PUNE, India, March 27, 2024 /PRNewswire/ -- The report titled "Inhaled Nitric Oxide Market by Application (Acute Respiratory Distress Syndrome, Chronic Obstructive Pulmonary Disease, Malaria Treatment), End-Users (Clinic, Hospital) - Global Forecast 2024-2030" is now available on 360iResearch.com's offering, presents an analysis indicating that the market projected to grow from a size of $778.21 million in 2023 to reach $1,157.38 million by 2030, at a CAGR of 5.83% over the forecast period.

360 iResearch Logo360 iResearch Logo

360 iResearch Logo

"Expanding Boundaries Revolutionizing Respiratory Care Using Inhaled Nitric Oxide Globally"

Using inhaled nitric oxide in intensive care is a significant therapy, primarily benefiting newborns and children suffering from severe pulmonary conditions such as persistent pulmonary hypertension of the newborn (PPHN) and acute respiratory distress syndrome (ARDS). This innovative treatment, delivered directly to the lungs, effectively enhances oxygenation without influencing blood pressure elsewhere, marking a significant stride in medical care. Its application has broadened beyond hospital settings to include home care, thereby promising a better quality of life for patients as the incidence of conditions treated by inhaled nitric oxide rises with technological advancements in portable delivery systems. Nonetheless, the market faces challenges due to the high costs and rigorous regulatory standards governing its use. The continued research into new therapeutic uses and improvements in delivery technology are setting the stage for more accessible and cost-effective treatments. Globally, inhaled nitric oxide is gaining traction, especially in the Americas, driven by a high rate of respiratory illnesses and a robust healthcare infrastructure. Europe is witnessing a growing demand, backed by innovation and robust regulatory frameworks, whereas the Asia-Pacific region is rapidly adopting this therapy, fueled by healthcare advancements and an increasing awareness of cutting-edge treatments.

Download Sample Report @ www.360iresearch.com/library/intelligence/inhaled-nitric-oxide

"Enhancing Respiratory Care: The Increasing Role of Inhaled Nitric Oxide Amid Rising Respiratory Disorders"

The medical community is turning toward innovative treatments such as inhaled nitric oxide (iNO)owing to the global increase in respiratory diseases, such as chronic obstructive pulmonary disease (COPD), the ongoing impacts of conditions such as acute respiratory distress syndrome (ARDS), and the long-term effects of COVID-19. Renowned for improving oxygenation in the lungs through vasodilation, iNO therapy is a groundbreaking solution in treating various respiratory issues, including pulmonary hypertension and ARDS. Its role in enhancing lung function while reducing reliance on mechanical ventilation is particularly notable in neonatal care, where it offers hope for premature infants facing hypoxic respiratory failure. The adoption of iNO in healthcare settings is gaining pace as respiratory disorders continue to affect millions globally due to respiratory illness. This treatment's integration into patient care routines highlights a critical advancement in addressing the urgent need for effective, non-invasive therapies, driving improvements in respiratory health and patient recovery rates.

"Revolutionizing Respiratory Care: The Expanding Role of Inhaled Nitric Oxide"

Inhaled nitric oxide (iNO) is a treatment crucial in managing various respiratory conditions by enhancing oxygenation and easing pulmonary arterial pressures. Its capability to dilate lung blood vessels offers significant benefits, particularly for chronic obstructive pulmonary disease (COPD) patients. These individuals often face severe flare-ups that worsen their breathing difficulties. iNO offers expectancy during critical times, potentially improving gas exchange and lessening the effects of pulmonary hypertension. Emerging research highlights iNO's potential in combating severe malaria, owing to its inflammation-reducing capabilities and improvement in blood flow. Furthermore, its established success in treating newborns with hypoxic respiratory failure highlights its life-saving impact. Additionally, exploring iNO in treating tuberculosis opens a new frontier, especially for combating drug-resistant strains, showcasing its versatility and potential as an adjunctive therapy. This multipurpose application of inhaled nitric oxide highlights its pivotal role in advancing respiratory care and offering hope to patients across a spectrum of conditions.

Request Analyst Support @ www.360iresearch.com/library/intelligence/inhaled-nitric-oxide

"Merck KGaA at the Forefront of Inhaled Nitric Oxide Market with a Strong 11.95% Market Share"

The key players in the Inhaled Nitric Oxide Market include VERO Biotech Inc., Getinge AB, Air Liquide SA, Merck KGaA, GE HealthCare Technologies, Inc., and others. These prominent players focus on strategies such as expansions, acquisitions, joint ventures, and developing new products to strengthen their market positions.

"Introducing ThinkMi: Revolutionizing Market Intelligence with AI-Powered Insights for the Inhaled Nitric Oxide Market"

We proudly unveil ThinkMi, a cutting-edge AI product designed to transform how businesses interact with the Inhaled Nitric Oxide Market. ThinkMi stands out as your premier market intelligence partner, delivering unparalleled insights with the power of artificial intelligence. Whether deciphering market trends or offering actionable intelligence, ThinkMi is engineered to provide precise, relevant answers to your most critical business questions. This revolutionary tool is more than just an information source; it's a strategic asset that empowers your decision-making with up-to-the-minute data, ensuring you stay ahead in the fiercely competitive Inhaled Nitric Oxide Market. Embrace the future of market analysis with ThinkMi, where informed decisions lead to remarkable growth.

Ask Question to ThinkMi @ app.360iresearch.com/library/intelligence/inhaled-nitric-oxide

"Dive into the Inhaled Nitric Oxide Market Landscape: Explore 180 Pages of Insights, 198 Tables, and 20 Figures"

  1. Preface

  2. Research Methodology

  3. Executive Summary

  4. Market Overview

  5. Market Insights

  6. Inhaled Nitric Oxide Market, by Application

  7. Inhaled Nitric Oxide Market, by End-Users

  8. Americas Inhaled Nitric Oxide Market

  9. Asia-Pacific Inhaled Nitric Oxide Market

  10. Europe, Middle East & Africa Inhaled Nitric Oxide Market

  11. Competitive Landscape

  12. Competitive Portfolio

Inquire Before Buying @ www.360iresearch.com/library/intelligence/inhaled-nitric-oxide

Related Reports:

  1. Inhaled Nitric Oxide Delivery Systems Market - Global Forecast 2024-2030

  2. Medical Nitrous Oxide Market - Global Forecast 2024-2030

  3. Concentrated Nitric Acid Market - Global Forecast 2024-2030

About 360iResearch

Founded in 2017, 360iResearch is a market research and business consulting company headquartered in India, with clients and focus markets spanning the globe.

We are a dynamic, nimble company that believes in carving ambitious, purposeful goals and achieving them with the backing of our greatest asset — our people.

Quick on our feet, we have our ear to the ground when it comes to market intelligence and volatility. Our market intelligence is diligent, real-time and tailored to your needs, and arms you with all the insight that empowers strategic decision-making.

Our clientele encompasses about 80% of the Fortune Global 500, and leading consulting and research companies and academic institutions that rely on our expertise in compiling data in niche markets. Our meta-insights are intelligent, impactful and infinite, and translate into actionable data that support your quest for enhanced profitability, tapping into niche markets, and exploring new revenue opportunities.

Contact 360iResearch

Mr. Ketan Rohom
360iResearch Private Limited,
Office No. 519, Nyati Empress,
Opposite Phoenix Market City,
Vimannagar, Pune, Maharashtra,
India - 411014.
Email: [email protected]
USA: +1-530-264-8485
India: +91-922-607-7550

To learn more, visit 360iresearch.com or follow us on LinkedIn, Twitter, and Facebook.

Logo: mma.prnewswire.com/media/2359256/360iResearch_Logo.jpg

 

CisionCision

Cision

View original content:www.prnewswire.com/news-releases/inhaled-nitric-oxide-market-projected-to-reach-1-157-38-million-by-2030---exclusive-report-by-360iresearch-302101075.html

SOURCE 360iResearch



Source link

In 2024, pulmonary rehabilitation turned 50.1 Yet even after being around for half a century and documenting consistent improvements in patient outcomes, pulmonary rehabilitation “remains underused and underresourced,” according to the 2023 American Thoracic Society (ATS) clinical guidelines for pulmonary rehabilitation.2

Pulmonary rehabilitation “reduces dyspnea; increases exercise capacity; improves health-related quality of life (HRQoL) and emotional function; confers social support; and, for those with chronic obstructive pulmonary disease (COPD), reduces hospital admissions and mortality risk after hospitalization,” according to the ATS guidelines.2

“Pulmonary rehabilitation (PR) is an essential component of the integrated care of people with chronic respiratory disease,” said ATS guideline authors, who went on to offer recommendations on when pulmonary rehabilitation should be used, based on evidence showing that PR led to improved patient outcomes. The guidelines recommend offering2:

  • pulmonary rehabilitation for adults with stable chronic obstructive pulmonary disease (COPD) and for adults following hospitalization for COPD exacerbation (strong recommendations);
  • center-based pulmonary rehabilitation or telerehabilitation for chronic respiratory disease (strong recommendation);
  • pulmonary rehabilitation for patients with interstitial lung disease (strong recommendation);
  • either supervised maintenance pulmonary rehabilitation or usual care after initial pulmonary rehabilitation for adults with COPD (conditional recommendation); and
  • pulmonary rehabilitation for patients with pulmonary hypertension (conditional recommendation).

You can’t do pulmonology and ICU medicine without RTs…It’s good to be hand in hand with RTs, especially when you’re dealing with respiratory problems. In the ICU world, that might mean assisting with ventilator management, oxygen delivery, bilevel positive airway pressure, and treatments like that.

Respiratory therapists (RTs) are among the health care providers who offer pulmonary rehabilitation to patients. These specially trained health care providers can bridge gaps between patients and pulmonologists and improve care in a health care system that’s stretched beyond its limits.

How can RTs and pulmonary/critical care physicians best work together? An example of the kind of effective teamwork that makes for better patient outcomes can be found at Temple Lung Center in Philadelphia, where such teamwork is encouraged. To gain insight into the role and value of RTs in improving patients care, we spoke with Temple Health pulmonologist Lijo C. Illipparambil, MD, who is also an assistant professor of clinical thoracic medicine and surgery at Temple’s Lewis Katz School of Medicine, and Temple respiratory therapist Noel Rice-Ham.

RT/Physician Collaboration at Temple Lung Center

All patients with pulmonary problems can benefit from RT, said Dr Illipparambil. Patients that benefit the most are those with chronic ventilator needs or chronic or advanced lung diseases, who require additional assistance due to their respiratory status, he added.

“Success stories are most often with chronic ventilator patients who an RT has worked with before or knows them very well. When you come on as a new attending or new team taking care of that patient, and you try to make changes or adjustments, the RT already knows the lung physiology and the mechanics of what works for that patient, so it can be very helpful to discuss [this] with the RT before you make any changes,” he shared.

At Temple Lung Center, pulmonologists and RTs work together in a system that fosters referrals and collaboration. From the physician point of view, RTs are generally very accessible, said Dr Illipparambil. “They’re very much integrated with us, and we work with them almost every day, both on the pulmonology and ICU side.”

“You can’t do pulmonology and ICU medicine without RTs,” said Dr Illipparambil. “It’s good to be hand in hand with RTs, especially when you’re dealing with respiratory problems. In the ICU world, that might mean assisting with ventilator management, oxygen delivery, bilevel positive airway pressure , and treatments like that.”

Pulmonologists at Temple meet with RTs every morning to discuss which patients will be extubated and to review the results of spontaneous breathing trials. “An RT is always there to help out with getting patients on other devices like HiFlo or BiPAP or even helping with clearance,” Dr Illipparambil noted. In pulmonology, RTs help with testing to identify diseases and get patients on the appropriate devices or pressure settings.

RTs also have a lot of experience with different settings and different machines like cough assist, which can help the patient clear mucus and feel better, noted Dr Illipparambil.

Rice-Ham said she works with a lot of patients undergoing lung transplantation at Temple. “I came from working inpatient, where I’d see patients right after transplants or in the ICU setting. Now, I see patients who come in regularly for testing prior to or after the transplant.”

How RTs Benefit the Patient Care Team

As a respiratory therapist, Rice-Ham knows from experience that RTs often remember patients from past visits and may spend substantial time watching how patients react to different treatments in critical and noncritical settings. “I get to know the patients from the inside out and observe how they’re progressing. Physicians rely on us to see the things they don’t always see,” she said.

In her current position, Rice-Ham estimated that she spends an equal amount of time doing testing and speaking to patients. “We find ourselves having personal talks with patients and families, especially in the outpatient setting. Education can be as simple as discussing how someone wears their oxygen tank or cleans their equipment. We’re always prepared for whatever question comes up. Many patients want to know about using inhalers properly,” she explained.

Although 75% of RTs are employed by a hospital, studies highlight the advantages of RTs in community settings as well.3 As part of a multidisciplinary team, RTs can help identify the early stages of diseases like COPD by reviewing lung function and other risk factors, like social determinants of health. Earlier interventions and care can shift the health care system into a more preventative versus reactive mode, ultimately resulting in cost savings and improvements in patients’ quality of life.

While physicians like Dr Illipparambil consider RTs to be a vital part of the patient care team, Rice-Ham said that some collaborative barriers remain, particularly in the inpatient setting. “At the lung center, we see a lot of patients. In the inpatient setting, it’s not as often. I don’t know if the inpatient physicians include us as much as they could. It depends on the physician’s experience with RTs,” she explained.

Why Is Pulmonary Rehabilitation Underutilized?

Although PR was originally developed for patients with COPD, its scope has expanded to address the needs of patients with other chronic respiratory diseases as well as those with cancer and undergoing lung transplantation.2

Yet, as the ATS pulmonary rehabilitation guidelines acknowledge, PR is underutilized. “Less than 5% of people with COPD who may benefit from PR receive it,” the ATS guideline authors noted.2 

The availability of these services is not the only problem, said the guideline authors; another reason for underuse of PR is “insufficient HCP [health care provider] and patient knowledge and awareness of the process and benefits of PR” and the fact that “HCPs’ referral of patients to PR is suboptimal.”2

“There needs to be more recognition of what a respiratory therapist is,” said Rice-Ham. “A lot of times, we don’t get that respect because other providers don’t know about our qualifications and training. There’s a barrier of the unknown about who we are.”

In some places, there are “respiratory-therapist-driven protocols” for patient care, she noted. Where such protocols exist, they help facilitate better relationships between RTs and physicians.

Another barrier to collaboration between physicians and RTs can be inadequate communication among busy health care professionals. Because RTs see so many patients, they need to know the plan for the day, especially if there are changes to a patient’s settings or recommendations. Physicians, nurses, and RTs must communicate and ensure everyone is on the same page.

The RT’s Evolving Role

Traditionally, respiratory therapists were thought of as technicians rather than practitioners, but their role has since evolved, said Rice-Ham, who has a bachelor of science degree in respiratory therapy as well as a master’s degree in health care administration.

RTs who conduct pulmonary rehabilitation are trained clinicians who can support patients with a range of pulmonary issues. Typical duties of an RT include analyzing blood and sputum in the lab, helping physicians diagnose lung and breathing disorders, assisting with the development of treatment plans, managing breathing equipment and devices, and providing education to patients and families.

Over the past several years, the RT’s role has evolved to meet the growing demands of patients beyond the critical care setting.3 In addition to specializing in critical care and pulmonary rehabilitation, RTs may also specialize in polysomnography, geriatrics, home care, pediatrics, or neonatal care.

