?

Hospitalized COPD patients are 82% less likely to survive within the next 15 years compared to the general population [46].

Patients who experience worsening COPD are 7.3% likely to survive the next 15 years compared to the general population at 40.6% [46].

The survival rate in COPD patients depends on the GOLD stage of the disease [46].

COPD patients in the GOLD I stage have a 15-year survival of 24.0% compared to 11.1% and 5.3% survival at GOLD stages II and III, respectively [46].

43.7% of patients will survive the 5-year mark after COPD exacerbation, and 19.9% will survive a decade compared to 57.2% of the general population [46].

COPD patients have a reduced overall 15-year survival after diagnosis at an early stage and an even lower survival after hospitalization and exacerbation of symptoms [46].

This data is based on a study published in Respiratory Medicine that studied the mortality risks of people diagnosed with COPD — including hospitalized COPD patients versus subjects from the general population [46].

When undergoing non-invasive ventilation (NIV) treatment, women showed a survival tendency at a survival rate of 25.7%, compared to men at 19.2% [45].

A study published in the International Journal of Chronic Obstructive Pulmonary Disease treated patients with non-invasive ventilation (NIV) for acute respiratory failure for the first time. The study was conducted at a university hospital in Denmark on 253 patients at a median age of 72 years [45].

In general, patients with acute respiratory failure don’t leave long after receiving NIV. This study noted a 30-day mortality rate of 29.3% and a survival rate of 23.7% [45].

What's the Annual Cost of COPD?

The US spent an estimated $49 billion in 2020, an increase from 2010s $32.1 billion. It's a costly condition, especially due to the high rate of hospitalization among older adults over 65 [29].

51% of the annual 2010 COPD costs went to Medicare, and 18% were covered by private insurance [29]. The annual cost of COPD was three times higher in patients with severe COPD ($18,070) compared to patients with mild COPD ($5,945) [19].

In 2010, this condition caused a loss of 16.4 million days of work at the cost of $3.9 billion [29].

COPD is expensive, but luckily, the Social Security Administration (SSA) considers it a disability. If you’re not able to work due to advanced COPD, the SSA has a few assistance programs to help with the payments. Severe enough stages of COPD that don’t allow you to work for at least 12 months mean you’ll likely qualify for disability [7].

How Long Does It Take to Get Disability for COPD?

On average, it takes three to five months to find out whether the person qualifies for a disability for COPD. After getting approved, it takes another five months until the person receives their first disability benefit payment [7].

Call out text box saying it takes another 5 months to receive the first disability payment after waiting 3 to 5 months to know whether the patient qualifies for it.

Call out text box saying it takes another 5 months to receive the first disability payment after waiting 3 to 5 months to know whether the patient qualifies for it.

Common Treatments for COPD

While there’s no proven cure for COPD, several treatment options have shown more or less effective in treating this condition.

Amoxicillin/Clavulanic Acid

74.1% or 117 patients with nonsevere worsening of mild to moderate COPD improved on a combination of amoxicillin and clavulanic acid compared to placebo at 59.9% or 91 patients [22].

The patients who participated in this multicenter trial took a dosage of 500/125 mg amoxicillin/clavulanic acid three times a day for eight days and noticed a prolonged time between the last and the next interval of acute exacerbation of mild to moderate COPD (AECOPD) [22].

Corticosteroids

Four-week treatment with a high dose of oral steroids (over 30 mg) improves lung function in some COPD patients by up to 20% [17].

The researchers noted a significant improvement in patients’ FEV1 after two weeks of this treatment. However, they concluded that such high doses of corticosteroids are unsustainable in the long run due to the harm they do to the body [47].

Salmeterol/Fluticasone Combination

A salmeterol/fluticasone blend reduced the exacerbations in moderate and severe COPD cases but there was still a 64% increase in the risk of developing pneumonia compared to placebo [11].

The researchers have concluded that an extra case of pneumonia will develop for every 31 patients undergoing this therapy over a year [11].

In an attempt to improve COPD treatment and reduce the appearance of pneumonia as an adverse event, researchers studied the impact of a corticosteroid combination. The patients took part in a three year study and were treated with fluticasone alone or a combination of salmeterol and fluticasone [11].

Multifactorial Intervention

56.8% out of 146 patients diagnosed with COPD had reduced mobility impairment and 23.7% experienced increased cognition after a multifactorial intervention. The trial consisted of 91.8% male patients at a mean age of 69.8 years [21].

A study published in BM Pulmonary Medicine evaluated the effectiveness of a multifactorial intervention in COPD patients with scheduled inhalation therapy. This intervention included multiple components such as [21]:

  • Information on COPD
  • Training in inhalation techniques
  • Audio-visual materials
  • Dose reminders
  • Motivational aspects

Carbocysteine

Carbocysteine therapy decreases acute exacerbations in patients with COPD by 24% compared to placebo. The participants of the study took 1500 mg of this mucolytic for a year [36].

Final Thoughts — COPD Facts & Statistics

Chronic obstructive pulmonary disease (COPD) affects nearly 16 million Americans and is the cause of over 150,000 deaths per year. Smoking is the root cause of COPD, with cigarette smoking causing about 75% or nearly 8 out of 10 deaths.

Adults 75 and older have the highest number and rate of COPD deaths. Only 7.3% of the patients diagnosed with COPD will survive the next 15 years after admission for worsening COPD.

Once hospitalized, COPD patients at Stage I have a 24% chance of survival within the next 15 years compared to patients at Stage III at 5.3%. Treating chronic pulmonary obstructive disease is costly and amounts to 16.4 million days of total absenteeism.

References

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  11. Crim, C., Calverley, P. M. A., Anderson, J. A., Celli, B., Ferguson, G. T., Jenkins, C., Jones, P. W., Willits, L. R., Yates, J. C., & Vestbo, J. (2009). Pneumonia risk in COPD patients receiving inhaled corticosteroids alone or in combination: TORCH study results. European Respiratory Journal, 34(3), 641–647. [11]
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  13. Elflein, J. (2022b). Leading ten causes of death in the world 2019. Statista. [13]
  14. Fu, Z., Jiang, H., Xu, Z., Li, H., Wu, N., & Yin, P. (2020). Objective secondhand smoke exposure in chronic obstructive pulmonary disease patients without active smoking: the U.S. National Health and Nutrition Examination Survey (NHANES) 2007–2012. Annals of Translational Medicine, 8(7), 445. [14]
  15. Gilkes, A., Ashworth, M., Schofield, P., Harries, T. H., Durbaba, S., Weston, C., & White, P. (2016). Does COPD risk vary by ethnicity? A retrospective cross-sectional study. International Journal of Chronic Obstructive Pulmonary Disease, 11, 739–746. [15]
  16. Grahn, K., Gustavsson, P., Andersson, T., Lindén, A., Hemmingsson, T., Selander, J., & Wiebert, P. (2021). Occupational exposure to particles and increased risk of developing chronic obstructive pulmonary disease (COPD): A population-based cohort study in Stockholm, Sweden. Environmental Research, 200. [16]
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  19. Larsen, D. L., Gandhi, H., Pollack, M., Feigler, N., Patel, S., & Wise, R. (2022). The Quality of Care and Economic Burden of COPD in the United States: Considerations for Managing Patients and Improving Outcomes. American Health and Drug Benefits, 15(2), 57–64. [19]
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  21. Leiva-Fernández, J., Leiva-Fernández, F., García-Ruiz, A., Prados-Torres, D., & Barnestein-Fonseca, P. (2014). Efficacy of a multifactorial intervention on therapeutic adherence in patients with chronic obstructive pulmonary disease (COPD): a randomized controlled trial. BMC Pulmonary Medicine, 14, 70. [21]
  22. Llor, C., Moragas, A., Hernández, S., Bayona, C., & Miravitlles, M. (2012). Efficacy of Antibiotic Therapy for Acute Exacerbations of Mild to Moderate Chronic Obstructive Pulmonary Disease. American Journal of Respiratory and Critical Care Medicine, 186(8), 716–723. [22]
  23. Løkke, A., Lange, P., Scharling, H., Fabricius, P., & Vestbo, J. (2006). Developing COPD: a 25 year follow up study of the general population. Thorax, 61(11), 935–939. [23]
  24. Lung development may explain why some non-smokers get COPD and some heavy smokers do not. (2020). National Institutes of Health. [24]
  25. Menga, G., Fernandez Acquier, M., Echazarreta, A. L., Sorroche, P. B., Lorenzon, M. V., Fernández, M. E., & Saez, M. S. (2020). Prevalence of Alpha-1 Antitrypsin Deficiency in COPD Patients in Argentina. The DAAT.AR Study. Archivos De Bronconeumología, 56(9), 571–577. [25]
  26. Monge, M. B., Silva, R., Czischke, K., Saldías, F., Pavié, J., Jalón, M., Benavides, M. G., San Martín, B., Cea, X., Mendoza, L., Roldán, R., Soto, L., De La Prida, M., Zambrano, A., Villalobos, J., Gutiérrez, M., Riquelme, M., Tapia, M., & Dreyse, J. (2021). Prevalence of alpha-1-antitrypsin deficiency (A1AD) in patients with COPD. European Respiratory Journal, 58(65). [26]
  27. Most Polluted Places to Live. (2022). American Lung Association. [27]
  28. National Center for Chronic Disease Prevention and Health Promotion. (2015). Chronic Obstructive Pulmonary Disease (COPD). Centers for Disease Control and Prevention. [28]
  29. National Center for Chronic Disease Prevention and Health Promotion. (2018). COPD Costs. Centers for Disease Control and Prevention. [29]
  30. National Center for Chronic Disease Prevention and Health Promotion. (2022a). Burden of Cigarette Use in the U.S. Centers for Disease Control and Prevention. [30]
  31. National Center for Chronic Disease Prevention and Health Promotion. (2022b). Smoking and COPD. Centers for Disease Control and Prevention. [31]
  32. National Center for Health Statistics. (2022). Percentage of COPD, emphysema, or chronic bronchitis for adults aged 18 and over, United States, 2021. National Health Interview Survey. [32]
  33. National Heart, Lung, and Blood Institute. (2017). COPD National Action Plan. National Institutes of Health. [33]
  34. National Heart, Lung, and Blood Institute. (2018). COPD: The More You Know, The Better For You and Your Loved Ones. In National Institutes of Health (No. 13–5840). [34]
  35. National Heart, Lung, and Blood Institute. (2021). What Is COPD? National Institutes of Health. [35]
  36. Pace, E., Cerveri, I., Lacedonia, D., Paone, G., Sanduzzi Zamparelli, A., Sorbo, R., Allegretti, M., Lanata, L., & Scaglione, F. (2022). Clinical Efficacy of Carbocysteine in COPD: Beyond the Mucolytic Action. Pharmaceutics, 14(6), 1261. [36]
  37. Paulin, L. M., Halenar, M. J., Edwards, K. C., Lauten, K., Stanton, C. A., Taylor, K., Hatsukami, D., Hyland, A., MacKenzie, T., Mahoney, M. C., Niaura, R., Trinidad, D., Blanco, C., Compton, W. M., Gardner, L. D., Kimmel, H. L., Lauterstein, D., Marshall, D., & Sargent, J. D. (2022). Association of tobacco product use with chronic obstructive pulmonary disease (COPD) prevalence and incidence in Waves 1 through 5 (2013–2019) of the Population Assessment of Tobacco and Health (PATH) Study. Respiratory Research, 23, 273. [37]
  38. Sharma, B. B., & Singh, V. (2017). Nonsmoker COPD: Is it a reality? Lung India, 34(2), 117–119. [38]
  39. Shavelle, R. M., Paculdo, D. R., Kush, S. J., Mannino, D. M., & Strauss, D. J. (2009). Life expectancy and years of life lost in chronic obstructive pulmonary disease: Findings from the NHANES III Follow-up Study. International Journal of Chronic Obstructive Pulmonary Disease, 4, 137–148. [39]
  40. Smoking and Respiratory Diseases. (2022). Centers for Disease Control and Prevention. [40]
  41. Smoking Rates by State 2022. (2022). World Population Review. [41]
  42. Stages of COPD and Spirometric Classifications. (2008). Oklahoma Department of Human Services. [42]
  43. Summarizing the 2021 Updated GOLD Guidelines for COPD. (2021). US Pharmacist. [43]
  44. The National Institute for Occupational Safety and Health. (2011). Spirometry Quick calculation of FEV1 decline. Centers for Disease Control and Prevention. [44]
  45. Titlestad, I. L., Lassen, A. T., & Vestbo, J. (2013). Long-term survival for COPD patients receiving noninvasive ventilation for acute respiratory failure. International Journal of Chronic Obstructive Pulmonary Disease, 8, 215–219. [45]
  46. van Hirtum, P. V., Sprooten, R. T. M., van Noord, J. A., van Vliet, M., & de Kruif, M. D. (2018). Long term survival after admission for COPD exacerbation: A comparison with the general population. Respiratory Medicine, 137, 77–82. [46]
  47. Walters, J. A., Walters, E. H., & Wood-Baker, R. (2005). Oral corticosteroids for stable chronic obstructive pulmonary disease. Cochrane Database of Systematic Reviews, 3. [47]
  48. What is A1ATD? (2013). Asthma and Lung UK. [48]