RTs can start working with an associate’s degree, although many programs expect therapists to have a bachelor’s degree. RTs take boards similar to nursing, and many obtain specialty certifications in a particular area of expertise, said Rice-Ham. Every state besides Alaska also requires RTs to have a license to practice,4 and RTs must also undergo continuing education and renew their certification every 5 years.5

Some physicians, particularly in smaller community settings, may be unaware of the education and training required to become an RT, said Rice-Ham. Notably, this is not the case at Temple Lung Center, she added, where physicians have a high level of experience working with RTs and can see their capabilities firsthand.

The Future of Respiratory Therapy

The occupation of respiratory therapy is projected to grow by 13% to 23% over the next decade, outpacing many other professions.4,5 This increase is timely, as the Association of American Medical Colleges predicts the US physician shortage will reach 140,000 unfilled roles by 2033.6

In addition, respiratory therapy is among the many allied health professions that are expanding their advanced practice certifications to support rising patient demands. An Advanced Practice Respiratory Therapist (APRT) accreditation became available in June 2022. To complete the program, registered RTs must complete a graduate-level education and training program approved by the Commission on Accreditation for Respiratory Care.7

APRTs will practice as part of a physician-led team to document medical histories and progress noted and examine, treat, and educate patients. They’ll also order and interpret labs and diagnostic tests, reducing administrative work for physicians and enabling more efficient and hands-on care. As RTs and physicians continue joining forces, patients will undoubtedly benefit.

Source link

Dyspnea, also known as shortness of breath or breathlessness, is a subjective sensation that refers to the discomfort or difficulty in breathing.

Market Overview:  

The dyspnea market is expected to exhibit a CAGR of 5.24% during 2024-2034. The report offers a comprehensive analysis of the dyspnea market in the United States, EU5 (including Germany, Spain, Italy, France, and the United Kingdom), and Japan.

It covers aspects such as treatment methods, drugs available in the market, drugs in development, the proportion of various therapies, and the market’s performance in the seven major regions. Additionally, the report evaluates the performance of leading companies and their pharmaceutical products.

Current and projected patient numbers across these key markets are also detailed in the report. This study is essential for manufacturers, investors, business planners, researchers, consultants, and anyone interested or involved in the dyspnea market.

Request for a Sample of this Report : www.imarcgroup.com/dyspnea…uestsample

Dyspnea Market Trends:

The dyspnea market is experiencing significant growth, influenced by several key factors. Primarily, the increasing incidence of respiratory diseases such as asthma, chronic obstructive pulmonary disease (COPD), and pulmonary hypertension contributes to the rising prevalence of dyspnea.

These respiratory conditions are becoming widespread due to factors like air pollution, smoking, and lifestyle changes, driving the demand for effective dyspnea management solutions. Additionally, the aging population, which is more susceptible to respiratory disorders, is another vital factor propelling the growth of the dyspnea market.

Advances in medical technology have led to the development of innovative diagnostic tools and treatment methods for respiratory ailments, further fueling market expansion. The growing awareness of respiratory health and early diagnosis techniques has also resulted in more people seeking treatment for dyspnea, thereby boosting the market.

The pharmaceutical and healthcare sectors are increasingly focusing on the research and development of new drugs and therapies, offering effective and targeted treatments for dyspnea. Furthermore, the adoption of digital health solutions, such as telemedicine and remote patient monitoring, has been accelerated by the COVID-19 pandemic, offering new avenues for managing dyspnea effectively.

This trend is expected to continue, significantly influencing dyspnea market dynamics in the foreseeable future.

Countries Covered:

  • United States
  • Germany
  • France
  • United Kingdom
  • Italy
  • Spain
  • Japan

Analysis Covered Across Each Country:

• Historical, current, and future epidemiology scenario
• Historical, current, and future performance of the dyspnea market
• Historical, current, and future performance of various therapeutic categories in the market
• Sales of various drugs across the dyspnea market
• Reimbursement scenario in the market
• In-market and pipeline drugs

This report also provides a detailed analysis of the current dyspnea marketed drugs and late-stage pipeline drugs.

In-Market Drugs

  • Drug Overview
  • Mechanism of Action
  • Regulatory Status
  • Clinical Trial Results
  • Drug Uptake and Market Performance

Late-Stage Pipeline Drugs

  • Drug Overview
  • Mechanism of Action
  • Regulatory Status
  • Clinical Trial Results
  • Regulatory Status

Competitive Landscape:

The competitive landscape of the dyspnea market has been studied in the report with the detailed profiles of the key players operating in the market.

Ask Analyst for Customization and Explore Full Report With TOC & List of Figures: www.imarcgroup.com/request…amp;flag=C

If you need specific information that is not currently within the scope of the report, we will provide it to you as a part of the customization.

News From

IMARC Group - Market ResearchIMARC Group
Category: Market Research Publishers and Retailers Profile: IMARC is a leading market research company that provides market and business research intelligence across the globe. We partner with clients in all regions and industry verticals to identify their highest-value opportunities, address their most critical challenges, and transform their businesses.We make an effort to fulfill specific and niche requirements of the industry while balancing the quantum of quality with stipulated time and trace major trends at both the domestic and global levels. The ...

This email address is being protected from spambots. You need JavaScript enabled to view it.

Source link

  • Grana, R., Benowitz, N. & Glantz, S. A. ECs: A scientific review. Circulation 129, 1972–1986 (2014).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Liu, Y. et al. Smoking duration, respiratory symptoms, and COPD in adults aged ≥ 45 years with a smoking history. Int. J. Chron. Obstruct. Pulmon. Dis. 21(10), 1409–1416. doi.org/10.2147/COPD.S82259 (2015).

    Article 

    Google Scholar
     

  • Dhariwal, J. et al. Smoking cessation in COPD causes a transient improvement in spirometry and decreases micronodules on high-resolution CT imaging. Chest 145(5), 1006–1015. doi.org/10.1378/chest.13-2220 (2014).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Zhao, Z. et al. E-cigarette use among adults in China: Findings from repeated cross-sectional surveys in 2015–16 and 2018–19. Lancet Public Health 5(12), e639–e649. doi.org/10.1016/S2468-2667(20)30145-6 (2020).

    Article 
    PubMed 

    Google Scholar
     

  • Xiao, L. et al. Awareness and prevalence of EC use among Chinese adults: Policy implications. Tob. Control 31, 498–504. doi.org/10.1136/tobaccocontrol-2020-056114 (2020).

    Article 

    Google Scholar
     

  • Xiao, L., Parascandola, M., Wang, C. & Jiang, Y. Perception and current use of ECs among youth in China. Nicotine Tob. Res. Off. J. Soc. Res. Nicotine Tob. 21, 1401–1407 (2019).

    Article 

    Google Scholar
     

  • Chinese Center for Disease Control and Prevention. Tobacco control: 2019 China’s national youth tobacco survey. 2020. www.chinacdc.cn/jkzt/sthd_3844/slhd_12885/202005/t20200531_216942.html.

  • Bhatta, D. N. & Glantz, S. A. Association of EC use with respiratory disease among adults: A longitudinal analysis. Am. J. Prev. Med. 58, 182–190. doi.org/10.1016/j.amepre.2019.07.028 (2020).

    Article 
    PubMed 

    Google Scholar
     

  • Kalininskiy, A. et al. E-cigarette, or vaping, product use associated lung injury (EVALI): Case series and diagnostic approach. Lancet Respir. Med. 7(12), 1017–1026. doi.org/10.1016/S2213-2600(19)30415-1 (2019).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Hartnett, K. P. et al. Syndromic surveillance for EC, or vaping, product use-associated lung injury. N. Engl. J. Med. 382, 766–772. doi.org/10.1056/NEJMsr1915313 (2020).

    Article 
    PubMed 

    Google Scholar
     

  • Fang, L. et al. Chronic obstructive pulmonary disease in China: A nationwide prevalence study. Lancet Respir. Med. 6(6), 421–430. doi.org/10.1016/S2213-2600(18)30103-6 (2018).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Tackett, A. P. et al. Evaluation of respiratory symptoms among youth e-cigarette users. JAMA Netw. Open 3(10), e2020671. doi.org/10.1001/jamanetworkopen.2020.20671 (2020).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Varella, M. H. et al. E-cigarette use and respiratory symptoms in residents of the United States: A BRFSS report. PLoS ONE 17(12), e0269760. doi.org/10.1371/journal.pone.0269760 (2022).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Osei, A. D. et al. Association between EC use and chronic obstructive pulmonary disease by smoking status: Behavioral risk factor surveillance system 2016 and 2017. Am. J. Prev. Med. 58, 336–342 (2020).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Xie, Z., Ossip, D. J., Rahman, I. & Li, D. Use of electronic cigarettes and self-reported chronic obstructive pulmonary disease diagnosis in adults. Nicotine Tob. Res. 22(7), 1155–1161. doi.org/10.1093/ntr/ntz234 (2020).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Physical Examination Standards for Civil Servants of China. www.chinagwy.org.

  • McConnell, R. et al. Electronic cigarette use and respiratory symptoms in adolescents. Am. J. Respir. Crit. Care Med. 195(8), 1043–1049. doi.org/10.1164/rccm.201604-0804OC (2017).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Wang, M. P., Ho, S. Y., Leung, L. T. & Lam, T. H. Electronic cigarette use and respiratory symptoms in Chinese adolescents in Hong Kong. JAMA Pediatr. 170(1), 89–91. doi.org/10.1001/jamapediatrics.2015.3024 (2016).

    Article 
    PubMed 

    Google Scholar
     

  • Varella, M. H. et al. E-cigarette use and respiratory symptoms in residents of the United States: A BRFSS report. PLoS ONE 17(12), e0269760. doi.org/10.1371/journal.pone.0269760 (2022).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease (2017 report) (2007).

  • Marcoa, A. R. et al. Classification of chronic obstructive pulmonary disease (COPD) according to the new global initiative for chronic obstructive lung disease (GOLD). J. Chron. Obstruct. Pulmon. Dis. 15(1), 21–26 (2017).

    Article 

    Google Scholar
     

  • Ash, J. S. et al. Standard practices for computerized clinical decision support in community hospitals: A national survey. J. Am. Med. Inform. Assoc. 19(6), 980–987. doi.org/10.1136/amiajnl-2011-000705 (2012).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Zhou, B. F. Predictive values of body mass index and waist circumference for risk factors of certain related diseases in Chinese adults study on optimal cut-off points of body mass index and waist circumference in Chinese adults. Biomed. Environ. Sci. 15(1), 83–96 (2002).

    PubMed 

    Google Scholar
     

  • Kim, S. J. et al. Age-related annual decline of lung function in patients with COPD. Int. J. Chron. Obstruct. Pulmon. Dis. 30(11), 51–60. doi.org/10.2147/COPD.S95028 (2015).

    Article 

    Google Scholar
     

  • Ntritsos, G. et al. Gender-specific estimates of COPD prevalence: A systematic review and meta-analysis. Int. J. Chron. Obstruct. Pulmon. Dis. 10(13), 1507–1514. doi.org/10.2147/COPD.S146390 (2018).

    Article 

    Google Scholar
     

  • Zhai, M. et al. DALY trend and predictive analysis of COPD in China and its provinces: Findings from the global burden of disease study. Front. Public Health 23(10), 1046773. doi.org/10.3389/fpubh.2022.1046773 (2022).

    Article 

    Google Scholar
     

  • Tabak, C. et al. Alcohol consumption in relation to 20-year COPD mortality and pulmonary function in middle-aged men from three European countries. Epidemiology 12(2), 239–245. doi.org/10.1097/00001648-200103000-00018 (2001).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Zhang, L. et al. The incidence and prevalence of pulmonary hypertension in the COPD population: A systematic review and meta-analysis. Int. J. Chron. Obstruct. Pulmon. Dis. 10(17), 1365–1379. doi.org/10.2147/COPD.S359873 (2022).

    Article 

    Google Scholar
     

  • Ekroos, K. et al. Lipid-based biomarkers for CVD, COPD, and aging—A translational perspective. Prog. Lipid Res. 78, 101030. doi.org/10.1016/j.plipres.2020.101030 (2020).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Bowler, R. P. et al. Plasma sphingolipids associated with chronic obstructive pulmonary disease phenotypes. Am. J. Respir. Crit. Care Med. 191(3), 275–284. doi.org/10.1164/rccm.201410-1771OC (2015).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Kisiel, M. A. et al. Association between abdominal and general obesity and respiratory symptoms, asthma and COPD. Results from the RHINE study. Respir. Med. 211, 107213. doi.org/10.1016/j.rmed.2023.107213 (2023).

    Article 
    PubMed 

    Google Scholar
     

  • Harrell, Jr. F. E. Regression Modeling Strategies 2nd edn. (Springer, 2015).

    Book 

    Google Scholar
     

  • Xiao, L. et al. Awareness and prevalence of e-cigarette use among Chinese adults: Policy implications. Tob. Control 31(4), 498–504. doi.org/10.1136/tobaccocontrol-2020-056114 (2022).

    Article 
    PubMed 

    Google Scholar
     

  • Polosa, R. et al. Evidence for harm reduction in COPD smokers who switch to electronic cigarettes. Respir. Res. 17(1), 166. doi.org/10.1186/s12931-016-0481-x (2016).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Hartnett, K. P. et al. Syndromic surveillance for e-cigarette, or vaping, product use-associated lung injury. N. Engl. J. Med. 382(8), 766–772. doi.org/10.1056/NEJMsr1915313 (2020).

    Article 
    PubMed 

    Google Scholar
     

  • Adkins, S. H. et al. Lung injury clinical task force and the lung injury epidemiology/surveillance task force. Demographics, substance use behaviors, and clinical characteristics of adolescents with e-cigarette, or vaping, product use-associated lung injury (EVALI) in the United States in 2019. JAMA Pediatr. 174(7), e200756. doi.org/10.1001/jamapediatrics.2020.0756 (2020).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Li, D. & Xie, Z. Cross-sectional association of lifetime electronic cigarette use with wheezing and related respiratory symptoms in U.S. adults. Nicotine Tob. Res. 22(Suppl 1), S85–S92. doi.org/10.1093/ntr/ntaa195 (2020).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Wills, T. A., Pagano, I., Williams, R. J. & Tam, E. K. E-cigarette use and respiratory disorder in an adult sample. Drug Alcohol Depend. 1(194), 363–370. doi.org/10.1016/j.drugalcdep.2018.10.004 (2019).

    Article 

    Google Scholar
     

  • Pettigrew, S. et al. E-cigarette-related beliefs, behaviors, and policy support among young people in China. Tob. Induc. Dis. 23(21), 09. doi.org/10.18332/tid/156836 (2023).

    Article 

    Google Scholar
     

  • McConnell, R. et al. Electronic cigarette use and respiratory symptoms in adolescents. Am. J. Respir. Crit. Care Med. 195(8), 1043–1049. doi.org/10.1164/rccm.201604-0804OC (2017).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Chaffee, B. W. et al. E-cigarette use and adverse respiratory symptoms among adolescents and young adults in the United States. Prev. Med. 153, 106766. doi.org/10.1016/j.ypmed.2021.106766 (2021).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Wills, T. A., Soneji, S. S., Choi, K., Jaspers, I. & Tam, E. K. E-cigarette use and respiratory disorders: An integrative review of converging evidence from epidemiological and laboratory studies. Eur. Respir. J. 57(1), 1901815. doi.org/10.1183/13993003.01815-2019 (2021).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Bircan, E., Bezirhan, U., Porter, A., Fagan, P. & Orloff, M. S. Electronic cigarette use and its association with asthma, chronic obstructive pulmonary disease (COPD) and asthma-COPD overlap syndrome among never cigarette smokers. Tob Induc Dis. 21(19), 75. doi.org/10.18332/tid/142579 (2021).

    Article 
    CAS 

    Google Scholar
     

  • Bhatta, D. N. & Glantz, S. A. Association of E-cigarette use with respiratory disease among adults: A longitudinal analysis. Am. J. Prev. Med. 58(2), 182–190. doi.org/10.1016/j.amepre.2019.07.028 (2020).

    Article 
    PubMed 

    Google Scholar
     

  • Wieslander, G., Norback, D. & Lindgren, T. Experimental exposure to propylene glycol mist in aviation emergency training: Acute ocular and respiratory effects. Occup. Environ. Med. 58(10), 649–655. doi.org/10.1136/oem.58.10.649 (2001).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Farsalinos, K. E., Kistler, K. A., Gillman, G. & Voudris, V. Evaluation of electronic cigarette liquids and aerosol for the presence of selected inhalation toxins. Nicotine Tob. Res. 17(2), 168–174. doi.org/10.1093/ntr/ntu176 (2015).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Olmedo, P. et al. Metal concentrations in e-cigarette liquid and aerosol samples: The contribution of metallic coils. Environ. Health Perspect. 126(2), 027010. doi.org/10.1289/ehp2175 (2018).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Omaiye, E. E. et al. High-nicotine electronic cigarette products: Toxicity of JUUL fluids and aerosols correlates strongly with nicotine and some flavor chemical concentrations. Chem. Res. Toxicol 32, 1058–1069 (2019).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Shampa, C. et al. Acute exposure to e-cigarettes causes inflammation and pulmonary endothelial oxidative stress in nonsmoking, healthy young subjects. Am. J. Physiol. Lung Cell Mol. Physiol. 317, L155–L166 (2019).

    Article 

    Google Scholar
     

  • Gilpin, D. F. et al. Electronic cigarette vapour increases virulence and inflammatory potential of respiratory pathogens. Respir. Res. 20, 267 (2019).

    Article 
    CAS 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Garcia-Arcos, I. et al. Chronic electronic cigarette exposure in mice induces features of COPD in a nicotine-dependent manner. Thorax 71, 1119–1129 (2016).

    Article 
    PubMed 

    Google Scholar
     

  • Yu, V. et al. Electronic cigarettes induce DNA strand breaks and cell death independently of nicotine in cell lines. Oral Oncol. 52, 58–65 (2016).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • World Health Organization. Electronic Nicotine Delivery Systems Report (FCTCCOP/6/10). In Conference of the Parties to the WHO Framework Convention on Tobacco Control (2014).

  • Jamal, A. et al. Tobacco use among middle and high school students—United States, 2011–2016. MMWR Morb. Mortal. Wkly. Rep. 66(23), 597–603. doi.org/10.15585/mmwr.mm6623a1.Erratum.In:MMWRMorbMortalWklyRep.2017Jul21;66(28):765 (2017).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Rose, A., Filion, K. B., Eisenberg, M. J. & Franck, C. Electronic cigarettes: A comparison of national regulatory approaches. Can. J. Public Health. 106(6), e450–e453. doi.org/10.17269/cjph.106.5043 (2015).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar
     

  • Douglas, H., Hall, W. & Gartner, C. E-cigarettes and the law in Australia. Aust. Fam. Physician 44(6), 415–418 (2015).

    PubMed 

    Google Scholar
     

  • Czoli, C. D., Fong, G. T., Goniewicz, M. L. & Hammond, D. Biomarkers of exposure among “dual users” of tobacco cigarettes and electronic cigarettes in Canada. Nicotine Tob. Res. 21(9), 1259–1266. doi.org/10.1093/ntr/nty174 (2019).

    Article 
    CAS 
    PubMed 

    Google Scholar
     

  • Source link

    STARVING for air sounds like something from a horror film.

    But "air hunger" is a real condition that leaves sufferers feeling like they can't take a full breath. Sound familiar?

    1

    Credit: Getty

    Up to one in ten Brits will experience dyspnea - as it's medically known - at some point in their lives,

    "It happens when your brain detects low levels of oxygen," Dr Sarah Jarvis, a GP and clinical consultant to Patient.info, told the Sun.

    "It’s common in lung problems like asthma and chronic obstructive pulmonary disease (COPD) when not enough air gets to the lungs.

    "It can also be caused by heart problems, where the heart isn’t pumping out efficiently and isn’t getting oxygen-rich blood to the organs," she added.

    Heart conditions such as angina, heart attacks, heart failure and some abnormal heart rhythms like atrial fibrillation can all cause shortness of breath, according to the NHS.

    The terrifying feeling can also be a sign of anxiety, explained psychologist Dr Kirren Schnack, from Oxford.

    "One of the physical changes anxiety causes in your body is the redirection of oxygen to large muscle groups," she said in a video posted on TikTok.

    It’s like there’s no oxygen in the air

    Dr Kwan Kin

    "This means the demand for oxygen increases, so you try to inhale more and more air to meet that demand," she added.

    "You then feel short of breath, which triggers more anxiety about your breathing and that feeling of air hunger."

    The term has gone viral on social media after Dr Kwan Kin Pang, a US-based board-certified chiropractor specialising in functional neurology, posted a video about it.

    “You try to breathe, but your breath doesn’t feel like its enough," Dr Kwan said when explaining the condition.

    "You force a yawn but still can’t get the air to fill your lungs. It’s like there’s no oxygen in the air or like your lungs are too weak."

    The video has been viewed over 18.2million times, and thousands of people turned to the comments, thanking the expert for finally placing a name to the sneaky symptom.

    "I’ve been trying to explain this feeling for so long thank you for this," a user named @catcudmoree wrote.

    Another, called @jaclynamber, added: "This happens to me a lot, it makes me start to panic when I can’t get my lungs to feel satisfied."

    "Finally found the suitable description of what I feel," a user called @hulyalala said.

    How can I fix it?

    In a follow-up video, Dr Kirren demonstrated an exercise that can help stabilise breathing.

    "Instead of taking short, shallow breaths from your chest, you need to breathe from your stomach," she said.

    She started by placing her hands below her ribcage and breathing in through her nose.

    As you do this you should feel your diaphragm (a dome-shaped muscle that sits below your lungs and heart) move down towards your stomach, she said.

    "Now, hold your breath for about five seconds before you breathe out from a pouted mouth," she added.

    Make sure you try and get "every last bit of air out" while doing this, she said.

    "The feeling of air hunger will stop once you are breathing at a normal rate and the balance of gasses in your brain and blood go back to normal."

    When to get help

    Shortness of breath might not be anything to worry about, but sometimes it can be serious and you'll need to get medical help.

    You should seen your GP if your shortness of breath gets worse when you've been doing your normal activities, or when you lie down, accoridng to the NHS.

    But if you have severe difficulty breathing difficulties and are not able to get any words out, you should call 999.

    Full list of condions that cause 'air hunger'

    HEART or lung disease and other conditions can cause shortness of breath.

    Lung and airway conditions

    • Asthma
    • Allergies
    • Chronic obstructive pulmonary disease (COPD)
    • Respiratory illness (like bronchitis, Covid-19, the flu or other viral or bacterial infections)
    • Pneumonia
    • Inflammation (pleurisy) or fluid (pleural effusion) around your lungs
    • Fluid (pulmonary oedema) or scarring (fibrosis) inside your lungs.
    • Lung cancer or pleural mesothelioma
    • High blood pressure in your lungs (pulmonary hypertension)
    • Sarcoidosis
    • Tuberculosis
    • Partial or complete collapsed lung (pneumothorax or atelectasis)
    • Blood clot (pulmonary embolism)
    • Choking

    Heart and blood conditions

    • Anemia
    • Heart failure
    • Conditions that affect your heart muscle (cardiomyopathy)
    • Abnormal heart rhythm (arrhythmia)
    • Inflammation in or around your heart (endocarditis, pericarditis or myocarditis)

    Other conditions

    • Anxiety
    • Injury that makes breathing difficult (like a broken rib)
    • Medication: Statins (cholesterol-lowering drugs) and beta-blockers (used to treat high blood pressure) are two types of medications that can cause dyspnea
    • Extreme temperatures (being very hot or very cold)
    • Body mass index (BMI) over 30
    • Lack of exercise (muscle deconditioning)
    • Sleep apnea can cause paroxysmal nocturnal dyspnea (PND)

    Source: Cleveland Clinic

    Source link

    An algorithm based on artificial intelligence (AI) and machine learning may help in diagnosing pulmonary hypertension (PH), a new study shows.

    Its findings are particularly important for people suspected of having PH but whose disease remains uncertain using echocardiography, a noninvasive imaging method to examine heart structure and function. These individuals, who may not have PH, often are referred for further evaluations requiring invasive tests.

    “Our model may allow physicians to make a more accurate and reproducible echocardiographic estimation of normal vs elevated pulmonary pressures with greater efficiency and reduce referral for invasive testing,” the researchers wrote in “Machine Learning for Diagnosis of Pulmonary Hypertension by Echocardiography,” a study published in Mayo Clinical Proceedings.

    Recommended Reading

    banner image for

    Noninvasive echocardiography is among initial diagnostic PH tests

    “The study  … is timely, clinically relevant, and innovative in its application of machine learning in diagnosing pulmonary hypertension,” wrote Karl A. Nath, MD, the journal’s editor-in-chief, in its monthly highlights.

    PH is marked by the narrowing of the pulmonary arteries, the blood vessels that transport blood through the lungs, causing high blood pressure and making the heart work harder.

    Diagnosing PH can require multiple tests, including echocardiography. This technique estimates pulmonary artery pressure (PAP) by assessing the tricuspid valve, which controls blood flow from the heart’s right atrium to the right ventricle. Tricuspid regurgitation frequently is associated with PH, and it occurs when the valve does not close properly and blood flows backwards.

    When artery pressure is elevated, diagnosis is confirmed by an invasive technique called right heart catheterization (RHC), in which a flexible tube, a catheter, is passed into the right side of the heart and into the pulmonary arteries to measure PAP.

    People with normal findings on echocardiography often do not require further assessments. However, in more than a third of PH patients, PAP cannot be determined by echocardiography, making RHC necessary, the researchers noted.

    A number of small studies suggest that other measures of heart function and blood tests are associated with PH. But no computer-based models exist to evaluate “with high sensitivity” the risk of PH when tricuspid regurgitation is unavailable.

    Researchers at Mayo Clinic developed a predictive algorithm based on AI and machine learning that uses data obtained from echocardiography. To develop the algorithm, they analyzed data from 7,853 patients (mean age 64, 56% men) who underwent echocardiography and right heart catheterization at the Mayo Clinic in Minnesota between January 2012 and December 2019.

    A total of 6,323 patients (81%) were diagnosed with PH, following the criteria proposed in 2018 at the 6th World Symposium on Pulmonary Hypertension: a mean PAP greater than 20 millimeters of mercury (mm Hg).

    The heart’s right and left ventricles also had an abnormal size in 68% and 32% of the patients, respectively.

    But for another 2,007 people (26%), tricuspid regurgitation velocity could not be measured.

    Patients’ data were randomly divided into three groups: one for training the algorithm (5,024 people, 64%), another for validation (1,275 patients, 16%), and the third for testing (1,554 people, 20%).

    The final model had 19 features, including patients’ age, sex, body mass index (a measure of body fat), estimated PAP, the functioning of the tricuspid valve, and heart rate.

    Researchers first calculated the area under the receiver operating characteristic curve (AUC). This measure tells how well a given parameter can differentiate between two groups (i.e., PH or not). AUC values range from 0.5 to 1, with higher numbers indicating a better ability to differentiate.

    Based on the validation data, an AUC threshold of 0.65 or higher had a sensitivity of 90% in identifying correctly those with the disease.

    This threshold then was selected to assess the model’s performance in the testing datasets. Results showed that the model had high discrimination for the detection of PH with an accuracy of 82% and a sensitivity of 88%.

    Model had good positive predictive value, but less effective in disease’s absence

    In addition, the model’s positive predictive value was 89%, which refers to the percentage of patients who truly have PH after screening positive. The negative predictive value was 54%, meaning that 54% of cases truly did not have PH after a negative test.

    “We hypothesize that future research that combines echocardiography (derived features and image processing techniques) with electrocardiographic [EKG] analysis may be required to come closer to the goal of 90% negative predictive value. The importance of this accomplishment will be that RHC to determine PH may become unnecessary in patients who do not have PH,” the researchers wrote.

    The top five features supporting the model’s performance were estimated right atrial pressure, atrial fibrillation or flutter (an irregular or rapid beating of the heart’s atria), impression of the right ventricle’s normal function, body mass index, and heart rate.

    Finally, in a group of 412 patients (27%) whose tricuspid regurgitation could not be measured, AUC was 0.785

    An “AI assessment of echocardiographic data appears promising for estimating the presence of PH even when the [tricuspid regurgitation] velocity cannot be measured,” the team concluded, noting that larger validation studies are needed.

    Among the study’s limitations, the researchers noted the nearly 80% of participants whose mean PAP was higher than 20 mm Hg, “which is a value much higher than one would expect under a more general screening setting,” and may have led to overtraining or “overfitting the model to the data.”

    Study findings “demonstrate that the application of machine learning to the transthoracic echocardiogram enables the detection of pulmonary hypertension and may be used to identify patients with a low likelihood of pulmonary hypertension,” Nath wrote.

    Source link

    A few years ago, I shared an image on social media of my growing library. I love thrifting books just as much as I love reading them. It’s been a joy to invest in my collection of secondhand books in adulthood.

    A friend and fellow chronic illness warrior commented on the post with an insight. They shared the idea that the collection might indicate some sort of belief in a permanent future. Owning a library of books that I can’t read in the immediate future was a way for me to invest in the idea of an intangible “someday.”

    I think about this sentiment often. My ability to believe in the concept of my future self is heavily dependent on the stability of my health at any given time. Sometimes, when I’m considering buying a new piece of furniture or other substantial investment, I struggle to take the leap unless I’m in optimal health. Even then, I’m not always certain about it. It’s easy to believe I’ll be OK in a week, but what about in a month or a year? If things are about to go downhill for me, what’s the point?

    Recommended Reading

    The needle of a RISK dial points to HIGH in this illustration.

    Solutions can be found

    This dilemma works its way into the strangest spaces of my life. I’ve recently started knitting again, which was a small hobby of mine in childhood. But when I considered purchasing an expensive set of knitting needles, I hesitated. I had a few appointments coming up and felt like I shouldn’t hit the checkout button until I was assured that all was well.

    This mindset, of course, is irrational. But I don’t want to jinx my future health by buying something to enjoy for years to come. I’m worried the universe will say, “Ha! You thought you’d have time to enjoy these? Think again!”

    This tension was present when I was living with pulmonary hypertension for nearly two decades, before I received a heart-lung transplant in 2018. In those earlier years, decisions about the future were always intertwined with my health and often made at the last minute. Deciding whether to go to college was heavily influenced by the course of my disease progression. Even decisions like weekend plans depended on how I was feeling. I never really believed something would happen until it actually did.

    Living with severe illness makes future-oriented thinking difficult. It can feel as if few aspects of my life and my body are reliable, which makes planning hard. But aside from pausing plans with friends or not knowing how I’ll feel in a couple months, the part that causes me the most grief is that I’m unable to picture myself in future iterations of my life.