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An international team including Australian researchers has identified a potential new approach for treating chronic obstructive pulmonary disease (COPD) – a group of diseases that includes emphysema and chronic bronchitis.

In COPD airway inflammation, blockage, and lung damage causes airflow blockage making it difficult to breathe. According to the World Health Organization (WHO) COPD is the third leading cause of death worldwide, causing 3.23 million deaths in 2019.

Lung Foundation Australia says: “Around 1 in 13 Australians aged 40 years and over have some form of COPD however around half of these people living with COPD symptoms do not know they have the condition. Indigenous Australians are 2.5 times more likely to have COPD than non-Indigenous Australians. About 20% of people with COPD also have asthma. COPD is not contagious.

Existing treatments and lifestyle changes like quitting smoking, can slow the progression of the disease but cannot reverse the damage. There is currently no cure.

Now, a new study in the European Respiratory Journal has found that there are increased levels of an enzyme called Receptor-interacting protein kinase 1 (RIPK1) in the lungs of people suffering from COPD.

Inhibiting this enzyme helped protect against COPD in mouse models and may represents a new approach for treatment in humans.

According to co-senior author Professor Phil Hansbro, Director of the Centenary UTS Centre for Inflammation at the University of Technology Sydney, while smoking is the primary risk factor for developing COPD, the disease can also be caused by breathing in dust, fumes, chemicals, and air pollution.

“Cigarette smoke or exposure to other irritants triggers inflammation and can induce cell death in the lungs and airways, which directly contributes to the development of COPD,” explains Hansbro.


Read more: How are we studying firefighter health risks? (Part 1 of 2)


In emphysema, damage to the walls between air sacs (alveoli) in the lungs makes it more difficult to move air out of the body when exhaling. As a result, old air is trapped which leaves no room for fresh, oxygen-rich air to enter.

People with emphysema often also suffer from chronic bronchitis: an inflammation in the lining of the airways that carry air to the lungs (bronchial tubes) which causes thick mucus and a persistent cough to form.

“We investigated RIPK1 as it plays a key role in cell survival and death as well as inflammation. We found that there were far higher levels of RIPK1 in patients suffering from COPD, as well as in our COPD mouse models,” says Hansbro.

The team found that inhibiting RIPK1 activity in mice, through both knocking out the gene that produces it or introducing a compound (GSK’547) that inhibits the enzyme, had a significant protective effect against the disease.

“We saw reduced structural changes to the airways and decreased damage to the air sacs of the lungs. Our data indicates that inhibiting RIPK1 lessened both inflammation and the death of healthy lung and airway cells meaning less tissue damage overall,” adds Hansbro.

This finding represents a new promising therapeutic approach to treating COPD.



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Lütfiye Kiliç,1 Seda Tural Önür,2 Aslı Gorek Dilektasli,3 Gaye Ulubay,4 Arif Balcı5

1Yedikule Chest Diseases and Thoracic Surgery Training and Research Hospital, Pulmonologist, Department of Pulmonary Rehabilitation, University of Health Sciences, Istanbul, Turkey; 2Yedikule Chest Diseases and Thoracic Surgery Training and Research Hospital, Associate Professor, Department of Chest Diseases, University of Health Sciences, Istanbul, Turkey; 3Uludağ University, Faculty of Medicine, Associate professor, Department of Chest Diseases, Bursa, Turkey; 4Başkent University, Faculty of Medicine, Professor, Department of Chest Diseases, Ankara, Turkey; 5Yedikule Chest Diseases and Thoracic Surgery Training and Research Hospital, Physiotherapist, Department of Pulmonary Rehabilitation, University of Health Sciences, Istanbul, Turkey

Correspondence: Lütfiye Kiliç, Yedikule Chest Diseases and Thoracic Surgery Training and Research Hospital, Istanbul, Turkey, Tel +90 532 397 7172, Email [email protected]

Purpose: We investigated the effect of pulmonary rehabilitation (PR) on airway resistance in chronic obstructive pulmonary disease (COPD) patients with severe airway obstruction and hyperinflation.
Patients and Methods: This retrospective cohort study was conducted with data from severe COPD cases with those who underwent an 8-week PR program. Main inclusion criteria were having severe airflow obstruction (defined as a forced expiratory volume in one second (FEV1) < 50%) and plethysmographic evaluation findings being compatible with hyperinflation supporting the diagnosis of emphysema (presence of hyperinflation defined as functional residual capacity ratio of residual volume to total lung capacity (RV/TLC) > 120%). Primary outcomes were airway resistance (Raw) and airway conductance (Gaw) which were measured by body plethysmography, and other measurements were performed, including 6-minute walk test (6-MWT), modified Medical Research Council dyspnea scale (mMRC) and COPD assessment test (CAT).
Results: Twenty-six severe and very severe COPD patients (FEV1, 35.0 ± 13.1%; RV/TLC, 163.5 ± 29.4) were included in the analyses, mean age 62.6 ± 5.8 years and 88.5% males. Following rehabilitation, significant improvements in total specific airway resistance percentage (sRawtot%, p = 0.040) and total specific airway conductance percentage (sGawtot%; p = 0.010) were observed. The post-rehabilitation mMRC scores and CAT values were significantly decreased compared to baseline results (p < 0.001 and p < 0.001, respectively). Although there were significant improvements in 6-MWT value (p < 0.001), exercise desaturation (ΔSaO2, p = 0.026), the changes in measured lung capacity and volume values were not significant.
Conclusion: We concluded that PR may have a positive effect on airway resistance and airway conductance in COPD patients with severe airflow obstruction.

Keywords: airway resistance, body plethysmography, airflow limitation, emphysema, lung mechanics

Introduction

Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation caused by a combination of many factors,1 including increased airway resistance, impaired airway-parenchymal tethering due to emphysema, and lumen narrowing due to mucus occlusion and bronchoconstriction.2–5 Among the conditions referred to as COPD, patients with emphysema have highest airway resistance.6 In patients with emphysema, peripheral airway resistance may be increased by four to 40-fold.7

Although activity limitation in COPD is multifactorial (reduced cardiac function, hypoperfusion of the working muscle, limb muscle dysfunction and impaired neural regulation),8 therapies aimed at partially reversing pulmonary hyperinflation represent the first step in improving dyspnea and exercise capacity.

Various pharmacological and non-pharmacological interventions have been shown to reduce hyperinflation and delay the onset of airflow restriction in patients with COPD.4 For instance, bronchodilators reduce expiratory airflow resistance by increasing the diameter of the airways, emptying of peripheral airways with trapped air is facilitated, thus reducing hyperinflation and improving breathing mechanics.9 Previous studies showed that inhaled long-acting bronchodilators (LABA/LAMA combination) have been proven to be able to reduce hyperinflation and therefore to improve dyspnea and tolerance to physical activity.10 Inhaled low-dose short-acting β-agonists (SABAs) have been demonstrated to reduce lung hyperinflation despite no change in forced expiratory volume within one second (FEV1) in patients with advanced emphysema.5,11–13

Pulmonary rehabilitation (PR) is the most effective non-pharmacological therapy that has emerged as a standard of care for patients with COPD.14 PR reduces ventilatory requirements and improves breathing efficiency, thereby reducing hyperinflation and improving exertional dyspnea.5 Although there is a limited data to draw a firm conclusion as to the mechanism by which this PR effect occurs, it may be attributable to the multifactorial effects of the rich PR content.15

To date, the benefit of PR in COPD patients has been mostly evaluated by investigating effects on exercise capacity, dyspnea and health-related quality of life.16 Due to variabilities in perceptions and interpretations, assessing benefit based solely on symptoms and clinical response may lead to incomplete or inaccurate outcomes. Moreover, the relationship of improvements in the degree of hyperinflation, which is attributed to the effect of PR on respiratory mechanics in patients with COPD,15 with intra-alveolar pressure and airway conductance has not been elucidated yet. Previous investigations have shown that body plethysmography can potentially provide additional insights into the respiratory mechanics of COPD patients.17

Body plethysmography is an integrative diagnostic procedure in respiratory medicine for comprehensive pulmonary function testing to evaluate static lung volumes and airway resistance (Raw), as well as specific airway conductance (sGaw).18–20 Raw reflects changes in alveolar pressure over changes in flow, representing true resistance of the airways. In this context, it may be a good parameter for the diagnosis of airflow obstruction.21,22 In contrast, sRaw can be interpreted as the work to be performed to establish this flow rate; Raw is calculated as the ratio of sRaw to FRC;23 sGaw is the inverse of sRaw and therefore reflects the conductance of the airways independent of lung volumes.23 In obstructive lung diseases, the Raw value is higher and the sGaw value is lower than both healthy controls and non-obstructive respiratory diseases.18 Furthermore, some authors have suggested that sGaw is more sensitive to changes in airway resistance than FEV1.24

The use of different functional markers to evaluate the effectiveness of PR in COPD may provide a better understanding of its effects on lung mechanics. Assessment of airway resistance is, therefore, important to characterize respiratory mechanisms that contribute to improved exercise capacity after PR in patients adopting different breathing strategies during exercise. To the best of our knowledge, no previous studies have addressed the effects of PR on airway resistance and specific airway conductance in patients with COPD. Accordingly, the primary aim of this study was to examine the effects of PR on airway resistance in patients with advanced COPD who had clinical and physiological features of emphysema, and secondarily, to assess whether airway resistance tests could be used as a physiological biomarker for PR.

Patients and Methods

Study Design and Patient Selection

This observational study involved a retrospective analysis of COPD patients admitted to the PR outpatient clinic of a tertiary-level training and research hospital, between December 2012 and June 2019. The study protocol was approved by the ethics committee of Yedikule Chest Diseases and Thoracic Surgery Training and Research Hospital (Approval Number: 2020–27; September 17, 2020). Written informed consent was obtained from all participants before PR. This study complied with the principles of the Declaration of Helsinki and Good Clinical Practice guidelines.