    I do my best to cope with these doubts and anxieties. One of my biggest fears is receiving news that I’m ailing from something fatal that can’t be treated or reversed. In response, I meditate on the idea that even if I face health changes, solutions can often be found, along with opportunities for recovery. Even if I do have setbacks, it doesn’t mean I won’t return to having functional health. That’s an important mantra for me as I attempt to visualize myself months or years down the road.

    I also try to live each day for what it is. If I want to buy knitting needles or books, why not do it? Despite how it sometimes feels, I know that making these decisions has no impact on what tomorrow will bring. If nothing changes tomorrow, then I’ll have time to enjoy those things.

    When I look at my books or my collection of art supplies, I can sense the accumulation of the nearly six years that have passed since my transplant. August will be a milestone that would’ve seemed inconceivable to me. It reminds me that anything is possible. I work hard to lean into that truth.

    In case you’re wondering, I did end up buying those knitting needles. Now, as I prepare for a post-transplant checkup next month, I’ll work hard to visualize myself reading and knitting and living my life for many years to come.


    Note: Pulmonary Hypertension News is strictly a news and information website about the disease. It does not provide medical advice, diagnosis, or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. The opinions expressed in this column are not those of Pulmonary Hypertension News or its parent company, BioNews, and are intended to spark discussion about issues pertaining to pulmonary hypertension.

    Source link

    Transparency Market Research

    Transparency Market Research

    The increasing prevalence of asthma and COPD, and increasing demand for effective nebulizer inhalation tools drive market demand.

    Wilmington, Delaware, United States, Feb. 29, 2024 (GLOBE NEWSWIRE) -- Transparency Market Research Inc. - The global soft mist inhalers market is projected to grow at a CAGR of 6.8% from 2022 to 2031. As per the report published by TMR, a valuation of US$ 4.4 billion is anticipated for the market in 2031. As of 2023, the demand for soft mist inhalers is expected to close at US$ 2.5 billion.

    With an increasing incidence of respiratory conditions such as asthma, COPD (Chronic Obstructive Pulmonary Disease), and bronchitis globally, there's a growing demand for effective inhalation therapy, thus boosting the market for soft mist inhalers.

    Many patients prefer inhalation therapy over traditional oral medications due to its convenience, faster onset of action, and targeted delivery to the lungs. Soft mist inhalers offer a user-friendly alternative, further fueling market growth.

    Download Sample PDF Report: www.transparencymarketresearch.com/sample/sample.php?flag=S&rep_id=85947

    The global aging population is prone to respiratory ailments, which is driving the demand for respiratory care devices, including soft mist inhalers. As the elderly population grows, so does the market for respiratory devices, creating opportunities for market expansion.

    Rising awareness about respiratory diseases and the importance of effective management, coupled with increased healthcare expenditure, particularly in emerging markets, is boosting the adoption of soft mist inhalers. Governments and healthcare organizations are also focusing on promoting inhalation therapy, further propelling market growth.

    Soft mist inhalers are increasingly being used for a wide range of indications beyond asthma and COPD, including cystic fibrosis, pulmonary hypertension, and respiratory infections. This expansion of indications broadens the market base and drives demand for soft mist inhalers.

    Key Takeaways from the Market Study

    • As of 2022, the soft mist inhalers market was valued at US$ 2.4 billion.

    • In terms of type, the reusable inhalers segment held a prominent share of the global soft mist inhalers market in 2021.

    Soft Mist Inhalers Market: Key Trends and Opportunistic Frontiers

    • The rising incidence of respiratory conditions such as asthma, COPD, and bronchitis is driving demand for soft mist inhalers as effective treatment options.

    • Growing emphasis on patient-centered care in respiratory medicine, leading to increased adoption of soft mist inhalers due to their ease of use, improved compliance, and better patient outcomes.

    • Soft mist inhalers are being explored for a wider range of respiratory conditions beyond asthma and COPD, such as cystic fibrosis and respiratory infections, expanding the market potential.

    • Ongoing innovations in soft mist inhaler technology, including improvements in dose accuracy, breath-actuation synchronization, and portability, are enhancing patient convenience and driving market growth.

    Unlock Growth Potential in Your Industry ! Download PDF Brochure @ www.transparencymarketresearch.com/sample/sample.php?flag=S&rep_id=85947

    Soft Mist Inhalers Market: Regional Analysis

    • North America dominates the soft mist inhalers market due to the high prevalence of respiratory diseases, well-established healthcare infrastructure, and favorable reimbursement policies. Additionally, the presence of key market players and ongoing technological advancements further bolster market growth in this region.

    • The Asia Pacific region is witnessing rapid growth in the soft mist inhalers market, propelled by factors such as the growing prevalence of respiratory disorders, rising healthcare awareness, and improving access to healthcare services. Increasing disposable income levels and expanding healthcare infrastructure also play a crucial role in driving market growth in countries like China, India, and Japan.

    Competitive Landscape

    The soft mist inhalers market is characterized by its fragmented nature, hosting numerous players vying for market dominance. These companies are strategically prioritizing investments in research and development as well as forging collaborations to bolster their market presence and enhance their competitive edge.

    Key Players Profiled

    Key Developments in the Market

    • Merxin Ltd. introduced MRX004 represents a soft mist inhaler device designed to offer an interchangeable AB rated opportunity for tiotropium/olodaterol, formulated similarly to the Respimat.
      MRX004 is versatile, serving as a soft mist inhaler suitable for various applications, including delivering new molecules to the lungs, repurposing existing ones, managing product life cycles, and reformulating compounds from nebulizers or pMDI/DPI devices.

    • In January 2024 - Recipharm, a prominent contract development and manufacturing organization (CDMO), is excited to unveil an exclusive license and collaboration agreement with Medspray and Resyca. Together, they will focus on the development of soft mist nasal delivery devices intended for both single and combination drug products.

    Soft Mist Inhalers Market – Key Segments

    Type

    Application

    Age Group

    End User

    • Hospitals

    • Clinics

    • Others (Home Care, etc.)

    Region

    • North America

    • Latin America

    • Europe

    • Asia Pacific

    • Middle East & Africa

    Purchase the Premium Report Now for a Competitive Edge! www.transparencymarketresearch.com/checkout.php?rep_id=85947&ltype=S

    Go through further research published by Transparency Market Research:

    Tumor Ablation Market - The global tumor ablation market was projected to attain US$ 1.3 billion in 2022. It is anticipated to garner a 6.9% CAGR from 2023 to 2031 and by 2031, the market is likely to attain US$ 2.3 billion by 2031.

    Medical Robotic Systems Market - The global medical robotic systems market is estimated to flourish at a CAGR of 11.2% from 2023 to 2031. According to Transparency Market Research, sales of medical robotic systems are slated to total US$ 21.3 billion by the end of the aforementioned period of assessment.

    About Transparency Market Research

    Transparency Market Research, a global market research company registered at Wilmington, Delaware, United States, provides custom research and consulting services. Our exclusive blend of quantitative forecasting and trends analysis provides forward-looking insights for thousands of decision makers. Our experienced team of Analysts, Researchers, and Consultants use proprietary data sources and various tools & techniques to gather and analyses information.

    Our data repository is continuously updated and revised by a team of research experts, so that it always reflects the latest trends and information. With a broad research and analysis capability, Transparency Market Research employs rigorous primary and secondary research techniques in developing distinctive data sets and research material for business reports.

    Contact:

    Transparency Market Research Inc.
    CORPORATE HEADQUARTER DOWNTOWN,
    1000 N. West Street,
    Suite 1200, Wilmington, Delaware 19801 USA
    Tel: +1-518-618-1030
    USA – Canada Toll Free: 866-552-3453
    Website: www.transparencymarketresearch.com    
    Email: [email protected]
    Follow Us: LinkedIn| Twitter| Blog | YouTube

    Source link

    Interstitial Lung Disease Market Size

    Interstitial Lung Disease Market Size

    The Business Research Company has updated its global market reports, featuring the latest data for 2024 and projections up to 2033

    The Business Research Company offers in-depth market insights through Interstitial Lung Disease Global Market Report 2024, providing businesses with a competitive advantage by thoroughly analyzing the market structure, including estimates for numerous segments and sub-segments.

    Market Size And Growth Forecast:

    The interstitial lung disease market size has grown strongly in recent years. It will grow from $1.83 billion in 2023 to $1.97 billion in 2024 at a compound annual growth rate (CAGR) of 7.3%. The growth in the historic period can be attributed to awareness and diagnosis improvement, immune system modulation therapies, respiratory rehabilitation programs, multidisciplinary care teams.

    The interstitial lung disease market size is expected to see strong growth in the next few years. It will grow to $2.62 billion in 2028 at a compound annual growth rate (CAGR) of 7.4%. The growth in the forecast period can be attributed to precision medicine, novel drug development, regenerative medicine, telehealth and remote monitoring. Major trends in the forecast period include advancements in imaging technology, ai in imaging, fibrosis subtype differentiation, supportive care services.

    Get Free Sample Of This Report-

    www.thebusinessresearchcompany.com/sample.aspx?id=13019&type=smp

    Market Segmentation:

    The main types of drugs used for interstitial lung disease are oral corticosteroids, immune-suppressing, anti-fibrotic medication and others. Interstitial pneumonia, also known as non-infectious interstitial pneumonia, is a type of interstitial lung disease (ILD) that affects the interstitium, which is the tissue that surrounds and supports the air sacs (alveoli) in the lungs. They are indicated for the treatment of interstitial pneumonia, idiopathic pulmonary fibrosis, nonspecific interstitial pneumonitis, hypersensitivity pneumonitis, cryptogenic organizing pneumonia (COP), sarcoidosis and acute interstitial pneumonitis for adults and children. It is distributed by various channels such as hospital pharmacies, retail pharmacies and online pharmacies.

    Major Driver - Role Of Allergic Conditions In Driving Growth Of The Interstitial Lung Disease Market

    The growing prevalence of allergic conditions is expected to propel the growth of the interstitial lung disease market going forward. An allergic condition is when the immune system overreacts to an allergen, often known as a harmless substance. Allergic reactions might result in interstitial lung disease (ILD), specifically hypersensitivity pneumonitis, which causes an allergic reaction in the body causes hypersensitivity pneumonitis. For instance, in January 2023, according to the Centers for Disease Control and Prevention (CDC), a US-based federal agency for public health, over one-third of American adults and more than one-fourth of American children had a seasonal allergy, eczema, or food allergy in 2021. Further, anaphylaxis (a severe allergic reaction to food) is estimated to cause 90,000 emergency room visits in the United States each year. Therefore, the growing prevalence of allergic conditions is driving the growth of the interstitial lung disease market.

    Competitive Landscape:

    Major players in the interstitial lung disease market are Roche Laboratories Inc., Merck & Co. Inc., Bayer AG, Novartis Pharmaceuticals Corporation, The Bristol-Myers Squibb Company, Amgen Inc., Boehringer Ingelheim, Siemens Healthineers, Koninklijke Philips N.V., Teva Pharmaceuticals USA Inc., AstraZeneca PLC, Horizon Pharma USA Inc., Genentech Inc., Amneal Pharmaceuticals LLC, Fujirebio Diagnostics Inc., Insmed Inc., VIDA Diagnostics Inc., EmphyCorp Inc., Verseau Therapeutics, Regend Therapeutics Co., LTT Bio-Pharma Co. Ltd., Galecto Biotech, Pulmatrix Inc., PureTech Health PLC, Pneuma Respiratory Inc., Bellerophon Therapeutics Inc., MediciNova Inc., Altavant Sciences Inc., Verona Pharma plc.

    Get Access To The Full Market Report -

    www.thebusinessresearchcompany.com/report/interstitial-lung-disease-global-market-report

    Top Trend - Innovative Drug Development Initiatives To Improve Interstitial Lung Disease Treatment

    Major Companies operating in the interstitial lung disease market are focusing on developing innovative drugs to treat their customers and sustain their position in the market. The development of new drugs can improve treatment outcomes for patients with lung-related diseases. For instance, in April 2021, United Therapeutics, a US-based biotechnology company, launched Tyvaso, a medication for treating patients with pulmonary hypertension associated with interstitial lung disease (PH-ILD; WHO Group 3) to improve exercise ability. Tyvaso is a treatment for patients with Pulmonary Hypertension associated with Interstitial Lung Disease (PH-ILD). It is a sterile version of the prostacyclin-mimicking drug treprostinil that is meant to be inhaled orally utilizing the Tyvaso inhalation system.

    The Table Of Content For The Market Report Include:

    1. Executive Summary

    2. Interstitial Lung Disease Market Characteristics

    3. Interstitial Lung Disease Market Trends And Strategies

    4. Interstitial Lung Disease Market - Macro Economic Scenario

    5. Interstitial Lung Disease Market Size And Growth

    …..

    27. Interstitial Lung Disease Market Competitor Landscape And Company Profiles

    28. Key Mergers And Acquisitions

    29. Future Outlook and Potential Analysis

    30. Appendix

    Contact Us:

    The Business Research Company

    Europe: +44 207 1930 708

    Asia: +91 88972 63534

    Americas: +1 315 623 0293

    Email: [email protected]

    Follow Us On:

    LinkedIn: in.linkedin.com/company/the-business-research-company

    Twitter: twitter.com/tbrc_info

    Facebook: www.facebook.com/TheBusinessResearchCompany

    YouTube: www.youtube.com/channel/UC24_fI0rV8cR5DxlCpgmyFQ

    Blog: blog.tbrc.info/

    Healthcare Blog: healthcareresearchreports.com/

    Global Market Model: www.thebusinessresearchcompany.com/global-market-model

    About The Business Research Company

    The Business Research Company (www.thebusinessresearchcompany.com) is a market intelligence firm that pioneers in company, market, and consumer research. Located globally, TBRC's consultants specialize in various industries including manufacturing, healthcare, financial services, chemicals, and technology. The firm has offices located in the UK, the US, and India, along with a network of proficient researchers in 28 countries.

    This release was published on openPR.



    Source link

    Introduction

    Chronic obstructive pulmonary disease (COPD) is a common respiratory disease that can be prevented and treated. It primarily involves various airway and/or alveolar abnormalities caused by excessive exposure to the toxic particles or gases, and can result in persistent and progressively worsening chronic respiratory symptoms and airflow limitations.1 It is estimated that COPD would become the fourth leading cause of premature death by 2040.2 Meanwhile, COPD is ranked as sixth leading cause of all-age mortality and years of life loss (YLLs) by 2019, and its rank was proportional to the age.3

    The enormous financial burden of COPD is closely related to both itself and its multiple comorbidities.4 In 2011, the ‘comorbidities’ were included in the Global Initiative for Chronic Obstructive Lung Disease (GOLD) and used for the comprehensive evaluation of COPD. In the 2023 GOLD guidelines, the concept of “heterogeneous lung condition” was proposed,1 emphasizing the diversity and individual differences in clinical manifestations of COPD patients. The reason for this is that various factors, such as hypoxia, oxidative stress (OS), systemic inflammation and other mechanisms, can lead to damage in multiple organs and tissues throughout the body. These include the cardiovascular, endocrine, hematological, locomotor, neuropsychiatric, and digestive system.5 The risk of comorbidities in COPD patients is also elevated by factors such as smoking history and advanced age.6 In addition, several extrapulmonary comorbidities of COPD have been found to considerably increase the risk of acute exacerbation, complicate the treatment, and impose a heavy medical burden on COPD patients.4,7

    Therefore, a comprehensive understanding and early diagnosis of comorbidities are extremely important to optimize the treatment and prognosis of COPD. This review summarizes recent advances in the study of such above extrapulmonary comorbidities in COPD.