Records of 154 COPD patients with predominant pathology to emphysema who had attended an 8-week outpatient PR program were reviewed. The criteria for inclusion into the study for all participants were 1) having completed the 8-week outpatient PR program; 2) having a post-bronchodilator ratio of forced expiratory volume per second to forced vital capacity (FEV1 / FVC) less than 0.7 to qualify for the definition of COPD;25 3) having severe airflow obstruction (defined as a FEV1 less than 50% of the predicted value); 4) presence of hyperinflation defined as functional residual capacity (FRC) ≥120% and/or RV/TLC >120% of the predicted value;26 5) having undergone a body plethysmography test, including measures of lung volumes, airway resistance (Raw) and specific airway conductance (sGaw), and 6) no change in dose or use of bronchodilator treatment, prior to, and throughout the duration of the PR program. Patients were excluded in the presence of 1) patients who only participated in a home-based pulmonary rehabilitation program, even if having severe or very severe COPD; 2) patients whose data is missing from their file; 3) patients who could not complete the eight-week PR program due to various reasons; 4) patients whose COPD treatment was changed for an attack and/or other reason during the PR program; 5) patients whose body plethysmography test measurement was discordant; 6) those who have another chronic obstructive pulmonary disease (chronic bronchitis, asthma, bronchiectasis, etc.) other than emphysema, and 7) significant diseases other than COPD that could contribute to dyspnea and exercise limitation (interstitial lung disease, advanced heart disease, anemia, thyroid dysfunction).

Baseline data included age, sex, body mass index (BMI), smoking status, pulmonary function tests (PFTs), and comorbid diseases. The outcome measures were body plethysmography test, 6-minute walk test (6-MWT), modified Medical Research Council (mMRC) dyspnea scale, and COPD Assessment Test (CAT). Disease classification was made according to the GOLD staging.25

Pulmonary Rehabilitation Program

The comprehensive PR program consisted of 1) education (lung anatomy, physiology and pathophysiology etc.) and self-management aimed at improving disease status; 2) training for controlled breathing techniques (slow and deep breathing, pursed-lip breathing, diaphragmatic breathing, and restructuring of breath); 3) teaching effective use of inhaler medication and management of breathing difficulties, both aimed maximizing bronchodilation; 4) at least twice supervised cycle ergometer or treadmill training session (30 min) per a week, the intensity of which was set at 60–80% of maximal workload based on 6-MWT results; 5) supervised upper and lower limb strengthening exercises and inspiratory/expiratory muscle training; 6) psychiatric and social counseling/assistance, and 7) nutritional management (patient counselling and nutritional therapy). All patients underwent a supervised exercise program at the hospital two days per week, for a total of 8 weeks. A home-based program (3 days per week) was also provided, comprising various exercises during the same period. All patients completed a follow-up form for the exercise program.

Functional and Pulmonary Testing

Exercise tolerance was evaluated with the distance covered during a 6-MWT, according to guidelines put forth by the American Thoracic Society (ATS).27 Before and after the test, oxygen saturation, heart rate, dyspnea, and Borg fatigue scores were recorded, and the distance covered was documented.25,28 Oxygen desaturation was defined according to the Royal College of Physicians’ guidelines as a ≥ 4% reduction between arterial oxygen saturation measured by pulse oximetry pre-test and post-test (ΔSpO2 ≥4%) and post-test SpO2 <90%.29 Patients were introduced to a 10-point Borg category scale.30 Patients were asked to describe their perception of dyspnea before exercise testing and at the end of tests.

Lung function testing was performed according to current ATS/ERS recommendations with a Sensor Medics model 2400 (Yorba Linda, CA, USA).31,32 Static, dynamic lung volumes and total specific airway resistances (sRawtot) were assessed by means of an ultrasonic flow measurement plethysmograph (Ganshorn PowerCube Body+, SCHILLER, Germany). The system automatically derived total specific conductance (sGawtot) from the breathing loops and determined total respiratory resistance (Rawtot).

Perceived levels of effort dyspnea were assessed through the modified medical research council (mMRC) dyspnea scale which performs evaluations with respect to daily activities.33 Patient-reported CAT results were obtained to identify COPD impact on health status (ie, cough, sputum and dyspnea).33

Statistical Analysis

Statistical analysis was performed using the SPSS software for Windows, version 15.0 (IBM, Armonk, NY, USA). Continuous variables were expressed with minimum–maximum (median) values (for non-normally distributed variables) or with mean ± standard deviation values (for normally distributed variables), while categorical variables were depicted with number (absolute frequency) and percentage (relative frequency). When continuous variables in dependent groups met normal distribution, they were examined using the paired samples t-test; otherwise, the Wilcoxon test was utilized. A p value of <0.05 was considered statistically significant.

Results

A total of 26 emphysema patients (88.5% males) with severe airflow limitation (FEV1, mean ± SD, 35.0 ± 13.15%) and static hyperinflation (RV/TLC, mean ± SD, 163.5 ± 29.4%) were included in the study, mean age 62.6 ± 5.8 year. The number of patients with at least one comorbidity was 10 (38%), diabetes mellitus was the most common (others: hypertension, hypercholesterolemia and osteoporosis). The demographic characteristics and baseline values of the patients are shown in Table 1. Following PR, there were significant improvements in total specific airway resistance percentage (sRawtot%, p = 0.040) and total specific airway conductance percentage (sGawtot%, p = 0.010) (Table 2; Figures 1 and 2). Of note, after PR, some limited improvements in plethysmographic respiratory measurement values [pre-PR vs post-PR, % of pred (IC: inspiratory capacity; 49.0 ± 24.6 vs 49.2 ± 20.7; p = 0.970), (FVC: forced vital capacity; 57.8 ± 17.0 vs 60.4 ± 15.8; p = 0.054), (FRC: functional residual capacity; 133.7 ± 37.2% vs 132.0 ± 39.9%; p = 0.788), (ERV: expiratory reserve volume; 80.8 ± 29.2% vs 88.5 ± 36.6%; p = 0.364)] were identified in our group of patients, especially in RV and RV/TLC [pre-PR vs post-PR, % of pred (169.9 ± 51.3 vs 163.8 ± 67.9) and (163.5 ± 29.4 vs 156.0 ± 42.5)], albeit statistical significance was not achieved (p > 0.05).

Table 1 Patient Characteristics

Table 2 Changes in Lung Volumes in Plethysmography Measurements After PR

Figure 1 A graph showing the parameters for which statistically significant differences were observed in patients who has participated in an eight-weeks PR program.

Abbreviations: PR, pulmonary rehabilitation; sRawtot, total specific resistance of airways; sGawtot, total specific conductance of airways; ΔSaO2, delta of haemoglobin O2 saturation; mMRC, modified Medical Research Council; CAT, COPD assessment test.

Figure 2 A Body plethysmography data samples of a 57-year-old male patient with a history of smoking 60 pk/year, who has attended sixteen sessions (8 weeks) of PR program; before attending (A) and after attending (B).

The post-rehabilitation mMRC scores and CAT values were significantly decreased compared to the baseline results (p < 0.001 and p < 0.001, respectively) (Table 2 and Figure 1). We observed significant differences between baseline and post-PR measurements in terms of 6-MWT results, including walking distance (Mean ± SD; 307.7 ± 98.3 meters vs 363.7 ± 105.7 meters; p < 0.001) and delta of haemoglobin O2 saturation (ΔSpO2, difference between rest and maximal exercise values; p = 0.026) (Table 3 and Figure 1). In addition, the post-rehabilitation median change in distance (Mean ± SD, 55.9 ± 64.6 meters) observed in the 6-MWT was above the minimal clinically important difference defined for COPD and other chronic respiratory patients.28 Although an improvement in Borg scores was observed, comparisons did not show significant improvement (p = 0.314) (Table 3).

Table 3 Comparison of 6-MWT Data

Discussion

The main new finding of this study is that PR may have a positive effect on airway resistance and airway conductivity in COPD patients with severe airway resistance. The present study is the first to demonstrate that the Raw and sGaw plethysmography parameters have the potential to assess the effect of PR on COPD.

Previous studies have shown that airway resistance and specific conductance have a valuable and potentially important role in the diagnosis of obstructive diseases.18 In a study including 51 participants with emphysema, the variability and sensitivity of plethysmography and spirometry measurements were compared in order to assess bronchodilation in COPD.17 The findings of this study demonstrated the high sensitivity of plethysmography in the detection of minor physiological effects, which resulted in improved airway conductance. In COPD, both specific conductance and airway resistance are more sensitive for assessing short-acting bronchodilator effects than FEV1.24 Moreover, body plethysmography can be a favorable alternative tool in evaluating the effect of PR, especially in elderly patients with COPD who have difficulty in performing spirometry.34

The significant decrease in plethysmography-determined airway resistance, the significant increase in airway conductance, and improvements in lung volumes may be attributed to the mechanical effects of PR on respiratory function.33 We observed limited improvements in the respiratory functions of our cases, as demonstrated by RV and RV/TLC results; however, comparisons did not demonstrate statistical significance (p > 0.05) which is similar to the literature on this topic.35 The changes in Raw and sGaw were also relatively greater compared to the changes in lung volume, and therefore, these parameters are possibly better for the purpose of detecting significant reductions in airflow restriction following PR interventions.

In our cases, there was a statistically significant improvement in exercise-induced hypoxaemia levels observed in 6-MWT after PR compared to baseline (Table 3 and Figure 1). We speculate that the improvement in desaturation during exercise following PR may be achieved by both the reduction in the effort required to breath and the decrease in the oxygen demand associated with the improvement of the oxygen utilization in peripheral muscles.36 In addition, controlled pursed-lip breathing and deeper and longer breaths to decrease the frequency of hyperventilation can reduce the O2 cost caused by the unit force.37,38 It was thought that the decrease in Raw would improve hypoxemia, as it would increase air conduction and reduce the O2 cost caused by the resistant respiratory workload. The clinical equivalent of this was interpreted as an increase in effort capacity and improvement in dyspnea levels in our cases. Although the patients in this study were under optimal pharmacological treatment and there was minimal change in lung function after rehabilitation, improvements in exertional dyspnea and capacity should be mainly attributed to the effect of rehabilitation. This is important as it demonstrates that even patients with advanced emphysema may experience considerable benefit from PR.

In previous studies, the addition of inspiratory muscle training to a PR program for COPD was reported to contribute to improved outcomes.39,40 However, patients with predominant pathologies such as chronic bronchitis or emphysema were not evaluated separately in these studies, whereas, in emphysematous lungs, the radial traction exerted by the surrounding alveoli to the airway decreases, correlated with the degree of parenchymal destruction.41 Accordingly, the bronchodilation effect of deep and strong inspiration is not proportional to the severity of emphysema, and may even cause bronchoconstriction.42 Therefore, in patients with emphysema, it would be more appropriate to focus on PR interventions that affect the expiratory rather than the inspiratory phase of respiratory mechanics, altering the breathing pattern and reducing air trapping.

The impact of PR on airway resistance-related respiratory mechanics cannot be resolved through this study design, but some assumptions are worth testing. The PR interventions that may lead to improved airflow resistance in emphysema may be summarized as follows: 1) breathing training, particularly pursed-lip breathing and controlled breathing techniques, prevent early airway closing, providing enough time to expel trapped air;37,43 2) deep inspiration is established to increase the production of surfactant, which maintains alveolar and airway stability;44 3) effective inhalation techniques allow inhaled medications to reach higher concentrations in the airways, facilitating stronger bronchodilation effect; 4) effective coughing and expectoration techniques eliminate secretions that cause airway obstruction and increased resistance;45 5) exercise training of leg muscles reduces lactate production and decreases ventilator load.46 A lower ventilation load allows COPD patients to breathe more slowly during exercise, consequently reducing dynamic hyperinflation.15,47 We speculate that airway resistance may be significantly reduced by the cumulative effect of PR interventions.48,49 It is clear that breathing exercises in COPD patients yield complex changes in pulmonary physiology.39,49 Therefore, body plethysmography can be beneficial in assessing the different aspects of these physiological changes.24

Although the expansion of airway diameter achieved by bronchodilator drugs in patients with COPD is smaller than in patients with asthma, the decrease in Raw provides an above-expected resistance reduction in relation to Poiseuille’s law (a reduction correlated with the 4th power of airway diameter).50 In addition, according to our clinical experience, we recommend that severe COPD patients take their short-acting bronchodilator drugs (with a nebulizer if necessary) 15–20 minutes before exercise, thus reducing the level of exercise limitation due to shortness of breath.51,52 Similarly, it would be more appropriate to focus on reducing airway resistance before respiratory muscle exercises with an incentive spirometry device.33 Otherwise, in the patient trying to breathe against the high resistance caused by the narrowed airway, the increased respiratory workload may increase O2 cost and cause more harm than benefit.

There are several limitations to this study. The main limitation is the single-center study design and small sample size. Inclusion of only patients with emphysema was the main reason for the low number of patients, but this was necessary for accurate analysis in this particular population. Another reason that plethysmography tests were expensive and had limited indications (preoperatively or before volume reduction intervention, etc.) in our hospital. We realize that the small size of the group does not allow generalization of results beyond this select group of patients. However, our group represents a fairly homogeneous group of patients with severe COPD and hyperinflation of the lungs, which is an important strength of the study.

In conclusion, our study suggests that the PR is effective in reducing airway resistance in COPD patients with severe hyperinflation. In addition, we believe that Raw and sGaw can be used as physiological biomarkers in the evaluation of PR benefit, especially in a select group of patients with severe airflow obstruction.

Funding

There is no funding to report.

Disclosure

The authors report no conflicts of interest in this study.

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It is estimated that 37 million Americans live with a chronic respiratory disease, and this dreadful condition led to the deaths of over 152,000 people in the United States in 2020 [1,2]. Chronic respiratory disease encompasses many disorders, including chronic obstructive pulmonary disease (COPD), asthma, interstitial lung fibrosis, and others [3]. Historically, of all the respiratory disorders, COPD is by far the deadliest. In 2020, 5% of Americans had a diagnosis of COPD, emphysema, or chronic bronchitis, which caused over 140,000 deaths [3]. COPD is the third leading cause of death worldwide, killing more than 3.23 million people in 2019 [4]. COPD is a common lung disorder that causes many abnormalities of the airflow in and out of the lungs. COPD comprises two main disorders: emphysema and chronic bronchitis [5]. Emphysema results from the destruction of alveoli, which are the terminal points of the lung allowing for the proper gaseous exchange of oxygen and carbon dioxide [5]. Chronic bronchitis is caused by excess mucus production in the lungs, leading to mucus plugging within the airways [5]. Both disorders are usually associated with smoking or exposure to tobacco, but they can also result from occupational exposures, restrictions of normal lung growth during childhood or adolescent years, and even genetic causes [5]. While both disorders are different, they are linked by the common symptoms of shortness of breath and difficulty breathing. Diagnosing COPD can be challenging; the most effective diagnostic test involves measuring lung function through spirometry [6]. The most commonly used pulmonary function tests together with spirometry for diagnosing COPD are the FEV1 (forced expiratory ventilation in the first second of expiration), FVC (forced vital capacity in an effortful expiration), and FEV1%/FVC (the proportion of FEV1 in an entire effortful expiration) [6]. Typically, FEV1%/FVC should be greater than 70%, and a value less than 70% would be indicative of COPD [6].

While there are many medications and treatments for COPD, there is no definitive cure for the disease. Treatment modalities like oxygen therapy and medications such as bronchodilators, anticholinergic agents, and inhaled/oral steroids are aimed at achieving symptomatic relief and preventing or treating disease exacerbations or flare-ups [7]. However, currently, there is no cure for the disease, and progression to mortality is a major concern.

While COPD is the most common lung disorder historically, with the emergence of the ongoing coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), many other variants of lung disorders have been reported. To date, there have been over 95 million confirmed cases in the US, killing over one million Americans [8]. The most common severe complication of COVID-19 is acute respiratory distress syndrome (ARDS) [9]. Though this pandemic is still ongoing, the long-lasting effects on recovered COVID-19 patients are already starting to be seen. ARDS could lead to many chronic effects, including lung fibrosis and scarring [10]. ARDS is caused by the buildup of fluid within the alveoli of the lungs, which can cause acute lung injury [10]. While pulmonary fibrosis affects the interstitium of the lung (cells that surround structures inside the lung) and COPD affects the alveoli and actual airways, they both result from lung damage and are considered terminal illnesses [11,12].

Chronic respiratory disease progression is unfortunately inevitable. While the current protocol of medications focuses on relieving symptoms and preventing and controlling exacerbations, many researchers are hopefully looking to mesenchymal stem cell (MSC) therapy for lung regeneration [13]. The current ways to obtain MSC are either via umbilical cords/embryonic tissue, bone marrow, or adipose tissue [13,14]. While MSC therapy looks promising, there are many challenges in obtaining these cells. Collecting these cells from umbilical cords or embryonic tissue is controversial in nature and acquiring MSC from bone marrow or adipose tissue requires a painful, invasive procedure with many possible complications [14]. An alternative is platelet-rich plasma (PRP). PRP is essentially plasma and serum, without erythrocytes, or red blood cells (RBC) [15]. To obtain PRP, a standard blood draw is done, and the blood is centrifuged to separate the RBCs from the remaining plasma [15]. This remaining plasma has a higher concentration of platelets, which contain many growth factors to aid in tissue repair. Some of these factors include platelet-derived growth factor (PDGF), insulin-like growth factor (IGF), vascular endothelial growth factor (VEGF), epidermal growth factor (EGF), transforming growth factor (TGF), and platelet-derived angiogenesis factor (PDAF); all of which play key roles in tissue regeneration by accelerating the healing process [15]. PRP’s application in orthopedic injuries, oral and maxilla-facial surgeries, and dermatologic and cosmetic surgeries to accelerate healing has been shown to be beneficial [16]. While the exact mechanism of how PRP regenerates tissue is yet to be understood, the effects that platelets have on pulmonary endothelium by releasing these growth factors include maintenance of barrier integrity via cell proliferation, enhancement of endothelial cell growth, and the neutralization of barrier permeability [17].

The purpose of this study is to determine if patients with COPD or other chronic lung disorders can benefit from PRP therapy, which accelerates lung regeneration. Although there is vast evidence of clinical progression in these patients, the current treatment of COPD is symptomatic in nature, and most patients deteriorate to the point where they either require lung transplantation or unfortunately die [7]. Since PRP therapy is quite effective in many fields of medicine in terms of accelerating natural tissue healing, the benefits of its application for chronic respiratory disease patients will be thoroughly reviewed in this study [16,18].

Methods

The following databases were used to obtain relevant material for this study: Google Scholar, PubMed, NCBI, Medscape, and clinicaltrials.gov. The specific keywords used to search for relevant articles were “Platelet Rich Plasma” AND “Chronic Respiratory Disease” AND/OR “Chronic Obstructive Pulmonary Disease”. To narrow down the material to a level of absolute relevance, the additional keywords used were “Autologous PRP” AND “Lung Regeneration”, but NOT “Stem Cell”.

Studies that were considered relevant included those that were published in or after 2006. Different types of studies were chosen, including case series, controlled clinical trials, non-controlled clinical trials, cohort studies, animal studies, and lab studies. Initially, the choice of studies was limited to human trials, but since PRP therapy is a rather new field of medicine and there is a limited number of published articles available regarding lung regeneration via PRP, case series, non-controlled clinical trials, animal trials, and lab studies were also considered relevant for this review.

Articles were excluded if they involved terms relating to “mesenchymal stem cells”, “drug therapy”, and “musculoskeletal injuries”. However, one study regarding “musculoskeletal injuries” was included as it helped explain the anti-inflammatory and tissue-regenerating capabilities of PRP therapy. Articles were excluded if proper statistics were not available. The exclusion criteria also included any articles that provided access to study abstracts only and reports from before 2006.

Initially, 32 articles were chosen for review. However, after eliminating duplicates and analyzing bias and the quality of the studies, this was reduced to 15 relevant articles, which were used to explore the topic and establish the hypothesis of this study. The reason for choosing a high number of primary articles was due to the limited availability of studies with a high level of evidence. Thus, including many reports with a lower level of evidence assisted in preventing biases and preferred outcomes.

All statistical data presented in the results section of this paper were considered significant if the p-value (the value that a given outcome could have occurred by chance alone) was less than 5%, or 0.05. Statistical analysis of the results section was performed using the following tests: t-test, analysis of variance (ANOVA), chi-squared test, two-tailed Wilcoxon signed-rank test, Shapiro-Wilk test, Fisher's exact test, and analysis of logistic regression. All data were considered statistically significant unless otherwise stated. Statistics and other data in the introduction were sourced from the World Health Organization (WHO), the Centers for Disease Control and Prevention (CDC), the American Lung Association (ALA), the Cleveland Clinic, the Mayo Clinic, and John Hopkins Coronavirus Resource Center to better outline the need for further research in the treatment of PRP in chronic respiratory disease patients. All primary articles used in this study are presented in a table in the next section, which provides a summary of the following: authors of the study, publication date, study design, the study population, therapy/exposure used in the study, the outcomes of the study, and the level of evidence. All published material was included in this table, except for articles that were used for background information provided in the introduction section.

Results

As previously mentioned in the introduction, the goal of this paper is to evaluate if patients with COPD or other chronic lung disorders can benefit from PRP therapy, which accelerates lung regeneration and slows the progression of the disease. If the natural progression of the disease is slowed, the belief is this will decrease mortality. However, just like stem cell therapy, PRP is not a cure for the disease, but rather potentially an adjunctive therapy to better control the mortality rate. Our review involved reviewing 15 articles that explored the use of PRP in chronic respiratory disease patients.

The information we present here explores the results of the 15 researched articles on PRP therapy in chronic respiratory disease patients. Four of the reviewed articles discuss the association between PRP use and the improvement of lung function and decreased exacerbations of the disease. The other 11 articles delve into the relationship between PRP therapy and tissue regeneration and anti-inflammatory effects. The remaining part of this section summarizes the results and data from the 15 articles selected and reviewed.