    Method

    We conducted a comprehensive search on Medline/PubMed and China national knowledge infrastructure (CNKI) up to December 2023 to identify studies relevant to this review. The combination of the following keywords was used as the potential search terms: “Comorbidities in COPD”, “Relationship”, “Prevalence”, “Risk factors”, “Treatment”, “Management”, “Survival and Quality of Life” and so on. In addition, the reference lists of the retrieved articles were further examined in order to determine their significance to the subject matter of this review.

    COPD and Cardiovascular Diseases (CVD)

    A meta-analysis of observational studies found that the probability of cardiovascular events was significantly increased in patients with COPD compared to patients without COPD [OR=2.46; 96% CI; 2.02–3.00; P<0.0001], and the risk of ischemic heart disease (IHD), cardiac dysrhythmia, heart failure, and arterial circulation diseases in COPD patients was two to five times higher than those in the non-COPD population.8

    COPD and CVD have a significant overlap in risk factors, pathophysiological mechanisms, clinical characteristics, and symptoms, which in turn worsen the prognosis for individuals affected by both conditions.9,10 Although smoking is a common and significant risk factor for the two diseases mentioned above, an increasing number of studies have indicated that smoking is not the only link between COPD and CVD. Obesity, hypoxia, aging, lifestyle, and genetics may also be common risk factors.11 In addition, under the stimulation of different factors (eg, inflammation, hypoxia, and OS), in some COPD patients, cardiovascular damage may occur in the early stages.12 Here, hypoxia can induce stress responses in hemodynamics, leading to an increase in cardiac output index, leading to increased peripheral vascular contraction and OS.12 Furthermore, increased oxidative stress can further stimulate persistent systemic inflammation, which in turn can effectively alter the vascular structure.13 The systemic inflammatory response, in turn can significantly enhance cytokine activity, contributing to platelet aggregation and blood coagulation.14,15 Additionally, OS not only causes extensive damage to the airway epithelium, but can also adversely affect both the function and quantity of endothelial cells. The dysfunction of endothelial cells can disrupt the vascular homeostasis, while excessive endothelial cell apoptosis can effectively reduce their antioxidant, anti-inflammatory, and antithrombotic abilities.16 This series of reactions can significantly increase the possibility of cardiovascular events.

    Clinically, patients with COPD and CVD may sometimes experience exertional dyspnea, and both can increase the patient’s fatigue, which can further limit their physical activity and continuously reduce their activity tolerance. Patients with both diseases develop severe symptoms. The most important drugs for COPD currently include bronchodilators (eg, β receptor agonists, anti-cholinergic drugs, and theophyllines), corticosteroids, and other symptomatic therapeutic drugs.4 It is important to emphasize that recent studies have indicated that the use of dual long-acting bronchodilators can significantly increase the risk of cardiovascular events.17 However, in the treatment of cardiovascular complications, treatment with β receptor agonist appears to violate the principles of COPD therapy. Interestingly, studies have reported that selective cardiac β receptor agonists exhibit more significant benefits than potential risks in mild to moderate reversible respiratory diseases or coronary artery disease with COPD.18,19 However, its use in COPD patients combined with heart failure remains controversial.20 Meanwhile, statins have shown numerous benefits such as antioxidant, anti-inflammatory, antithrombotic, and immunomodulatory properties.21 These effects prove effective in managing inflammation, reducing the severity of COPD, and lowering CVD-related mortality,22,23 in addition to reducing the risk of pulmonary hypertension.24 However, some studies have demonstrated that the beneficial effects of statins may depend on the patient’s age and corticosteroid use.25 Additionally, antiplatelet agents can significantly reduce the risk of ischemic events in patients with COPD.26 These agents can also contribute to delaying the progression of emphysema,27 improving dyspnea and quality of life in patients.28 Furthermore, angiotensin-converting enzyme inhibitor (ACEI) / angiotensin receptor block (ARB) have also been proposed to display a beneficial effect on the risk of cardiovascular events. These drugs may also potentially delay the progression of emphysema while improving the lung function,29,30 with dual cardiorespiratory protective properties. In addition, the imbalance between protease and antiproteinase is also a major pathogenic mechanism of COPD and CVD. Matrix metalloproteinases (MMPs) play an important role and antiproteinase inhibitors are expected to be employed as novel therapeutic targets.15 Although some MMP inhibitors were found to be safe in cancer trials, their success rate is relatively limited.31 Therefore, large-scale prospective studies are still needed to further evaluate the safety and effectiveness of MMP inhibitors in COPD patients affected with CVD. It is noteworthy that numerous studies have demonstrated that both COPD and CVD share common mechanisms such as oxidative stress and systemic inflammation. This suggests that antioxidant therapy could provide a novel and effective therapeutic direction for the treatment of COPD and its associated cardiovascular diseases. However, further extensive prospective studies are required to validate this potential therapeutic direction.

    COPD and Endocrine Diseases

    According to statistics, up to 40% of COPD cases are associated with one or more diseases related to metabolic syndrome (MetS), with diabetes being the most common.32,33 COPD is also regarded as a common comorbidity of diabetes, and they mutually increase the risk of disease and unfavorable prognostic factors.34,35 It is worth indicating that the severity of diabetes has been strongly related to the deterioration of lung function, which could be related to the limited activity and the reduced quality of life of COPD patients.36,37 In contrast, hyper glycaemia can also cause a decline in lung function and physical performance.38 For instance, in a 30-year follow-up study involving more than 27,000 non-smokers, low FEV1 was found to precede diabetes and has a significant predictive effect on diabetes incidence.39 Multiple shared risk factors and pathological changes play a vital role in their cooccurrence and interaction, including smoking, obesity, age, hypoxia, oxidative stress, inflammation, and so on.34

    A sustained systemic inflammatory response and OS are considered as major factors in the progression of these two diseases.33 The inflammation of airways can cause harm to pancreatic beta cells and obstruct the signaling pathway of insulin, resulting in insulin resistance.40,41 At the same time, the hyperglycemic state can lead to inflammation and oxidative stress, resulting in damage to the pulmonary blood vessels.42 Additionally, the damage to the endothelial cells in the pulmonary blood vessels can lead to connective tissue proliferation and subsequently reduce pulmonary compliance.43 In addition, the advanced glycation end products (AGEs) associated with hyper glycaemia can trigger inflammation and attenuate alveolar retraction, thus exacerbating the patient’s ventilatory deficits.44 At the same time, diabetic autonomic neuropathy can also dysregulate airway diastolic function.45 Additionally, hypoxia has the potential to impact glucose metabolism and insulin sensitivity,29 leading to an increased risk of excessive oxidation and oxidative stress. Furthermore, it can disrupt the defense provided by antioxidants as well as antiproteases, and evolve into a potential risk factor for diabetes mellitus.33 Interestingly, although corticosteroids can also increase the risk of diabetes.46 For instance, corticosteroids, which are commonly used in COPD patients, some studies have reported that the risk of diabetes was only significantly increased upon treatment with high-doses of corticosteroids.47,48 However, other studies have suggested that the combined use of inhaled corticosteroids (ICS) and statins could increase the risk of developing new-onset diabetes.49 Therefore, more long-term observational studies and randomized controlled trials should be conducted in the future to assess the potential safety of drug combinations.

    For the treatment of COPD cases combined with diabetes, blood sugar control is essential, as it has been linked to immune dysfunction.50 Recently, the hypoglycemic drug metformin has received significant attention because of its properties of anti-inflammatory and antioxidant. It effectively improves lung outcomes by reducing the production of pro-inflammatory factors through the activation of AMP-activated protein kinase (AMPK).51 Furthermore, it promotes the breakdown of inflammatory mediators by stimulating autophagy,52 with a primary focus on inhibiting the nuclear factor of kappa B (NF-κB) pathway, which is considered to play a crucial role in promoting inflammation.53,54 In addition, metformin can also attenuate oxidative stress-induced cytotoxicity and inhibit the inflammatory response in macrophages through an AMPK-dependent pathway.55 However, the use of metformin still remains controversial. Several large-scale cohort studies have demonstrated that metformin can significantly reduce the risk of exacerbation and all-cause mortality in COPD patients.56,57 However, another retrospective cohort study suggested that metformin failed to improve the blood glucose elevation caused by COPD in non-diabetic patients.58 Hence, additional clinical trials of metformin with stronger evidence are needed to validate its effectiveness in delaying progression. Among other oral hypoglycemic agents, thiazolidinedione drugs and dipeptidyl peptidase-4 (DPP-4) inhibitors can substantially attenuate the inflammatory reactions while lowering blood sugar, thereby protecting the lung tissues.59,60 Sulfonylureas can reduce risk of acute exacerbation of COPD, bacterial pneumonia and cardiovascular events.61 However, recently, there has been growing attention on glucagon-like peptide 1 (GLP-1) receptor agonist and sodium-glucose cotransporter 2 (SGLT-2) inhibitor. Research suggests that GLP-1 receptor agonists can enhance airway function and reduce the risk of exacerbation of COPD.62,63 Additionally, SGLT-2 inhibitors have shown a reduced risk of exacerbating obstructive airway disease when compared to DPP-4 inhibitors.64 In addition to medication, reducing sedentary time, increasing exercise, and implementing individual nutritional interventions can also effectively improve the quality of life and prognosis of COPD patients with diabetes.

    COPD and Hematological Diseases

    A number of previous studies have shown that high incidence of hypoxia in COPD patients could lead to a compensatory increase in erythropoietin (EPO), leading to secondary hyperhemoglobinemia. However, recent studies in China and abroad suggest that anemia was also one of the comorbidities of COPD and its incidence rate was even higher than that of hyperhemoglobinemia.65,66 It was found that compared to hyperhemoglobinemia, anemia has a greater impact on the disease severity and quality of life in COPD patients.67,68 As shown in a 9-year multicenter clinical study in Korea, anemia (WHO criteria) can serve as an independent risk factor for mortality in COPD.69 In addition, it has been observed that COPD patients affected with anemia had a higher comorbidity burden, especially CVD and MetS,70 which further increased their disease burden and risk of death.

    Currently, COPD combined with anemia is considered to belong to the anemia of chronic disease (ACD), commonly known as “inflammatory anemia”, which is essentially an immune- driven inflammatory response.71,72 Prolonged chronic inflammation in COPD patients can significantly weaken the proliferative stimulation response of EPO and shorten the lifespan of red blood cells.73 In addition, some inflammatory factors can directly inhibit hypoxia-induced activation of EPO, which leads to an increase in OS. These factors also interfere with EPO receptor-mediated signaling pathways, thus inhibiting the production of EPO.74 During chronic inflammation, phagocytes have been found to inhibit inflammation by depleting iron and affect iron metabolism as well as transport. This is primarily caused by high levels of hepcidin, leading to iron deficiency in the body, which evolves into iron deficiency anemia (IDA).75,76 Thus, iron deficiency can affect lung function and disease progression in COPD,77,78 forming a vicious circle. Furthermore, since COPD is a chronic wasting disease with malnutrition, there may be a deficiency of hematopoietic raw materials,79 resulting in a decrease in red blood cells.

    Hemoglobin can transport oxygen to the various tissues and organs. However, the decrease in hemoglobin in anemia patients leads to a reduction in oxygen supply capacity. Although the blood oxygen partial pressure is sometimes within the normal range, the patient may still be in a state of hypoxia. Therefore, patients with anemia are more likely to develop symptoms such as dyspnea, affecting the motor ability and quality of life.67 Therefore, it is important to actively improve the hemoglobin level. For clinical improvement of anemia, we generally choose direct blood transfusions, EPO injections, and supplementation with hematopoietic raw materials. However, it has been suggested that patients with COPD combined with anemia are resistant to EPO due to the inhibitory effect of inflammatory factors on erythroid progenitor cells.80 Furthermore, although iron supplementation has been found to be effective in reducing the levels of OS in COPD patients, recent studies have further shown that iron therapy could affect the composition of the microbiota as well as the distribution of fecal metabolites, to a certain extent, which has a potentially detrimental effect on the patients.81,82 It is worth noting that intravenous iron supplementation can be effective in increasing hemoglobin levels while reducing gastrointestinal adverse effects compared to oral iron supplementation. This is particularly significant as inflammation can impair iron absorption in the gut.83 In addition, the supplementation of essential nutrients like vitamins and amino acids plays a pivotal role in facilitating the production of hemoglobin and erythropoiesis, underscoring their potential importance. Vitamin C is recognized as a powerful antioxidant, while vitamin D has the potential to exhibit anti-inflammatory effects.84,85 Although it is currently unclear whether the effectiveness of treating the inflammation response is more effective in the primary disease. There are novel treatment strategies available related to the iron regulatory pathway and hypoxia-inducible factor stabilizers for inflammatory anemia, but their efficacy needs to be further evaluated in clinical trials.76

    COPD and Locomotor System Diseases

    Skeletal muscle dysfunction and osteoporosis are locomotor system comorbidities found in COPD, and the risk of incidence is 1.9 times higher than in normal individuals.86 The incidence of reduced muscle mass in COPD patients is about 15.5%-34%,87 and it is approximately 38.5% in patients affected with osteoporosis.88 Osteoporosis is a systemic metabolic bone disease characterized by a decrease in bone mass and structural deterioration of bone tissue, leading to an increase in bone fragility and the risk of fractures.89 In contrast, osteoporosis is mostly asymptomatic in COPD patients and is typically only detected when a fracture takes place. Therefore, special attention should be paid to the early identification of high-risk patients with COPD combined with osteoporosis.

    It has been found that most pathogenic factors can simultaneously affect muscle strength and bone strength in COPD patients. In addition to the patient’s low body mass index, malnutrition and decreased exercise tolerance, systemic inflammatory responses, OS, hypoxia, intake of hormone drugs and vitamin D deficiency are all considered as potential risk factors, increasing bone loss and even leading to fragility fractures.90,91 Furthermore, fractures associated with osteoporosis could further increase the poor prognosis of COPD due to lack of exercise and prolonged bed rest, such as deterioration of the lung function, poor quality of life, as well as increased hospitalization and mortality rates.92 This can potentially create a vicious cycle of these two diseases and places a heavy burden on patients. Under the normal circumstances, bone resorption by osteoclasts and bone formation by osteoblasts alternate in bone tissues to maintain the balance of bone mass.93 However, both the hypoxic state and systemic inflammation in COPD patients could effectively stimulate the proliferation and differentiation of osteoclasts, thus affecting the bone metabolism.94,95 In addition, in patients who smoke, nicotine not only stimulates osteoclast activity, but also triggers apoptosis in osteoblasts, thereby further contributing to osteoporosis.96,97 It is important not to overlook that COPD patients may suffer from deficiency of Vitamin D due to limited activity, reduced sunlight exposure, malnutrition, and the promotion of Vitamin D metabolism by corticosteroids. This deficiency can potentially lead to bone loss as a result of the inability to maintain calcium homeostasis.98

    In terms of pharmacological treatment, corticosteroid is an effective treatment for COPD, however, the potential development of secondary osteoporosis due to prolonged usage should not be ignored.99 Although oral administration has been reported to cause apoptosis of bone cells and loss of bone strength,100 there is still controversy regarding the impact of inhaled corticosteroids (ICS) on bone strength.91,101 Currently, the GOLD does not explicitly state that using ICS could lead to significant negative impacts associated with osteoporosis. However, numerous studies have indicated that the use of ICS raises the risk of osteoporosis regardless of the duration of exposure.102 In general, except in patients with COPD in the acute exacerbation stage, systemic application of corticosteroids should be avoided to reduce the risk of bone related adverse effects. In the treatment of osteoporosis, bisphosphonates have been shown to be effective in the treatment of hormone-related bone loss, and are usually combined with calcium and vitamin D.103 In addition, some novel drugs, including denosumab and teriparatide, have been found to have more potent effects in improving the bone density, preventing fractures, and have higher safety.104–106 Hence, these are expected to become a first-line medication for the treatment of osteoporosis-related corticosteroids.107 It has also been suggested that romosozumab, a sclerostin inhibitor that both induces bone formation and inhibits bone resorption, could possibly reduce the risk of fracture to a greater extent in comparison to alendronate.108 Additionally, the use of some antioxidants is considered as a new potential therapeutic direction to prevent and reduce the negative effects of OS on bone remodeling and osteoblastic cells.109 However, additional research is necessary in order to thoroughly investigate the potential risks associated with them.