From 2017 to 2020, Rubio conducted a prospective cohort study to establish a possible relationship between PRP use and the improvement of lung function and decreasing symptoms [19]. A total of 419 COPD patients provided a baseline FEV1/FVC using spirometry, as well as a self-reported questionnaire on quality of life [19]. The questionnaire used was the Clinical COPD Questionnaire (CCQ), which is validated and endorsed by the Global Initiative for Chronic Obstructive Lung Committee (GOLD) [19]. The CCQ is a 10-question survey, with a score for each question ranging from 0 to 6, where 0 indicates “never”, while 6 indicates “always” [19]. The higher the numerical value of each component, the worse it is for the patient [19]. The CCQ quantifies three important aspects: COPD/respiratory symptoms, mental health status, and functional health state [19]. These patients all had their blood drawn and centrifuged to formulate PRP and were then infused back into them intravenously [19]. All 419 patients completed a CCQ survey at three, six, and 12 months post-PRP treatment [19]. Regarding COPD symptoms, the average CCQ scores decreased from 3.56 at baseline to 2.80 at three months, 2.60 at six months, and 2.78 at 12 months post-PRP [19]. For mental health, the average CCQ score also decreased from 3.83 at baseline, to 2.65, 2.26, and 2.48, at three, six, and 12 months post-treatment, respectively [19]. Functional health scores also decreased from 3.47 at baseline, to 2.87, 2.88, and 0.62, at three, six, and 12 months post-treatment, respectively [19]. A paired sample t-test conducted on each pair of baseline and follow-up scores showed significantly decreased numbers with a p-value of less than 0.001, making this statistically significant [19]. Although the baseline FEV1 was ascertained for all 419 patients, only 150 of these patients fulfilled a three-month FEV1/FVC check [19]. For these 150 patients, the FEV1 increased from a baseline of 32.65% to 34.3% at three months post-PRP, with an average increase of 7.83% [19]. Of note, 101 out of the 150 patients who retested their FEV1 at three months had either improved scores or no change [19]. A paired sample t-test was conducted to assess the difference between baseline and three-month FEV1/FVC, which was also statistically significant with a p-value of 0.003 [19].

Another cohort study performed by Rubio assessed the changes in FEV1/FVC in 281 COPD patients after autologous PRP was administered intravenously [20]. A baseline FEV1//FVC was measured before any treatment. The 281 patients were classified into two groups: Group A had 150 patients and their FEV1% was reevaluated after three months, while Group B had 131 patients, whose FEV1% was remeasured after 12 months [20]. The PRP infusion was prepared in the same way as in her previous study, mentioned above. Group A had an increase of FEV1/FVC from 33.2% at baseline to 34.7% at three months, with an average increase of 7.2% per patient [20]. Group B also showed an increase in their FEV1/FVC from 35.8% at baseline to 38.1% at 12 months, with an average rise of 6.88% per patient [20]. Using the two-tailed Wilcoxon signed-rank test and the Shapiro-Wilk test, results were shown to be statistically significant (p-value less than 0.05) [20]. Analysis of variance (ANOVA) was conducted for both groups and the results showed the following: Group A had F=1.149 and a p-value of 0.011, while Group B had F=1.130 and a p-value of 0.004 [20]. Together both groups showed statistically significant increases in their respective group’s FEV1%, signaling an improved lung function after the PRP therapy [20].

A case series conducted by Coleman and Rubio in 2015 measured the changes in COPD patients and their quality of life after autologous PRP was administered intravenously [21]. This case series involved 568 patients with COPD stages 2-4 [21]. Each participant had a CCQ assessed at baseline to quantify their quality of life and again at six months post-therapy [21]. This study classified patients into different groups. Group 1 (n=495) had a single veinous harvest of PRP and was administered the autologous PRP for three consecutive days [21]. Group 2 (n=17) had a double veinous harvest; the first PRP harvest was administered for three consecutive days; then three months later, the second harvest of PRP was done and administered for another three consecutive days [21]. Group 3 (n=36) had a single veinous harvest and reinfusion for one day, a bone marrow harvest and reinfusion on the second day, and a reassessment of the bone marrow wound on the third consecutive day [21]. Group 4 (n=30) was the “booster” group, which followed the same protocols as group 1; however, with disease progression, a second PRP infusion was conducted [21]. It is important to note that higher scores indicate a poorer quality of life, and lower scores show a better quality of life for the patient. Group 1 had a decrease in their COPD symptoms from 3.5 at baseline to 2.2 at six months, a decrease in mental health scores from 3.8 at baseline to 2.3 at six months, and a decrease in functional health scores from 3.7 at baseline to 2.8 at six months [21]. Group 2 had a decrease in their COPD symptoms from 2.9 at baseline to 1.4 at six months, a decrease in mental health scores from 4.2 at baseline to 1.9 at six months, and a decrease in functional health scores from 2.7 at baseline to 1.9 at six months [21]. Group 3 had a decrease in their COPD symptoms from 3.0 at baseline to 1.9 at six months, a decrease in mental health scores from 3.6 at baseline to 2.0 at six months, and a decrease in functional health scores from 3.7 at baseline to 2.7 at six months [21]. Group 4 had a decrease in their COPD symptoms from 2.9 at baseline to 2.4 at six months, a decrease in mental health scores from 3.3 at baseline to 1.8 at six months, and a decrease in functional health scores from 3.2 at baseline to 2.5 at six months [21]. The results from the CCQ were deemed clinically significant if there was a difference of 0.4 or more at the follow-up [21]. Utilizing the ANOVA, with a p-value of 0.05, together with a significant change in the CCQ at the six-month follow-up, this case series showed clinically and statistically significant changes in the quality of life of these COPD patients [21]. Although there were differences based on the group treatment type, the PRP infusion treatment positively affected each component of the CCQ at six months compared to the baseline [21].

In a case series by Karina et al., activated platelet-rich plasma (aPRP) was administered to seven COVID-19 patients suffering from ARDS [22]. The aPRP was created using patients’ blood that was centrifuged, and the remaining plasma was combined with a calcium activator [22]. Before administration, blood clots were removed and the remaining solution was reinfused into patients on days one, three, and five while in the intensive care unit [22]. Before the administration of the aPRP, a baseline lab level of interleukin-1B (IL-1B) was obtained, together with their PaO2/FiO2 and lung injury score [22]. IL-1B is a useful biologic marker that can help determine the inflammation in the body [22]. PaO2/FiOmeasures the ratio of arterial oxygen pressure dissolved in the blood compared to the level of fractional inspired oxygen, and a completely normal level is between 500-600 mmHg, with a value under 300 mmHg being diagnostic of ARDS [22]. The seven patients were subdivided into two groups to distinguish between the different IL-1B levels: three had severe disease and four were critical [22]. On days two, four, and six (after each aPRP treatment), these levels were each remeasured. Three out of the four critical patients ended up dying shortly after day six [22]. The three severe patients’ IL-1B levels decreased on average from 4.71pg/ml to 2.48pg/ml from day one to six, while the four critical patients’ IL-1B levels increased on average from 3.095pg/ml to 18.77pg/ml within the same timeframe [22]. Although 75% of the critical patients died, this development was not statistically significant based on a paired t-test (p-value was greater than 0.05) [22]. While evaluating the lung injury scores and the change in PaO2/FiO2, all seven patients were grouped together. The lung injury scores increased from 5.33 at baseline to 6.0 on day 6 [22]. While there was a net increase in the scores, after the second aPRP infusion, they decreased from 6.50 on day four to 6.0 on day six [22]. However, these changes were also not statistically significant as per a paired t-test (p-value was above 0.05) [22]. The final measurement conducted - the difference in PaO2/FiO2 - did show meaningful results [22]. The seven COVID-19 patients had an average baseline PaO2/FiO2 of 71.33 mmHg, which was diagnostic of ARDS [22]. On day six, however, these scores increased to 144.97 mmHg on average [22]. This value was statistically significant based on a paired t-test, with a p-value less than 0.05 [22]. While these scores never went beyond 300 mmHg, signaling that they were still experiencing ARDS, their ARDS was less severe, highlighting improved lung function [22].

From 2018 to 2020, Pires et al. conducted a randomized controlled animal trial involving 37 racehorses suffering from exercise-induced pulmonary hemorrhage to evaluate PRP treatment efficacy [23]. Most racehorses were evaluated post-race, which included endoscopy, as it is quite common for these horses’ airways to become inflamed and edematous [23]. Thirty-seven horses that showed signs of mucosal edema, airway inflammation, and visible airway bleeds were included and were randomly assigned to either placebo (n=14) or treatment group (n=23) [23]. Three days after the races, blood was collected for PRP and bronchoalveolar lavage (BAL) was conducted, with specimens to be used as control. The placebo group was administered 10 mL of 0.9% normal saline, while the study group was given 10 mL of autologous PRP; both groups were given 10 mL intrabronchially [23]. Five weeks after the intrabronchial administration, all the horses participated in another race and were again evaluated endoscopically post-race with BAL. The BAL specimens were all scored from 0 to 5, with 0 indicating no bleeds or inflammation and five being the worst result [23]. The 14 placebo horses had a mean increase from 2.0 after the first race to 2.5 after the second race, while the PRP-treated horses had a mean decrease from 3.21 to 1.52, respectively [23]. This was statistically significant after analysis revealed p=0.002 when comparing the pre-and post-race results of the PRP group to those of the placebo group [23].

In 2015, Mammoto et al. conducted a controlled animal trial to assess whether PRP could be used to promote the angiogenesis of the lung [24]. Since it has been recognized that PRP promotes endothelial cell sprouting in vitro and in vivo and that endothelial cells stimulate alveolar morphogenesis, this animal study assessed whether PRP can cause better lung remodeling [24]. The study involved six mice that had undergone surgical left pneumonectomy and PRP was used to promote overall better compensatory lung growth in the remaining right lungs. Six other mice were used as controls and, after the unilateral pneumonectomy, the following parameters were compared with the control group: right lung weight, static lung compliance, pulmonary vascular permeability, alveolar-arterial oxygen difference, and exercise capacity [24]. After seven days, some mice underwent microscopy of the lung as well. Once the surgery was complete, PRP extract was given to the mice every day for 14 days, via intraperitoneal injection, and all measurements were reassessed at seven and 14 days post-surgery [24]. As expected, in all mice that had undergone unilateral left pneumonectomy, the right cardiac lung lobe increased significantly by 1.4-fold from days seven to 14 post-surgery (measured via the ratio of right cardiac lung lobe weight to total mouse weight) [24]. However, in the PRP-treated mice post-surgery, their ratio significantly increased by 14% compared to the control group (pneumonectomy without PRP treatment) [24]. Regarding right lung compliance, in PRP-treated mice, the total right lung compliance was 30% greater than the control group post-surgery [24]. Lung vascular permeability was measured by intravenously injecting dye and measuring the leakage into the alveolar space. However, there was no change between the PRP-treated group and the control group in terms of permeability, indicating that PRP did not cause inflammation of the tissue [24]. There was also no difference between the study and control group with regard to alveolar-arterial oxygen. However, microscopy using hematoxylin and eosin (H&E) stain showed thickened alveola septa, a decrease in the size of alveolar space, and an increase in the number of alveoli in PRP-treated mice post-pneumonectomy compared to the control group [24]. Additionally, the blood vessel density of the lung was analyzed using CD31, a blood vessel biomarker, and showed increased blood vessel density in the PRP group compared to controls [24]. These results indicate that PRP accelerates vascular and alveolar regeneration and remodeling post-pneumonectomy [24]. All analyses were performed by masked observers, to ensure unbiased findings. A student’s t-test and ANOVA were conducted, which showed the analysis of all measurements to be statistically significant (p-value was less than 0.05) [24].

Salama et al. conducted a randomized controlled trial from 2015 to 2017 in order to assess the efficacy of nebulized autologous PRP in smoke inhalation patients [25]. The study included a total of 40: 20 in the study group and 20 acted as the control group [25]. Each patient had between 25-50% of total body surface area burns, plus smoke inhalation lung injuries [25]. Each group, regardless of PRP, received the standard treatment regimen. Each patient required mechanical ventilation via intubation within 48 hours of admission. The study group was given autologous PRP via nebulization as an adjunctive treatment [25]. Throughout each patient’s hospital stay, the following variables were recorded for statistical use: day of extubation (patient no longer requiring mechanical ventilation), mortality rate, hospital length of stay, and PaO2/FiO2 [25]. The mean intubation length was seven days for the nebulized PRP group, compared to 14 days in the control group [25]. The average hospital stay was also less in the PRP group (15 days), compared to controls (23 days) [25]. The mortality rate was 10% in the PRP group and 20% in the control group [25]. The average PaO2/FiO2 was 36.24 in the PRP group and 25.17 in the control group [25]. Additionally, in the nebulized PRP group, there was a significant difference in biological changes in the upper airway, compared to the control group, which manifested as follows: decreased edema, decreased mucus formation, and decreased tissue inflammation [25]. The following statistical tests were used to ensure the value of this cohort study: Pearson's correlational coefficient for analyzing the association between different parameters, student’s t-test to assess the differences between the two groups, and logistic regression for evaluating all combined factors (age, gender, total body surface areas of burns, and PaO2/Fio2 ratio) [25]. The p-value level of significance was less than 0.01 for all tests, showing a statistically significant difference [25].

A controlled animal study performed by Gómez-Caro et al. assessed the relationship between PRP use and airway healing as well as the decrease in possible anastomotic complications [26]. This study involved 15 adult Yorkshire Duroc pigs. These pigs were randomly divided into three groups, with five pigs in each group. Group 1 was the sham treatment group; each pig underwent cervicotomy and cervical and tracheal dissection without resection [26]. This group acted as the control group. Group 2 underwent cervicotomy and cervical dissection with resection of 50% of the tracheal total length with end-to-end anastomosis [26]. This group was the non-PRP group. Group 3 underwent group 2’s protocols with the addition of PRP applied over the surgical area, including the anastomoses [26]. Blood was extracted from the animals via a jugular vein central line and was centrifuged to create the separation of RBCs and plasma [26]. The RBCs were removed and the PRP was left. A small sample of the PRP was analyzed and the remaining PRP was used during the surgery. This central line was also the point to extract blood for assessment of growth factors at one and six hours post-surgery, and laser Doppler flowmetry was used to measure the blood flow rates during the surgery and 30 days post-surgery [26]. After 30 days, the animals’ tracheas were viewed under microscopy and blindly assessed, to ensure unbiased findings [26]. All surgeries were completed successfully without complications; however, one pig in Group 2 (non-PRP) died at nine days due to pneumonia [26]. The sampled PRP showed a platelet count of 638 x 109 per cubic millimeter of blood (mm3), while the whole blood sample showed 176 x 109 mm3 (p=0.02) [26]. The following platelet-derived growth factors were assessed at one and six hours post-surgery: total growth factor-β (TGF-β), EGF, and VEGF [26]. Group 1 (sham) had an increase in TGF-β from 0.58 ng/ml at one hour to 0.69 ng/ml at six hours, an increase in EGF from 0.21 ng/ml at one hour to 0.23 ng/ml at six hours, while VEGF stayed the same (0.10 ng/ml) at one and six hours [26]. Group 2 (non-PRP) had an increase in TGF-β from 0.63 ng/ml at one hour to 0.66 ng/ml at six hours, a decrease in EGF from 0.50 ng/ml at one hour to 0.23 ng/ml at six hours, and an increase in VEGF from 0.12 ng/ml at one hour to 0.14 ng/ml at six hours [26]. Group 3 (PRP) had the same TGF-β values (0.86 ng/ml) at one and six hours, a decrease in EGF from 0.86 ng/ml at one hour to 0.69 ng/ml at six hours, and a decrease in VEGF from 0.30 ng/ml at one hour to 0.18 ng/ml at six hours [26]. The PRP group consistently showed the highest values with regard to platelet-derived growth factors (p=0.03), indicating a possible acceleration of healing [26]. Laser Doppler flowmetry showed that the average trans-anastomotic blood flow rate in Group 2 was +3.8%, while it measured +15.6% in Group 3 (p=0.04) [26]. After 30 days, the tracheas were blindly assessed by pathologists and showed higher vessel density and epithelial thickness in the PRP group, compared to the non-PRP group; but this was not statistically significant (p=0.08) [26]. All data values were determined to be significant via ANOVA and student’s t-test, except for the pathology report [26].

Maher et al. did a controlled animal study to assess the efficacy of PRP usage for the treatment of amiodarone-induced pulmonary fibrosis [27]. Amiodarone, a very useful medication in cardiology, is known to have many adverse effects, including pulmonary fibrosis [27]. This trial used 70 adult albino rats in total, divided into three groups, with each group consisting of 20 rats, while 10 rats functioned as PRP donors [27]. Group 1 acted as the control group. Group 2 (non-PRP) was given amiodarone via intraperitoneal injection daily for three weeks, followed by phosphate-buffered saline (PBS) twice weekly for three weeks via intra-peritoneum [27]. Group 3 (PRP) had a similar protocol to Group 2: amiodarone daily for three weeks intraperitoneally, followed by PRP twice weekly for three weeks [27]. The following data were collected between weeks four and six: hematological analysis, BAL fluid collection, and antioxidant biomarkers [27]. Glutathione reductase and malondialdehyde (MDA) were used as the antioxidant markers. Glutathione reductase is an important enzyme used to treat oxidative stress, and MDA is an important marker signifying if oxidative stress has occurred [27]. At the end of the study, lung tissue was examined using microscopy. All statistical analyses were performed using ANOVA. The study showed that Group 2 (non-PRP) experienced a significant decrease in white blood cells (WBC) and RBC compared to the control group [27]. However, Group 3 showed a significant increase in WBC at weeks four to six, and an increase in RBC at weeks five to six when compared to Group 2 [27]. Glutathione reductase levels were significantly decreased in Group 2 at weeks four to six, compared to the control group [27]. However, in Group 3, there was a significant increase in glutathione reductase at weeks five to six when compared to Group 2 [27]. Both Groups 2 and 3 showed significantly increased levels of MDA in the fourth week when compared to the control group [27]. However, in Group 2, this level remained high in weeks five to six, while Group 3’s MDA levels significantly decreased in weeks five to six, when compared to each other [27]. The BAL fluid was collected and stained with Giemsa stain and was examined under the microscope, as was the lung tissue. Microscopy determined that Group 2 (non-PRP) had significant leukocytosis, abundant macrophages, and suffered from interstitial pneumonia with emphysematous areas and bronchiolitis [27]. Group 3 (PRP) had a significantly lower leukocytosis with normal lung tissue, which was evident in PRP’s acceleration of healing [27]. All data were proven to be statistically significant via ANOVA with p-values less than 0.05 [27].

In another animal trial conducted by Dzyekanski et al., 10 racehorses with recurrent cough, wheezing, and other pulmonary symptoms were administered intrabronchial PRP for treatment analysis [28]. The BAL fluid was collected before treatment and again at seven days post-treatment. After analyzing the BAL specimen, the horses were grouped based on their diagnosis: recurrent airway obstruction (RAO) (n=2), inflammatory airway disease (IAD) (n=5), and normal lung (NL) (n=3) [28]. Although the three horses in the “normal” group experienced pulmonary symptoms, their BAL sample was inconclusive for diagnosis [28]. The PRP was prepared similarly to the previous studies reviewed and was administered into the right and left main bronchus (intrabronchial), using endoscopic guidance [28]. The BAL fluid was examined and analyzed for tracheal mucus grade and relative neutrophil count [28]. After examining the BAL fluid on day seven, the results were determined. The IAD group had an average tracheal mucus reduction of 2.4, compared to a reduction of 1.4 in the RAO group (p=0.034) [28]. Additionally, the relative neutrophil count was significantly decreased in the IAD group by 13.0, compared to 5.0 in the RAO group (p=0.014) [28]. The IAD horses were the only group to show clinically significant improvement in pulmonary effects in a physical exam, while both the RAO and NL groups showed little to no clinical improvement [28]. The NL group also showed very little change in mucus grade reduction and relative neutrophil reduction, per their BAL sample [28]. This trial showed the anti-inflammatory effect and improvement of PRP in IAD racehorses [28]. All statistical data were analyzed by a paired student’s t-test, to identify statistical significance [28].

In a human clinical trial conducted by Karina et al., the researchers investigated the safety and efficacy of aPRP as an adjunctive treatment in severely ill COVID-19 patients [29]. Ten COVID-19 patients suffering from ARDS were enrolled in the study and were given aPRP on days one, three, and five, via intravenous infusion [29]. The PRP was prepared similarly as in previously reviewed studies; however, a calcium activator was added to the mixture for activation [29]. On days two, four, and six (post-PRP), the following lab values were ascertained: C-reactive protein (CRP), neutrophil count, lymphocyte count, lymphocyte-to-CRP ratio (LCR), and neutrophil-to-lymphocyte ratio (NLR) [29]. A baseline level of these labs was also collected before any aPRP therapy, which was used to identify if aPRP had any anti-inflammatory effects in severely ill COVID-19 patients [29]. All statistical lab value changes were analyzed with a paired t-test, and the Shapiro-Wilk test was used for data distribution [29]. The average CRP level on day one was 10.89 and decreased to 2.53 on day six (p=0.005); the mean neutrophil count was 81.42 on day one and increased to 84.12 on day six (p=-0.389); and the average lymphocyte count was 19.37 on day one and decreased to 8.77 on day six (p=0.234) [29]. The average LCR increased from 1.64 on day one to 6.91 on day six (p=0.009), and the mean NLR increased from 11.79 on day one to 11.94 on day six (p=0.285) [29]. Although there were changes, the only statistically significant differences were in the average decreased CRP (p=0.005) and the increased LCR (p=0.009) [29]. Although these two differences prove the beneficial anti-inflammatory effect of aPRP in these patients, the other lab values neither prove nor disprove this, as they are statistically insignificant [29].

From 2009 to 2014 Alamdari et al. conducted a randomized controlled trial to evaluate the efficacy of pleurodesis with PRP and fibrin glue for the treatment of chylothorax post-esophagectomy [30]. A total of 52 patients diagnosed with esophageal cancer were included in this trial and were randomly assigned into two groups, with 26 patients in each group: one group underwent thoracic duct ligation via surgery and one group underwent pleurodesis with platelet-rich fibrin glue (PRFG) from PRP via chest tube [30]. Chylothorax refers to an accumulation of lymphomatous fluid within the lung pleura, commonly caused by damage in the thoracic duct [31,32]. Pleurodesis is a procedure to obliterate the pleural space between the visceral and parietal pleura of the lung [31,32]. PRFG was created by first centrifuging the blood to make PRP, as previously discussed. However, a portion was then centrifuged again to separate platelets from plasma, and this plasma combined with PRP constituted the final PRFG [30]. While all 26 PRFG pleurodesis patients were successfully treated, 20 of the 26 thoracic duct ligation patients had successful outcomes (p=0.009), although seven pleurodesis patients required an additional PRFG administration a week later [30]. The average hospital length of stay was 53.50 days in the thoracic duct group, compared to 36.04 days in the PRFG pleurodesis group (p<0.001) [30]. Additionally, the average ICU length of stay was 14.27 in the thoracic duct ligation group compared to 2.23 in the PRFG group (p=0.0001) [30]. The time to a successful outcome from the last intervention (surgery or PRFG) was also less in the PRFG group (3.90 days), compared to the thoracic duct ligation group (4.77 days), which was found to be statistically significant (p=0.004) [30]. Five patients in total died, four from the thoracic duct group and one from the PRFG group; however, this outcome was not statistically significant (p=0.1621) [30]. Statistical analysis was performed using the student’s t-test, Chi-square test, and Fisher's exact test, with p<0.05 considered statistically significant [30]. The results that showed statistically significant increased success rates and decreased hospital and ICU stay lengths suggest that pleurodesis with PRP and fibrin glue should be considered in all postoperative chylothorax patients [30].