    COPD and Mental Disorders

    The combined nervous system diseases associated with COPD mainly include emotional disorders, cognitive impairments, pulmonary encephalopathy and consciousness disorders. Emotional disorders (eg, anxiety and depression) are the most common and easily misdiagnosed. Interestingly, a systematic retrospective study found that the incidence of COPD patients developing emotional disorders was approximately three times higher in comparison to the control group.110 However, the incidence of COPD combined with anxiety and depression has been shown to be between 19.5% −50% in China, and the incidence varies between different studies due to various factors, such as sample size, diagnostic tools, and disease severity.111,112

    Patients with COPD often find themselves in a vicious cycle of “dyspnea- decreased activity- increased mental symptoms - dyspnea exacerbation”.113 However, a variety of factors such as behavior, societal influence, and the illness itself contribute to the development of anxiety and depression. In addition, COPD patients suffer from recurrent illness and reduced social engagement that perpetuates anxiety/depression, which in turn can increase the risk of acute exacerbation of COPD. In addition, to the emotional disorders caused by reduced social participation primarily induced by the degradation of body function, this phenomenon could also be related to the influences of hypoxemia and hypercapnia on areas of the brain areas involved in regulation of both ventilation and defensive behaviors.114,115 For chronic smokers, long-term inhalation of nicotine stimulates the body’s inflammatory response and can cause damage to the glial cells. Consequently, this leads to brain damage and the development of mood disorders,116 and potential impact of cigarette smoke on the regulation of neurohormonal secretion rhythms can also contribute to mood disorders in patients.117 Moreover, the chronic inflammatory response in COPD can also have a direct impact on the central nervous system, including an increase in negative emotions.118 In addition, imbalance of inflammatory factors can also increase risk of mood disorders in COPD patients119. Recently, the potential relationship between imbalance in immune system response and emotional disorders has also been suggested.120 However, the relationship between COPD combined with emotional disorders and immunological mechanisms is complex, and further research is still needed for more in-depth exploration.

    COPD catalyzes the development of emotional disorders, and emotional disorders can influence both the occurrence and development of COPD. Therefore, early intervention should be carried out in patients with COPD, focusing on the impact of psychological changes on the development and prognosis of the physical diseases. Currently, the main treatment includes pharmacological therapy and non-pharmacological therapy, while non-pharmacological therapy also includes various treatment methods, such as comprehensive pulmonary rehabilitation therapy, psychological therapy and collaborative nursing mode.121 Although pulmonary rehabilitation is known to improve mood and provide several other benefits to COPD patients, studies have found that it has inconsistent rates of continuation and completion, with only half of participants continuing in a rehabilitation center and merely 30% completing the full duration of their treatment.122 Therefore, it is imperative to conduct further studies on pulmonary rehabilitation programs aimed at providing adequate support and ensuring participants’ successful completion. Additionally, it is crucial to discover viable alternative interventions for patients who are unable to participate in routine pulmonary rehabilitation. It is worth noticing that there could be potential interactions between drugs for COPD and those for anxiety/depression. Tricyclic antidepressants (TCA) may potentiate other adverse effects of beta-2 adrenergic agonists and anticholinergic bronchodilators, but tricyclic antidepressants are not considered absolutely contraindicated for use in patients with COPD because of the above mentioned interactions.123,124 Therefore, both the efficacy and safety of anxiolytic/depressant medications for the treatment of COPD-associated mood disorders still needs to be confirmed by more clinical trials. Additionally, considering the potential influence of inflammatory cytokines on depression, the emergence of cytokine modulators as a potential treatment for depression in individuals with chronic inflammation chronic inflammation125 should be explored. However, it is crucial to conduct more extensive randomized controlled trials with robust evidence to thoroughly assess this field. Overall, to minimize the adverse effects of emotional disorders and improve quality of life, comprehensive interventions including medication, psychology and rehabilitation are required.

    COPD and Digestive System Diseases

    Common digestive system comorbidities associated with COPD include gastroesophageal reflux, chronic gastritis, peptic ulcer, irritable bowel syndrome and inflammatory bowel disease. Among these, gastroesophageal reflux disease (GERD) is a common but frequently overlooked condition, which can markedly increase the frequency of acute exacerbation of COPD. This primarily results because of airway irritation and damage from reflux of acidic gastric contents, bronchoconstriction due to the cough reflex triggered by vagal stimulation, bacterial reflux and even bacterial colonization due to aspiration.126–128 Similarly, changes in chest pressure due to COPD may increase the risk of GERD. Additionally, recurrent coughing in COPD patients can also exacerbate reflux, and the use of receptor agonists commonly prescribed for COPD have a diastolic effect on the esophageal sphincter while dilating the bronchial tubes, potentially increasing the likelihood of the development of gastroesophageal reflux.129–131 Thus, GERD and COPD can interact with each other. However, there remains a lack of comprehensive knowledge regarding the exact causal relationship between them.

    At present, there is a lack of sufficient information on the impact of anti-reflux therapy on COPD, and there is ongoing controversy regarding the appropriateness of using acid-inhibitory drugs, specifically proton pump inhibitors (PPIs). Several studies have indicated that PPI treatment could potentially exacerbate COPD,132 yet others have suggested that the risk of pneumonia was not increased by PPI treatment.133 In addition, some studies have demonstrated that acid-suppressing therapy could improve the scores of lung symptom,134 but paradoxically, the lung function of the majority of patients does not show significant improvement.135,136 In addition, use of azithromycin has been found to be noteworthy as it can promote cholinergic activity to accelerate gastric emptying.137 For the moment, the efficacy and safety of PPIs in patients with chronic obstructive pulmonary disease (COPD), as well as the relationship between increased gastric acidity and progression of COPD, still need to be studied on a larger scale.

    Conclusions

    COPD is usually accompanied by one or more comorbidities that interact with each other. Chronic inflammation, oxidative stress, hypoxia, and smoking serve as mutual links connecting COPD and comorbidities. Although the mechanisms remain elusive and the current guidelines recommend a management according to the principle of single-disease guideline-directed medical treatment,1 it’s appropriate to treat them as a whole (Figure 1).138 For almost every patient with COPD, the clinical reality is that the disease is a component of multimorbidity. Therefore, we need to find integrated multimorbidity management, considering both pharmacological and nonpharmacological strategies. It’s important for every clinician to realize that an effective patient-centered management approach is a more efficient treatment option. So, multi-disciplinary, multi-level, and effective research is necessary to thoroughly investigate and develop targeted treatment strategies that are more appropriate for COPD and its comorbidities. This strategy can provide strong theoretical support for the management and prevention of these conditions. Moreover, the clinicians should also improve their cognitive and diagnostic abilities in management of COPD-related comorbidities. They should develop personalized and effective diagnosis and treatment approaches for individual patients to optimize their clinical outcomes.

    Figure 1 COPD and multimorbidity. This conceptual framework represents the most important change in disease concept since the Review139 by Decramer and Janssens on COPD and comorbidities was published in the first volume of The Lancet Respiratory Medicine, and demands a shift in the management paradigm from an approach that focuses on COPD as a single disease of the respiratory system with comorbidities, to one in which COPD is viewed as a component of multimorbidity. (A) Previously COPD was seen as a single disease. (B) COPD and different comorbidities have generally gained attention because of the progress in understanding, but they were still viewed separately. (C) Patients with COPD and comorbidities should be considered as suffering from a multimorbid state, which should be treated as a whole. COPD=chronic obstructive pulmonary disease. FVC=forced vital capacity.

    Note: Reprinted from The Lancet Respiratory Medicine, 11/11, Leonardo M Fabbri, Bartolome R Celli, Alvar Agustí, Gerard J Criner, Mark T Dransfield, Miguel Divo, Jamuna K Krishnan, Lies Lahousse, Maria Montes de Oca, Sundeep S Salvi, Daiana Stolz, Lowie E G W Vanfleteren, Claus F Vogelmeier, COPD and multimorbidity: recognising and addressing a syndemic occurrence, 1020-1034, Copyright 2023, with permission from Elsevier.138

    Acknowledgments

    We thank all the reviewers who participated in the review, as well as MJE editor (www.mjeditor.com) for the linguistic editing and proof reading of the manuscript.

    Disclosure

    The authors declare that they have no conflicts of interest in this work.

    References

    1. GOLD Report. Global initiative for chronic obstructive lung disease; 2023. Available from: goldcopd.org/2023-gold-report-2/. Accessed February 24, 2024.

    2. Foreman KJ, Marquez N, Dolgert A, et al. Forecasting life expectancy, years of life lost, and all-cause and cause-specific mortality for 250 causes of death: reference and alternative scenarios for 2016–40 for 195 countries and territories. Lancet. 2018;392(10159):2052–2090. doi:10.1016/S0140-6736(18)31694-5

    3. GBD 2019 Diseases and Injuries Collaborators. Global burden of 369 diseases and injuries in 204 countries and territories, 1990–2019: a systematic analysis for the Global Burden of Disease Study 2019. Lancet. 2020;396(10258):1204–1222. doi:10.1016/S0140-6736(20)30925-9

    4. Chen YH. Interpretation of global strategy for the diagnosis, treatment, management and prevention of chronic obstructive pulmonary disease 2022 report. Chinese General Practice. 2022;25(11):1294–1304+1308.

    5. Huang YL, Min J, Li GH, et al. The clinical study of comorbidities and systemic inflammation in COPD. J Sichuan Univ. 2019;50(1):88–92.

    6. Divo MJ, Celli BR, Poblador-Plou B, et al. Chronic Obstructive Pulmonary Disease (COPD) as a disease of early aging: evidence from the EpiChron Cohort. PLoS One. 2018;13(2):e0193143. doi:10.1371/journal.pone.0193143

    7. Agustí A, Celli BR, Criner GJ, et al. Global initiative for chronic obstructive lung disease 2023 report: gold executive summary. Am J Res Crit Care Med. 2023;207(7):819–837.

    8. Chen W, Thomas J, Sadatsafavi M, et al. Risk of cardiovascular comorbidity in patients with chronic obstructive pulmonary disease: a systematic review and meta-analysis. Lancet Respir Med. 2015;3(8):631–639. doi:10.1016/S2213-2600(15)00241-6

    9. André S, Conde B, Fragoso E, et al. COPD and Cardiovascular Disease. Pulmonology. 2019;25(3):168–176. doi:10.1016/j.pulmoe.2018.09.006

    10. Kunisaki KM, Dransfield MT, Anderson JA, et al. Exacerbations of chronic obstructive pulmonary disease and cardiac events. A post hoc cohort analysis from the summit randomized clinical trial. Am J Respirat Crit Care Med. 2018;198(1):51–57.

    11. Shi Y, Zhang J, Huang Y. Prediction of cardiovascular risk in patients with chronic obstructive pulmonary disease: a study of the national health and nutrition examination survey database. BMC Cardiovascul Disord. 2021;21(1):417. doi:10.1186/s12872-021-02225-w

    12. Maclay JD, MacNee W. Cardiovascular disease in COPD: mechanisms. Chest. 2013;143(3):798–807. doi:10.1378/chest.12-0938

    13. Brassington K, Selemidis S, Bozinovski S, et al. New frontiers in the treatment of comorbid cardiovascular disease in chronic obstructive pulmonary disease. Clin Sci. 2019;133(7):885–904. doi:10.1042/CS20180316

    14. Sin DD, Man SFP. Why are patients with chronic obstructive pulmonary disease at increased risk of cardiovascular diseases? The potential role of systemic inflammation in chronic obstructive pulmonary disease. Circulation. 2003;107(11):1514–1519. doi:10.1161/01.CIR.0000056767.69054.B3

    15. Brassington K, Selemidis S, Bozinovski S, et al. Chronic obstructive pulmonary disease and atherosclerosis: common mechanisms and novel therapeutics. Clin Sci. 2022;136(6):405–423. doi:10.1042/CS20210835

    16. Karoli NA, Rebrov AP. Endothelial dysfunction in patients with chronic obstructive pulmonary disease in combination with coronary heart disease. Terapevticheskii Arkhiv. 2019;91(3):22–26. doi:10.26442/00403660.2019.03.000061

    17. Parkin L, Williams S, Sharples K, et al. Dual versus single long-acting bronchodilator use could raise acute coronary syndrome risk by over 50%: a population-based nested case-control study. J Intern Med. 2021;290(5):1028–1038. doi:10.1111/joim.13348

    18. Yang YL, Xiang ZJ, Yang JH, et al. Association of β-blocker use with survival and pulmonary function in patients with chronic obstructive pulmonary and cardiovascular disease: a systematic review and meta-analysis. Eur Heart J. 2020;41(46):4415–4422. doi:10.1093/eurheartj/ehaa793

    19. Gulea C, Zakeri R, Alderman V, et al. Beta-blocker therapy in patients with COPD: a systematic literature review and meta-analysis with multiple treatment comparison. Respir Res. 2021;22(1):64. doi:10.1186/s12931-021-01661-8

    20. Hawkins NM, Petrie MC, Macdonald MR, et al. Heart failure and chronic obstructive pulmonary disease the quandary of beta-blockers and beta-agonists. J Am Coll Cardiol. 2011;57(21):2127–2138. doi:10.1016/j.jacc.2011.02.020

    21. Zhang W, Li CW, Yang L, et al. Advances in the use of statins in chronic obstructive pulmonary disease and its comorbidities. Chin J Lung Dis. 2021;14(01):114–116.