In the only lab study reviewed here, Beitia et al. evaluated if nebulized PRP had a more beneficial effect on lung fibroblast growth compared to non-nebulized PRP [33]. Four healthy human donors were used for PRP collection. After the PRP was obtained, a calcium activator was added [33]. This article refers to the final solution as platelet lysate (PL), although there was no difference with activated PRP (aPRP) [33]. The PRP-PL was applied to lung fibroblast tissue contained in a fibroblast growth medium, via nebulization and non-nebulization (standard) [33]. A serum-free medium was used as a control. The researchers measured the growth rates of each for 96 hours, with data points collected at 24, 48, 72, and 96 hours [33]. Statistical analysis was performed using an unpaired t-test, with p-values under 0.05 identified as statistically significant [33]. Although the results indicate that both nebulized and non-nebulized PRP induced statistically significant fibroblast growth rates compared to controls, the study also showed that non-nebulized PRP has statistically higher rates than nebulized [33].

Between 2007 and 2012, Serraino et al. conducted a non-randomized controlled trial to evaluate the efficacy of PRP in preventing sternal wound infections in cardiac surgery patients [34]. After undergoing successful cardiac surgery, 671 patients, acting as controls, received standard closure of the chest, while 422 patients had the same closure but with PRP added to the edges of the sternum [34]. All patients had standard wound dressing changes daily for one month and received antibiotics prophylactically [34]. In the PRP group, two patients (0.5%) suffered from superficial sternal wound infection (SSWI), while the control group had 19 patients (2.8%) who experienced SSWI (p=0.006) [34]. In the PRP group, only one patient (0.2%) developed a deep sternal wound infection (DSWI), while the control group had 10 patients (1.5%) who experienced DSWI (p=0.043) [34]. Statistical analysis was performed using the unpaired t-test, with clinical significance determined by p-values <0.05 [34]. The control group had more incidents of deep and superficial sternal wound infections when compared to the PRP group [34].

Lastly, from 2009 to 2014, Huang et al. conducted a randomized controlled trial among patients with osteoarthritis of the knee to assess intra-articular PRP’s treatment capacity [35]. A total of 366 patients were randomly divided into two groups: 310 received PRP while 56 got the placebo (normal saline solution) [35]. All patients received 10 mL of either PRP or placebo via intra-articular injection with ultrasound guidance once a week, for a total of four weeks [35]. The following inflammatory plasma marker levels were evaluated: interleukin-17A (IL-17A), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), receptor activator of nuclear factor-κB ligand (RANKL), interleukin-6 (IL-6), and interferon-γ (IFN-γ) [35]. Additionally, the following plasma pro-angiogenic marker levels were assessed: hepatocyte growth factor (HGF), intercellular adhesion molecule-1 (ICAM-1), osteopontin (OPN), platelet-derived endothelial cell growth factor (PD-ECGF), VEGF, PDGF, insulin-like growth factor-1 (IGF-1), and TGF-β [35]. All lab values were taken at baseline (before injection) and again at eight weeks (four weeks post-injection) [35]. Additionally, MRI was performed at eight weeks to assess the degree of joint inflammation, synovial degeneration, and neovascularization [35]. At the eight-week assessment, all inflammatory marker levels were significantly lower in the PRP group compared to the placebo group (IFN-γ and IL-17A showed p-values <0.001; all other inflammatory markers had p-values <0.01) [35]. Conversely, at week eight, all pro-angiogenic marker levels were significantly greater in the PRP group compared to the placebo group (ICAM-1, OPN, and PDGF had p-values <0.01; all other pro-angiogenic markers had p-values <0.001) [35]. Joint inflammation, synovial degeneration, and percentage of the damaged area were significantly downregulated in the PRP group compared to the placebo on MRI (p<0.001), but neovascularization was significantly greater in the PRP group compared to the placebo (p<0.001) [35].

Discussion

The data from the 15 research articles that were used to test the hypothesis of this paper will be summarized and further discussed in this section. While four of the presented articles explore the relationship between PRP therapy and lung function improvement, which could decrease symptom severity and exacerbation, the remaining 11 studies expanded on the association between PRP treatment and anti-inflammatory qualities, which help accelerate the healing and regeneration of lung tissue. The following paragraphs will explore these connections further and describe the limitations of these studies. Table 1 summarizes all primary articles used in this study. It includes a summary of all published materials, except for articles that were used for background information in the Introduction section.

First author Publication date Study design Study population Therapy or exposure
Alamdari et al. [30] April 2018 Randomized controlled trial 52 patients with chylothorax Group 1: thoracic duct ligation (surgery); Group 2: pleurodesis with PRFG
Beitia et al. [33] February 2021 Preclinical lab study 4 healthy adult donors PRP-PL nebulized and non-nebulized (standard) on lung fibroblast cultures
Coleman and Rubio [21] March 2018 Case series 568 COPD patients Group 1: single PRP; Group 2: double PRP; Group 3: bone marrow and PRP; Group 4: booster
Dzyekanski et al. [28] December 2012 Animal trial 10 racehorses divided into 3 groups: 1: RAO, 2: IAD, 3: NL PRP was given intrabronchially and BAL fluid was assessed
Gómez-Caro et al. [26] December 2011 Animal trial 15 adult Yorkshire pigs Group 1: sham; Group 2: non-PRP; Group 3: PRP
Huang et al. [35] January 2018 Randomized controlled trial 366 patients with osteoarthritis of the knee Group 1: PRP injections; Group 2: placebo (normal saline) injections
Karina et al. [22] July 2021 Case series 7 COVID-19 patients with ARDS (3 severe, 4 critical) aPRP infusion on 1st, 3rd, and 5th day
Karina et al. [29] July 2021 Phase I/II clinical trial 10 severely ill COVID-19 patients aPRP infusion on 1st, 3rd, and 5th day in ICU
Maher et al. [27] July 2020 Animal trial 70 Albino rats with amiodarone-induced lung fibrosis Group 1: control; Group 2: amiodarone and phosphate buffer saline; Group 3: amiodarone and PRP
Mammoto et al. [24] January 2016 Animal trial 12 mice with left pneumonectomy 6 mice were given PRP; 6 mice acted as controls
Pires et al. [23] June 2021 Animal trial 37 racehorses with exercise-induced pulmonary hemorrhage Group 1: placebo; Group 2: PRP
Rubio [19] June 2021 Cohort study 419 COPD patients PRP infusion
Rubio [20] January 2021 Cohort study 281 COPD patients: Group A: FEV1% reassessed at 3 months; Group B: FEV1% reassessed at 12 months PRP infusion
Salama et al. [25] July 2019 Randomized controlled trial 40 adults with smoke inhalation injury: Group A: study; Group B: control Group A: nebulized PRP therapy plus a normal regimen; Group B: only normal treatment regimen
Serraino et al. [34] May 2013 Randomized controlled trial 1,093 post-cardiac surgery patients Group 1: Control Group 2: PRP at the wound

Two cohort studies by Rubio were included in this paper. In her first article, results showed an improvement in the self-reported CCQ scores after PRP treatment, compared to their baseline [19]. Since the CCQ measures COPD symptom severity and exacerbations, mental health, and functional health state, the improved scores correlate with a better outcome in terms of respiratory symptom control and an improvement in the quality of life of patients [19]. Additionally, 150 patients out of the original 419 had their FEV1/FVC re-evaluated at three months, which also showed an improvement in their scores [19]. Although this cohort had a respectable sample size, the limitations of this study include the lack of a control group, which the author stated was due to ethical grounds in not wanting to not treat COPD patients [19]. Another limitation of this study was the limited number of patients whose FEV1/FVC was remeasured at three months [19]. However, the results of this study highlight the beneficial effect that PRP therapy has on lung function in COPD patients, supporting the hypothesis of this paper, although with low evidence.

The second article by Rubio evaluated the change in FEV1/FVC scores in 281 COPD patients after PRP therapy [20]. This study divided the patients into two groups: Group A (150 patients) had their FEV1/FVC remeasured at three months, and Group B (131 patients) had theirs retaken at 12 months [20]. The results showed an improvement in both groups’ FEV1 scores after treatment compared to their baseline scores [20]. These results also show the benefit that PRP has on COPD patients’ lung function through their improved scores; however, there are limitations to this study [20]. Apart from the limitation associated with the small sample size, this study also did not have a control group for similar reasons to the author’s previous study. While the findings in this cohort do support the hypothesis of this paper, this article also had a low level of evidence.

In the case series by Coleman and Rubio, PRP usage in COPD patients was also shown to be beneficial based on self-reported decreases in symptom severity, and improvement of mental and functional health [21]. Group 2 (double PRP treatment) showed the highest rates of improvement in symptoms and mental health than the other three groups, but Group 3 (bone marrow and PRP therapy) displayed the best improvement in functional health [21]. While this study included many subjects, it was also hampered by the lack of a control group, and the results should be considered with caution [21]. This study also supports our hypothesis.

In the case series by Karina et al., seven patients were given adjunctive-activated PRP treatment for COVID-19-induced ARDS [22]. Although two of the three tested measurements were shown to be statistically insignificant (IL-1B levels and lung injury scores) before and after treatment, the overall increase in PaO2/FiO2 of the seven patients signifies that the PRP treatment improved their lung function [22]. The average increase of 73.64 mmHg in their PaO2/FiO2 showed improved lung function, supporting this paper’s hypothesis [22]. However, this series also lacked a control group, and the results should be viewed cautiously.

In the randomized controlled trial conducted by Salama et al. involving 40 smoke inhalation patients, results showed that PRP had a positive correlation with lower intubation day lengths, lower hospital stay lengths, lower mortality rates, and an increased PaO2/FiO2 when compared to the control group [25]. The PRP group also showed evidence of decreased pulmonary edema, decreased mucus formation, and lower inflammation of the airway [25]. This study suggests that PRP use in smoke inhalation patients can cause anti-inflammatory effects and overall better tissue regeneration, which supports the hypothesis of this paper [25].

We examined five studies involving animal trials in this review, and they showed positive tissue regeneration and anti-inflammatory effects of PRP treatment. Although the tested animal populations (two studies on mice, one on pigs, and two on horses) were different, each study showed accelerated pulmonary tissue healing.

In the randomized controlled animal trial in racehorses by Pires et al., the results showed that PRP decreased the level of intensity of bleeding and inflammation [23]. Although the exact mechanism is still under investigation, it was inferred that the platelet’s effect on releasing growth factors, which are involved in inflammation, clotting, cell adhesion, and proliferation, played a major role in controlling the bleeds [23]. Evidence showed that exercise-induced pulmonary hemorrhage leads to extensive lung vasculature remodeling and angiogenesis, and the high concentration of platelets in PRP enabled the control of the deposition, causing a more favorable remodeling with less inflammation [23]. Although the inability to measure PRP and growth factors in these subjects is a limitation [23], this study does suggest a positive remodeling of lung tissue with decreased inflammation, which supports the hypothesis of this paper.

In the study by Mammoto et al., the PRP-treated mice showed significant results in comparison to the control group [24]. The results showed an overall acceleration of lung healing based on an increased lung-to-body weight increase by 14%, increased lung compliance by 30%, thickened alveoli septa, decreased alveolar space size, increased number of alveoli, and increased blood vessel density [24]. This data imply that PRP usage improved overall lung regeneration in unilateral pneumonectomy mice [24]. Even though this article tested mice, its findings could be applied to humans with lung disease as well, supporting the tested hypothesis of this review [24].

In the other animal trial on mice, Maher et al. used PRP in amiodarone-induced pulmonary fibrosis [27]. In the study, both groups treated with amiodarone suffered from thrombocytopenia and hemolytic anemia, which were induced by the amiodarone injections [27]. Although these groups had hematologic issues, the mice showed improvement after one week of PRP treatment, compared to the non-PRP-treated mice [27]. Additionally, the PRP-treated mice had an acceleration of lung tissue healing when compared to the non-PRP group [27]. Their results indicate that the PRP treatment accelerated the regeneration of the lungs, which caused the normalization of lung tissue, thereby supporting the hypothesis of this paper [27]

In the controlled animal study by Gómez-Caro et al., researchers applied PRP therapy for surgically induced anastomosis in adult pigs [26]. Their results indicated that the PRP itself had higher platelet-derived growth factors (TGF-β, VEGF, and EGF) compared to whole blood analysis [26]. These growth factors have been proven to accelerate tissue repair and healing. Additionally, their results showed higher blood flow rates across the PRP-applied anastomoses, compared to the non-PRP and controlled ones [26]. Although pathology reported higher vessel density and epithelial thickness in the PRP group, this was ultimately deemed statistically insignificant (p-value greater than 0.05) [26]. The higher growth factor levels in the PRP and the increased blood flow rates indicate a faster tissue repair in these pigs, which ultimately supports the hypothesis of this paper that PRP induces an acceleration of pulmonary tissue repair [26].

In the final animal trial presented in this paper, Dzyekanski et al. examined the use of PRP therapy in racehorses that had recurrent coughs [28]. The results indicated that the horses with inflammatory airway disease had significant benefits from PRP therapy [28]. They showed anti-inflammatory effects via a reduction in relative neutrophil count and tracheal mucus grade of their BAL sample, as well as a clinically significant improvement in their cough [28]. However, the groups with recurrent airway obstruction and the undiagnosed (normal lung) showed no significant effects with the PRP treatment [28]. This study was limited by the lack of a control group and the use of animals instead of humans, and hence these results should be reviewed carefully [28]. The results of Dzyekanski et al. do support this paper’s hypothesis, but with weak evidence.

In the phase-I/II clinical trial performed by Karina et al., the researchers tested the safety and efficacy of PRP infusions in 10 severely ill COVID-19 patients suffering from ARDS [29]. Although their results indicated that only two out of the five tested lab measurements were proven to be statistically significant [29], the study did show a reduction of CRP levels by an average of 8.36 and an average increase of the lymphocyte-to-CRP ratio to 5.27 after three treatments of PRP infusions [29]. Since CRP is a useful marker of inflammation, its reduction provides an important indication of anti-inflammation [29]. However, the other three tested measurements (average neutrophil count, lymphocyte count, and neutrophil to lymphocyte ratio) were statistically insignificant, and could not be used [29]. Although the results indicate the anti-inflammatory properties of PRP therapy in COVID-19 patients, this study lacked a control group and should be viewed accordingly [29]. However, this article supports the hypothesis of this paper, indirectly, via the anti-inflammatory effects provided by PRP.

The randomized clinical trial by Alamdari et al. involving post-esophagectomy chylothorax patients with PRFG showed a massive success for PRFG pleurodesis when compared to thoracic duct ligation surgery [30]. All 26 patients in the PRFG pleurodesis group were successfully treated, had a lower average hospital and ICU stay length, and had a quicker time to success after intervention [30]. The researchers’ rationale for administering PRFG was PRP’s well-evidenced wound-healing capabilities [30]. These properties of PRP are made possible by the release of many growth factors and cytokines, which play a vital role in chemotaxis, cell proliferation, and differentiation [30]. Through these capabilities, PRP accelerates the framework required in the process of establishing successful pleurodesis [30]. Though this study does not directly support the hypothesis of this paper, it underlines the effect that PRP has on cell proliferation and differentiation through its released growth factors.

The human clinical trial conducted by Serraino et al. evaluated the use of PRP in preventing sternal wound infection in post-cardiac surgery patients [34]. The results of this study show that the patients who were given PRP at the wound site had significantly lower rates of superficial and deep sternal wound infections, compared to the control group [34]. Although this study was a controlled human trial, it was non-randomized, and hence the results should be viewed accordingly with caution [34]. The authors of this article suggest that the rich concentration of platelets and the growth factors secreted caused an accelerated migration of inflammatory cells, leading to improved angiogenesis and overall healing [34]. This mechanism during the inflammatory stage of healing indirectly supports the hypothesis of this paper that PRP can regenerate lung tissue.

The clinical trial discussed by Huang et al. highlights the anti-inflammatory properties of PRP, which were demonstrated by the reduction in inflammatory marker levels, as well as the reduction of the degree of joint inflammation seen on MRI when compared to the placebo group [35]. Additionally, PRP induces angiogenesis and regeneration through the growth factors secreted by the high concentration of platelets, which was shown by the increased pro-angiogenic marker levels and the increased neovascularization on MRI compared to the placebo [35]. MRI also revealed a reduction of synovial degeneration, and the extent of damaged tissue was lower compared to the placebo [35]. Although this article does not discuss the effect PRP has on lung tissue, this trial was double-blinded with a high level of evidence and can better illustrate the effects of PRP [35]. This human clinical trial indirectly supports the hypothesis of this paper by highlighting the anti-inflammatory and tissue-regenerating effects that PRP has on the body.

The final article that we reviewed in this paper was a lab study by Beitia et al., which tested the effects of nebulized PRP over standard PRP on lung fibroblast growth [33]. Although the standard aPRP had higher growth activity than the nebulized aPRP, both nebulized and non-nebulized variants had significantly more growth than the serum-free control [33]. These results indicate that aPRP causes an acceleration of fibroblast growth rates, and because fibroblast cells can help induce the differentiation and growth of other pulmonary cells, particularly alveolar cells (type 1 and 2) and endothelial cells, the increase of fibroblasts is directly associated with an acceleration of the natural healing of the lungs [33]. This lab study supports the hypothesis of this paper that PRP therapy can be beneficial for chronic respiratory disease patients by helping with the regeneration of the lung tissue, which ultimately would slow the natural progression of the disease [33].



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AirPhysio is an advanced product that is used for the expansion of the lungs and the clearance of mucus. The device is built in a way that it uses the natural process of Oscillating Positive Expiratory Pressure (OPEP). This process helps in reaching the goal of AirPhysio, which is to clear out the mucus for a better breathing experience.

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The links contained in this product review may result in a small commission if you opt to purchase the product recommended at no additional cost to you. This goes towards supporting our research and editorial team. Please know we only recommend high-quality products.

Disclaimer:

Please understand that any advice or guidelines revealed here are not even remotely substitutes for sound medical or financial advice from a licensed healthcare provider or certified financial advisor. Make sure to consult with a professional physician or financial consultant before making any purchasing decision if you use medications or have concerns following the review details shared above. Individual results may vary and are not guaranteed as the statements regarding these products have not been evaluated by the Food and Drug Administration or Health Canada. The efficacy of these products has not been confirmed by FDA, or Health Canada approved research. These products are not intended to diagnose, treat, cure or prevent any disease and do not provide any kind of get-rich money scheme. Reviewer is not responsible for pricing inaccuracies. Check product sales page for final prices.



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I overheard the EMS radio calling in to the emergency department and could immediately hear the urgency in the voice of the paramedic about a patient being brought in.

He told us they were bringing in a 43-year-old woman who was in respiratory distress. He advised of their prehospital treatment and that they would be there in about 5 minutes. I grabbed a quick sip of my coffee and assembled my team to be ready for the patient's arrival.

When I got to the room, the respiratory therapist was already there, getting his supplies ready. One of my nurses was getting the cardiac monitor and IV supplies ready, while another nurse was logging in to the computer at the patient’s bedside. I asked the pharmacist to be available as I hung up my white coat on the back of the door, secured my facemask and grabbed a pair of gloves. We were ready to go when the patient rolled through the door.

The paramedics had put Betsy on their cardiac monitor and were giving her breathing treatments through a mask over her mouth and nose. They had put an IV in her arm. They said they had taken care of Betsy previously and knew she had a history of chronic obstructive pulmonary disease (COPD) from a long history of smoking.  Unfortunately, Betsy had frequent episodes of respiratory distress that were occurring with increasing frequency in recent months.

Betsy looked uncomfortable and anxious when she arrived, sitting straight up on the ambulance cot and holding onto the sides of the bed. Her respiratory rate was increased, and I could hear her wheezing over the noise of the air blowing the medications into her facemask. She could only speak one or two words at a time when we were asking her questions, which seemed to make her even more anxious. We moved Betsy over to her emergency department bed, hooked her to our monitor and continued giving her breathing treatments. We also gave her a dose of steroids to decrease inflammation in her lungs and airway. I asked her to try to relax and to focus on slow, intentional breaths.

Emergency Medicine: Most of us still frazzled by effects of COVID pandemic

I put in orders for lab work and a chest X-ray, and I looked through her previous emergency department and hospital records since she could not initially give me much information. Betsy had been seen in the emergency department several times in the preceding month, each time for difficulty breathing and cough. Betsy had started smoking when she was in her early teens and tried to quit unsuccessfully many times. She had been diagnosed with COPD in her late 30s.

COPD is a chronic lung disease that includes chronic bronchitis and emphysema. With COPD, the airways become inflamed and thicken, which destroys the tissue where oxygen is exchanged and decreases the flow of air into and out of the lung. This results in a decrease in oxygen getting into the blood stream and to the body tissues and leads to the symptom of shortness of breath.

It is estimated that 16 million American’s are affected by COPD, and there are many more who have not been officially diagnosed. In the U.S., tobacco smoke is a primary cause for the development and progression of COPD. Other factors, such as exposure to air pollutants, respiratory infections and genetic factors, can contribute to developing COPD. 

While COPD is a chronic condition, there are treatments that can significantly lessen symptoms. For people who smoke, quitting smoking is the most important first step. There are medications, including inhaled medications, that treat symptoms like wheezing and coughing. Avoiding lung infections is also very important because patients with COPD have decreased reserve in their lung function. It is important to stay up to date with immunizations for infections that can seriously affect the lungs, such as flu, pneumonia and COVID-19. Some patients with COPD require supplemental oxygen to keep their oxygen levels in their blood within a normal range.

When I went back in to check on Betsy a short time later, she had finished her inhaled medications and the respiratory therapist was transitioning her to oxygen through her nose to keep her levels within a target range. She was still short of breath but was looking much better than when she had arrived. She said the recent bout of cold weather is what triggered this episode, adding that she would have terrible coughing fits and wheezing anytime she would go outside and breath the cold air. She said she was so short of breath the past week that she wasn’t even able to smoke a cigarette. I jumped at this opportunity to counsel Betsy on why she needed to quit smoking.

I explained to her that the health benefits of quitting smoking start right after the last cigarette smoked. Within 24 hours of the last cigarette, the risk of heart attack is lessened because of decreased constriction of the veins and arteries around the heart and increased oxygen levels in the blood. Once you make it to a week without smoking, you have a nine-times higher chance of successfully quitting. The benefits continue to add up. Within three years of quitting, your risk of heart attack is the same as a nonsmoker and within 10 years of quitting, your risk of dying of lung cancer decreases to the same risk as a nonsmoker.

Betsy, like many of my patients, feel that the damage is done and there is no point in quitting once they have smoked as long as they have. As I explained these benefits to her, she kept nodding her head. I reminded her that she has a lot of life left ahead of her and she could see real benefits in her health by committing to quit. Betsy improved enough to go home, and before she left, she told me that she made quitting smoking her New Year’s resolution and that she was committed to making it happen.

Dr. Erika Kube is an emergency physician who works for Mid-Ohio Emergency Services and OhioHealth.

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