    22. Lu Y, Chang R, Yao J, et al. Effectiveness of long-term using statins in COPD - a network meta-analysis. Respir Res. 2019;20(1):17. doi:10.1186/s12931-019-0984-3

    23. Ingebrigtsen TS, Marott JL, Nordestgaard BG, et al. Statin use and exacerbations in individuals with chronic obstructive pulmonary disease. Thorax. 2015;70(1):33–40. doi:10.1136/thoraxjnl-2014-205795

    24. Wu WT, Chen CY. Protective effect of statins on pulmonary hypertension in chronic obstructive pulmonary disease patients: a nationwide retrospective, matched cohort study. Sci Rep. 2020;10(1):3104. doi:10.1038/s41598-020-59828-0

    25. Huang YJ, Kao S, Kao LT, et al. Association between statin use and exacerbation of chronic obstructive pulmonary disease among patients receiving corticosteroids. Int J Chronic Obstr. 2021;16:591–602. doi:10.2147/COPD.S292026

    26. Andell P, James SK, Cannon CP, et al. Ticagrelor versus clopidogrel in patients with acute coronary syndromes and chronic obstructive pulmonary disease: an analysis from the platelet inhibition and patient outcomes (PLATO) trial. J Am Heart Assoc. 2015;4(10):e002490. doi:10.1161/JAHA.115.002490

    27. Aaron CP, Schwartz JE, Hoffman EA, et al. A longitudinal cohort study of aspirin use and progression of emphysema-like lung characteristics on CT imaging: the mesa lung study. Chest. 2018;154(1):41–50. doi:10.1016/j.chest.2017.11.031

    28. Fawzy A, Putcha N, Aaron CP, et al. Aspirin use and respiratory morbidity in COPD: a propensity score-matched analysis in subpopulations and intermediate outcome measures in COPD study. Chest. 2019;155(3):519–527. doi:10.1016/j.chest.2018.11.028

    29. Vasileiadis IE, Goudis CA, Giannakopoulou PT, et al. Angiotensin converting enzyme inhibitors and angiotensin receptor blockers: a promising medication for chronic obstructive pulmonary disease? COPD. 2018;15(2):148–156. doi:10.1080/15412555.2018.1432034

    30. Tejwani V, Fawzy A, Putcha N, et al. Emphysema progression and lung function decline among angiotensin converting enzyme inhibitors and angiotensin-receptor blockade users in the copdgene cohort. Chest. 2021;160(4):1245–1254. doi:10.1016/j.chest.2021.05.007

    31. Almutairi S, Kalloush HM, Manoon NA, et al. Matrix metalloproteinases inhibitors in cancer treatment: an updated review (2013–2023). Molecules. 2023;28(14):5567. doi:10.3390/molecules28145567

    32. Cebron Lipovec N, Beijers RJ, van den Borst B, Doehner W, Lainscak M, Schols AM. The prevalence of metabolic syndrome in chronic obstructive pulmonary disease: a systematic review. COPD. 2016;13(3):399–406. doi:10.3109/15412555.2016.1140732

    33. Chan SMH, Selemidis S, Bozinovski S, et al. Pathobiological mechanisms underlying metabolic syndrome (MetS) in chronic obstructive pulmonary disease (COPD): clinical significance and therapeutic strategies. Pharmacol Ther. 2019;198:160–188.

    34. Cazzola M, Rogliani P, Calzetta L, et al. Targeting mechanisms linking COPD to type 2 diabetes mellitus. Trends Pharmacol Sci. 2017;38(10):940–951. doi:10.1016/j.tips.2017.07.003

    35. Frizzelli A, Aiello M, Calzetta L, et al. The interplay between diabetes mellitus and chronic obstructive pulmonary disease. Minerva Med. 2023;114(1):68–73. doi:10.23736/S0026-4806.22.07742-4

    36. Kinney GL, Black-Shinn JL, Wan ES, et al. Pulmonary function reduction in diabetes with and without chronic obstructive pulmonary disease. Diabetes Care. 2014;37(2):389–395. doi:10.2337/dc13-1435

    37. Mekov EV, Slavova YG, Genova MP, et al. Diabetes mellitus type 2 in hospitalized COPD patients: impact on quality of life and lung function. Folia Medica. 2016;58(1):36–41. doi:10.1515/folmed-2016-0005

    38. Liu J, Song X, Zheng S, et al. A prospective study on physical performance of Chinese chronic obstructive pulmonary disease males with type 2 diabetes. Medicine. 2021;100:35.

    39. Zaigham S, Nilsson PM, Wollmer P, et al. The temporal relationship between poor lung function and the risk of diabetes. BMC Pulm Med. 2016;16(1):75. doi:10.1186/s12890-016-0227-z

    40. Cyphert TJ, Morris RT, House LM, et al. NF-κB-dependent airway inflammation triggers systemic insulin resistance. Am J Physiol Regulatory Integr Comp Physiol. 2015;309(9):R1144–1152. doi:10.1152/ajpregu.00442.2014

    41. Xu M. The changes of the inflammatory profiles and oxidative stress for insulin resistance in AECOPD patients with T2DM. Anhui Medical University. 2018;2018:1.

    42. Khateeb J, Fuchs E, Khamaisi M. Diabetes and lung disease: a neglected relationship. Rev Diabet Stud. 2019;15:1–15. doi:10.1900/RDS.2019.15.1

    43. Mauricio D, Gratacòs M, Franch-Nadal J. Diabetic microvascular disease in non-classical beds: the hidden impact beyond the retina, the kidney, and the peripheral nerves. Cardiovasc Diabetol. 2023;22(1):314. doi:10.1186/s12933-023-02056-3

    44. Dai Y, Zhou S, Qiao L, et al. Non-apoptotic programmed cell deaths in diabetic pulmonary dysfunction: the new side of advanced glycation end products. Front Endocrinol. 2023;14:1126661. doi:10.3389/fendo.2023.1126661

    45. Klein OL, Krishnan JA, Glick S, et al. Systematic review of the association between lung function and Type 2 diabetes mellitus. Diabet Med. 2010;27(9):977–987. doi:10.1111/j.1464-5491.2010.03073.x

    46. Price DB, Russell R, Mares R, et al. Metabolic effects associated with ICS in patients with COPD and comorbid type 2 diabetes: a historical matched cohort study. PLoS One. 2016;11(9):e0162903. doi:10.1371/journal.pone.0162903

    47. Miravitlles M, Auladell-Rispau A, Monteagudo M, et al. Systematic review on long-term adverse effects of inhaled corticosteroids in the treatment of COPD. Eur Respir Rev. 2021;30(160):210075. doi:10.1183/16000617.0075-2021

    48. Liu X. Effect of Corticosteroid use in chronic obstructive pulmonary disease with diabetes on diabetic complications. Genom Appl Biol. 2019;38(11):5204–5208.

    49. Ajmera M, Shen C, Sambamoorthi U. Concomitant medication use and new-onset diabetes among Medicaid beneficiaries with chronic obstructive pulmonary disease. Popul Health Manag. 2017;20(3):224–232. doi:10.1089/pop.2016.0047

    50. Jin Y, Liu A. The Changes and significance of immune function in chronic obstructive pulmonary disease patients with diabetes mellitus. J Clin Pulm Med. 2012;17(2):267–268.

    51. Deng HB, Long M, Jia KL. Experimental study of the effects of AMP-dependent protein kinase metformin on emphysema in aged rats. Chin J Mult Organ Dis Elderly. 2019;18(11):864–868.

    52. Saber S, El-Kader EMA. Novel complementary coloprotective effects of metformin and MCC950 by modulating HSP90/NLRP3 interaction and inducing autophagy in rats. Inflam-mopharmacology. 2021;29(1):237–251. doi:10.1007/s10787-020-00730-6

    53. Peng Q. Effects and mechanism of metformin on inflammatory and oxidative stress in COPD rats. Zheng Univer. 2019;2019:1.

    54. Zhang Y, Zhang H, Li S, et al. Metformin alleviates LPS-induced acute lung injury by regulating the SIRT1/NF-κB/NLRP3 pathway and inhibiting endothelial cell pyroptosis. Front Pharmacol. 2022;13:801337. doi:10.3389/fphar.2022.801337

    55. Cheng D, Xu Q, Wang Y, et al. Metformin attenuates silica-induced pulmonary fibrosis via AMPK signaling. J Transl Med. 2021;19(1):349. doi:10.1186/s12967-021-03036-5

    56. Tseng CH. Metformin and risk of chronic obstructive pulmonary disease in diabetes patients. Diabetes Metabolism. 2019;45(2):184–190. doi:10.1016/j.diabet.2018.05.001

    57. Yen FS, Chen W, Wei JCC, et al. Effects of metformin use on total mortality in patients with type 2 diabetes and chronic obstructive pulmonary disease: a matched-subject design. PLoS One. 2018;13(10):e0204859. doi:10.1371/journal.pone.0204859

    58. Ho TW, Huang CT, Tsai YJ, et al. Metformin use mitigates the adverse prognostic effect of diabetes mellitus in chronic obstructive pulmonary disease. Respir Res. 2019;20(1):69. doi:10.1186/s12931-019-1035-9

    59. Wang MT, Lai JH, Huang Y-L, et al. Use of antidiabetic medications and risk of chronic obstructive pulmonary disease exacerbation requiring hospitalization: a disease risk score-matched nested case-control study. Respir Res. 2020;21(1):319. doi:10.1186/s12931-020-01547-1

    60. Chen KY, Wu SM, Tseng CH, et al. Combination therapies with thiazolidinediones are associated with a lower risk of acute exacerbations in new-onset COPD patients with advanced diabetic mellitus: a cohort-based case-control study. BMC Pulm Med. 2021;21(1):141. doi:10.1186/s12890-021-01505-7

    61. Yen FS, Wei JC, Yu TS, et al. Sulfonylurea use in patients with type 2 diabetes and COPD: a nationwide population-based cohort study. Int J Environ Res Public Health. 2022;19(22):15013. doi:10.3390/ijerph192215013

    62. Rogliani P, Matera MG, Calzetta L, et al. Long-term observational study on the impact of GLP-1R agonists on lung function in diabetic patients. Respir Med. 2019;154:86–92. doi:10.1016/j.rmed.2019.06.015

    63. Pradhan R, Lu S, Yin H, et al. Novel antihyperglycaemic drugs and prevention of chronic obstructive pulmonary disease exacerbations among patients with type 2 diabetes: population based cohort study. BMJ. 2022;379:e071380.

    64. PCM A, Tan KCB, Lam DCL, et al. Association of sodium-glucose cotransporter 2 inhibitor vs dipeptidyl peptidase-4 inhibitor use with risk of incident obstructive airway disease and exacerbation events among patients with type 2 diabetes in Hong Kong. JAMA Network Open. 2023;6(1):e2251177. doi:10.1001/jamanetworkopen.2022.51177

    65. Cote C, Zilberberg MD, Mody SH, et al. Haemoglobin level and its clinical impact in a cohort of patients with COPD. Europ resp J. 2007;29(5):923–929. doi:10.1183/09031936.00137106

    66. Sarkar M, Rajta PN, Khatana J. Anemia in Chronic obstructive pulmonary disease: prevalence, pathogenesis, and potential impact. Lung India. 2015;32(2):142–151. doi:10.4103/0970-2113.152626

    67. Ferrari M, Manea L, Anton K, et al. Anemia and hemoglobin serum levels are associated with exercise capacity and quality of life in chronic obstructive pulmonary disease. BMC Pulm Med. 2015;15:58. doi:10.1186/s12890-015-0050-y

    68. Xu Y, Hu T, Ding H, et al. Effects of anemia on the survival of patients with chronic obstructive pulmonary disease: a systematic review and meta-analysis. Expert Rev Respir Med. 2020;14(12):1267–1277. doi:10.1080/17476348.2020.1816468

    69. Oh YM, Park JH, Kim EK, et al. Anemia as a clinical marker of stable chronic obstructive pulmonary disease in the Korean obstructive lung disease cohort. J Thorac Dis. 2017;9(12):5008–5016. doi:10.21037/jtd.2017.10.140

    70. Putcha N, Fawzy A, Paul GG, et al. Anemia and adverse outcomes in a chronic obstructive pulmonary disease population with a high burden of comorbidities. An Analysis from SPIROMICS. Ann Am Thoracic Soc. 2018;15(6):710–717. doi:10.1513/AnnalsATS.201708-687OC

    71. Chen H, Deng J, Feng YL. Anaemia associated with chronic obstructive pulmonary disease. Chin J Respir Crit Care Med. 2009;8(6):606–608.

    72. Lin HR, Deng C, Liu H, et al. Correlation analysis of incidences of anemia and hypoproteinemia and age and sex in patients with chronic obstructive pulmonary disease. Chin J Lung Dis. 2019;12(3):311–314.

    73. de Hoepers ATC, Menezes MM, Fröde TS. Systematic review of anaemia and inflammatory markers in chronic obstructive pulmonary disease. Clin Exp Pharmacol Physiol. 2015;42(3):231–239. doi:10.1111/1440-1681.12357

    74. Kuhrt D, Wojchowski DM. Emerging EPO and EPO receptor regulators and signal transducers. Blood. 2015;125(23):3536–3541. doi:10.1182/blood-2014-11-575357

    75. Lin SN, Wang FH, Shi HF, et al. Study on the mechanism of iron homeostasis disorder in mediating anemia in COPD patients with type II respiratory failure. Chin J Diffic and Compl Cas. 2021;20(10):1012–1016.

    76. Lanser L, Fuchs D, Kurz K, et al. Physiology and inflammation driven pathophysiology of iron homeostasis-mechanistic insights into anemia of inflammation and its treatment. Nutrients. 2021;13(11):3732. doi:10.3390/nu13113732

    77. Kim MH, Kim YH, Lee DC. Relationships of serum iron parameters and hemoglobin with forced expiratory volume in 1 second in patients with chronic obstructive pulmonary disease. Korean J Fam Med. 2018;39(2):85–89.

    78. Sato K, Inoue S, Igarashi A, et al. Effect of iron deficiency on a murine model of smoke-induced emphysema. Am J Respir Cell Mol Biol. 2020;62(5):588–597. doi:10.1165/rcmb.2018-0239OC

    79. Shi QF, Sheng Y, Wang SY. Progress in the study of the effect of anaemia on patients with chronic obstructive pulmonary disease. J Clin Pulm Med. 2019;24(1):144–147.

    80. Sharma RK, Chakrabarti S. Anaemia secondary to erythropoietin resistance: important predictor of adverse outcomes in chronic obstructive pulmonary disease. Postgrad Med J. 2016;92(1093):636–639. doi:10.1136/postgradmedj-2015-133814

    81. Pérez-Peiró M, Martín-Ontiyuelo C, Rodó-Pi A, et al. Iron replacement and redox balance in non-anemic and mildly anemic iron deficiency COPD Patients: insights from a clinical trial. Biomedicines. 2021;9(9):1191. doi:10.3390/biomedicines9091191

    82. Loveikyte R, Bourgonje AR, van Goor H, et al. The effect of iron therapy on oxidative stress and intestinal microbiota in inflammatory bowel diseases: a review on the conundrum. Redox Biol. 2023;68:102950. doi:10.1016/j.redox.2023.102950

    83. Bonovas S, Fiorino G, Allocca M, et al. Intravenous versus oral iron for the treatment of anemia in inflammatory bowel disease: a systematic review and meta-analysis of randomized controlled trials. Medicine. 2016;95(2):e2308. doi:10.1097/MD.0000000000002308

    84. Lei T, Lu T, Yu H, et al. Efficacy of Vitamin C supplementation on chronic obstructive pulmonary disease (COPD): a systematic review and meta-analysis. Int J Chron Obstruct Pulmon Dis. 2022;17:2201–2216. doi:10.2147/COPD.S368645

    85. Fletcher J, Cooper SC, Ghosh S, et al. The role of vitamin D in inflammatory bowel disease: mechanism to management. Nutrients. 2019;11(5):1019. doi:10.3390/nu11051019

    86. Schnell K, Weiss CO, Lee T, et al. The prevalence of clinically-relevant comorbid conditions in patients with physician-diagnosed COPD: a cross-sectional study using data from NHANES 1999–2008. BMC Pulm Med. 2012;12:26. doi:10.1186/1471-2466-12-26

    87. Sepúlveda-Loyola W, Osadnik C, Phu S, et al. Diagnosis, prevalence, and clinical impact of sarcopenia in COPD: a systematic review and meta-analysis. J Cach Sarcop Muscle. 2020;11(5):1164–1176. doi:10.1002/jcsm.12600

    88. Chen YW, Ramsook AH, Coxson HO, et al. Prevalence and risk factors for osteoporosis in individuals with COPD: a systematic review and meta-analysis. Chest. 2019;156(6):1092–1110. doi:10.1016/j.chest.2019.06.036

    89. Sözen T, Özışık L, Başaran NÇ. An overview and management of osteoporosis. Eur J Rheumatol. 2017;4(1):46–56. doi:10.5152/eurjrheum.2016.048

    90. Xiao YJ, Wang SP. Progress in the study of factors and mechanisms associated with skeletal muscle dysfunction in chronic obstructive pulmonary disease. J Clin Pulm Med. 2016;21(2):340–343.

    91. Song ZH, Song HP, Wang ZQ. Research progress on the effect of chronic obstructive pulmonary disease on bone strength. Chin J Osteoporos. 2022;28(4):613–618.

    92. Lehouck A, Boonen S, Decramer M, et al. COPD, bone metabolism, and osteoporosis. Chest. 2011;139(3):648–657. doi:10.1378/chest.10-1427

    93. Compston JE, McClung MR, Leslie WD. Osteoporosis. Lancet. 2019;393(10169):364–376. doi:10.1016/S0140-6736(18)32112-3

    94. Gorissen B, de Bruin A, Miranda-Bedate A, et al. Hypoxia negatively affects senescence in osteoclasts and delays osteoclastogenesis. J Cell Physiol. 2018;234(1):414–426. doi:10.1002/jcp.26511

    95. Liang B, Feng Y. The association of low bone mineral density with systemic inflammation in clinically stable COPD. Endocrine. 2012;42(1):190–195. doi:10.1007/s12020-011-9583-x

    96. Lu Y, Di YP, Chang M, et al. Cigarette smoke-associated inflammation impairs bone remodeling through NFκB activation. J Transl Med. 2021;19(1):163. doi:10.1186/s12967-021-02836-z

    97. Marinucci L, Balloni S, Fettucciari K, et al. Nicotine induces apoptosis in human osteoblasts via a novel mechanism driven by H2O2 and entailing Glyoxalase 1-dependent MG-H1 accumulation leading to TG2-mediated NF-kB desensitization: implication for smokers-related osteoporosis. Free Radic Biol Med. 2018;117:6–17. doi:10.1016/j.freeradbiomed.2018.01.017

    98. Kokturk N, Baha A, Oh YM, et al. Vitamin D deficiency: what does it mean for chronic obstructive pulmonary disease (COPD)? A compherensive review for pulmonologists. Clin Respir J. 2018;12(2):382–397. doi:10.1111/crj.12588

    99. Compston J. Glucocorticoid-induced osteoporosis: an update. Endocrine. 2018;61(1):7–16. doi:10.1007/s12020-018-1588-2

    100. Chotiyarnwong P, McCloskey EV. Pathogenesis of corticosteroids-induced osteoporosis and options for treatment. Nat Rev Endocrinol. 2020;16(8):437–447. doi:10.1038/s41574-020-0341-0

    101. Gonçalves PA, Dos Santos Neves R, Neto LV, et al. Inhaled glucocorticoids are associated with vertebral fractures in COPD patients. J Bone Mineral Metab. 2018;36(4):454–461. doi:10.1007/s00774-017-0854-3

    102. Chiu KL, Lee CC, Chen CY. Evaluating the association of osteoporosis with inhaled corticosteroid use in chronic obstructive pulmonary disease in Taiwan. Sci Rep. 2021;11(1):724. doi:10.1038/s41598-020-80815-y

    103. Allen CS, Yeung JH, Vandermeer B, et al. Bisphosphonates for steroid-induced osteoporosis. Cochrane Database Syst Rev. 2016;10(10):CD001347. doi:10.1002/14651858.CD001347.pub2

    104. Lewiecki EM. New and emerging concepts in the use of denosumab for the treatment of osteoporosis. Therapeutic Advan Musculosk Dis. 2018;10(11):209–223. doi:10.1177/1759720X18805759

    105. Saag KG, Wagman RB, Geusens P, et al. Denosumab versus risedronate in corticosteroids-induced osteoporosis: a multicentre, randomised, double-blind, active-controlled, double-dummy, non-inferiority study. Lancet Diabetes Endocrinol. 2018;6(6):445–454. doi:10.1016/S2213-8587(18)30075-5

    106. Ding L, Hu J, Wang D, et al. Efficacy and safety of first- and second-line drugs to prevent glucocorticoid-induced fractures. J Clin Endocrinol Metab. 2020;105(1):dgz023. doi:10.1210/clinem/dgz023

    107. Yuan C, Liang Y, Zhu K, et al. Clinical efficacy of denosumab, teriparatide, and oral bisphosphonates in the prevention of corticosteroids-induced osteoporosis: a systematic review and meta-analysis. J Orthopaedic Surg Res. 2023;18(1):447. doi:10.1186/s13018-023-03920-4

    108. Anagnostis P, Gkekas NK, Potoupnis M, et al. New therapeutic targets for osteoporosis. Maturitas. 2019;120:1–6. doi:10.1016/j.maturitas.2018.11.010

    109. Marcucci G, Domazetovic V, Nediani C, et al. Oxidative stress and natural antioxidants in osteoporosis: novel preventive and therapeutic approaches. Antioxidants. 2023;12(2):373. doi:10.3390/antiox12020373

    110. Zareifopoulos N, Bellou A, Spiropoulou A, et al. Prevalence, contribution to disease burden and management of comorbid depression and anxiety in chronic obstructive pulmonary disease: a narrative review. COPD. 2019;16(5–6):406–417. doi:10.1080/15412555.2019.1679102

    111. Huang J, Bian Y, Zhao Y, et al. The impact of depression and anxiety on chronic obstructive pulmonary disease acute exacerbations: a prospective cohort study. J Affective Disorders. 2021;281:147–152. doi:10.1016/j.jad.2020.12.030

    112. Liu YJ, Tian XL, Guo XH, et al. Prevalence of anxiety and depression in chronic obstructive pulmonary disease. Chin J Respir Crit Care Med. 2020;19(5):425–429.

    113. Montserrat-Capdevila J, Godoy P, Marsal JR, et al. Overview of the impact of depression and anxiety in chronic obstructive pulmonary disease. Lung. 2017;195(1):77–85. doi:10.1007/s00408-016-9966-0

    114. Riske L, Thomas RK, Baker GB, et al. Lactate in the brain: an update on its relevance to brain energy, neurons, glia and panic disorder. Therap Advan Psychopharmacol. 2017;7(2):85–89. doi:10.1177/2045125316675579

    115. Freire RC, Perna G, Nardi AE. Panic disorder respiratory subtype: psychopathology, laboratory challenge tests, and response to treatment. Harvard Rev Psych. 2010;18(4):220–229. doi:10.3109/10673229.2010.493744

    116. De Luca SN, Chan SMH, Dobric A, et al. Cigarette smoke-induced pulmonary impairment is associated with social recognition memory impairments and alterations in microglial profiles within the suprachiasmatic nucleus of the hypothalamus. Brain Behav Immun. 2023;109:292–307. doi:10.1016/j.bbi.2023.02.005

    117. Sundar IK, Yao H, Huang Y, et al. Serotonin and corticosterone rhythms in mice exposed to cigarette smoke and in patients with COPD: implication for COPD-associated neuropathogenesis. PLoS One. 2014;9(2):e87999. doi:10.1371/journal.pone.0087999

    118. Pelgrim CE, Peterson JD, Gosker HR, et al. Psychological co-morbidities in COPD: targeting systemic inflammation, a benefit for both? Eur J Pharmacol. 2019;842:99–110. doi:10.1016/j.ejphar.2018.10.001

    119. Zhang T, Wang G, Li Q, et al. Relationship between serum Th1/Th2 imbalance and depression in elderly patients with COPD and its clinical implications. Technol Health Care. 2023;31(6):2047–2058. doi:10.3233/THC-230665

    120. Foley ÉM, Parkinson JT, Mitchell RE, et al. Peripheral blood cellular immunophenotype in depression: a systematic review and meta-analysis. Mol Psychiatry. 2023;28(3):1004–1019. doi:10.1038/s41380-022-01919-7

    121. Recio Iglesias J, Díez-Manglano J, López García F, et al. Management of the COPD patient with comorbidities: an experts recommendation document. Int J Chronic Obstr. 2020;15:1015–1037. doi:10.2147/COPD.S242009

    122. Taylor SJC, Sohanpal R, Steed L, et al. Tailored psychological intervention for anxiety or depression in COPD (TANDEM): a randomised controlled trial. Eur Respir J. 2023;62(5):2300432. doi:10.1183/13993003.00432-2023

    123. Yohannes AM, Alexopoulos GS. Pharmacological treatment of depression in older patients with chronic obstructive pulmonary disease: impact on the course of the disease and health outcomes. Drugs Aging. 2014;31(7):483–492. doi:10.1007/s40266-014-0186-0

    124. Pollok J, van Agteren JE, Carson-Chahhoud KV. Pharmacological interventions for the treatment of depression in chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2018;12(12):CD012346. doi:10.1002/14651858.CD012346.pub2

    125. Kappelmann N, Lewis G, Dantzer R, et al. Antidepressant activity of anti-cytokine treatment: a systematic review and meta-analysis of clinical trials of chronic inflammatory conditions. Mol Psychiatry. 2018;23(2):335–343. doi:10.1038/mp.2016.167

    126. Huang C, Liu Y, Shi G. A systematic review with meta-analysis of gastroesophageal reflux disease and exacerbations of chronic obstructive pulmonary disease. BMC Pulm Med. 2020;20(1):2. doi:10.1186/s12890-019-1027-z

    127. Harding SM, Allen JE, Blumin JH, et al. Respiratory manifestations of gastroesophageal reflux disease. Ann N Y Acad Sci. 2013;1300:43–52. doi:10.1111/nyas.12231

    128. Lee AS, Lee JS, He Z, et al. Reflux-aspiration in chronic lung disease. Ann Am Thorac Soc. 2020;17(2):155–164. doi:10.1513/AnnalsATS.201906-427CME

    129. Broers C, Tack J, Pauwels A. Review article: gastro-oesophageal reflux disease in asthma and chronic obstructive pulmonary disease. Aliment Pharmacol Ther. 2018;47(2):176–191. doi:10.1111/apt.14416

    130. Lee AL, Goldstein RS. Gastroesophageal reflux disease in COPD: links and risks. Int J Chronic Obstr. 2015;10:1935–1949. doi:10.2147/COPD.S77562

    131. Zou M, Zhang W, Xu Y, et al. Relationship between COPD and GERD: a bibliometrics analysis. Int J Chronic Obstr. 2022;17:3045–3059. doi:10.2147/COPD.S391878

    132. Lee SW, Lien HC, Chang CS, et al. The impact of acid-suppressing drugs to the patients with chronic obstructive pulmonary disease: a nationwide, population-based, cohort study. J Res Med Sci. 2015;20(3):263–267. doi:10.4103/1735-1995.156174

    133. Kang J, Lee R, Lee SW. Effects of gastroesophageal reflux disease treatment with proton pump inhibitors on the risk of acute exacerbation and pneumonia in patients with COPD. Respir Res. 2023;24(1):75. doi:10.1186/s12931-023-02345-1

    134. Liu H. Assessment of anti-reflux treatment on pulmonary ventilation function and inflammatory cytokines in patients with stable chronic obstructive pulmonary disease combined with gastroesophageal reflux. Exp Ther Med. 2018;15(6):5528–5536. doi:10.3892/etm.2018.6077

    135. Kikuchi S, Imai H, Tani Y, et al. Proton pump inhibitors for chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2020;8(8):CD013113. doi:10.1002/14651858.CD013113.pub2

    136. Yu F, Huang Q, Ye Y, et al. Effectiveness of proton-pump inhibitors in chronic obstructive pulmonary disease: a meta-analysis of randomized controlled trials. Front Med Lausanne. 2022;9:841155. doi:10.3389/fmed.2022.841155

    137. Broad J, Sanger GJ. The antibiotic azithromycin is a motilin receptor agonist in human stomach: comparison with erythromycin. Br J Pharmacol. 2013;168(8):1859–1867. doi:10.1111/bph.12077

    138. Fabbri LM, Celli BR, Agustí A, et al. COPD and multimorbidity: recognising and addressing a syndemic occurrence. Lancet Respir Med. 2023;11(11):1020–1034. doi:10.1016/S2213-2600(23)00261-8

    139. Decramer M, Janssens W. Chronic obstructive pulmonary disease and comorbidities. Lancet Respir Med. 2013;1(1):73–83. doi:10.1016/S2213-2600(12)70060-7

    Source link

    Michelle Lyons, a 33-year-old social studies teacher, recalls the first time she noticed something was wrong. As she played with her 3-year-old daughter, she struggled to catch her breath. Since RSV and flu were going around, she thought it might be the beginning of a respiratory illness. By the evening, she felt better and went to sleep.

    But the breathless feeling continued, so Michelle sought care at the Emergency Department at Atrium Health Wake Forest Baptist Medical Center, where test results revealed she had a large blood clot, known as a pulmonary embolism, in her lung. In addition, she had two blood clots in her heart. Dr. Bart Imielski, cardiothoracic surgeon and professor of surgical sciences with Atrium Health Wake Forest Baptist, evaluated her in light of this potentially life-threatening condition.

    As her condition stabilized, Imielski recommended initial medical management and prescribed anticlotting medication to dissolve the clots. At that point, surgery would be a last resort. Performing a thrombectomy to remove some of the lung clot carried the risk of showering small emboli (portions of the blood clot) further into her lung. 

    After six months on the medication, Michelle still didn’t feel well. She couldn’t pick up her daughter without feeling out of breath, and a follow-up CT scan showed the blood clots were still in her lung and heart. Imielski diagnosed Michelle with chronic thromboembolism pulmonary hypertension, meaning the blood clot in her lung was stuck in her pulmonary artery.

    “As the embolism grows, it creates a lot of resistance to blood flow in the lungs,” explains Imielski. “It's a serious problem because it can eventually cause heart failure.”

    About 5% of patients with pulmonary embolisms will not reabsorb or dissolve them. While it's a relatively small patient population, it can be very debilitating, especially for young patients with busy schedules. Since Michelle’s quality of life continued to be affected, Imielski recommended surgery to remove the clots.

    Open-heart surgery

    Imielski’s team scheduled Michelle’s surgery during her summer break. Using open-heart surgery, he performed a pulmonary thromboembolectomy to remove the blood clots.

    “It's a complex procedure that requires periodically stopping the patient’s blood flow throughout the body,” Imielski explains. “We put the patient on cardiopulmonary bypass, which is a machine that takes over the patient’s breathing and blood circulation. This allows us to access the area where the pulmonary arteries are located and cut them open.”

    When Imielski entered Michelle’s chest and saw the lung clot, he noticed that it had grown into the wall of the pulmonary artery. He had to surgically remove the clot from the lung artery. While peeling it away, Imielski got to a point within the dependent portion of the pulmonary artery where the blood was pulling and there was still some clot remaining. The only way he could go deeper to finish removing the clot was by shutting off the bypass machine. This allows the team to work through the surgery without blood.

    Imielski’s surgical team cooled Michelle’s body to 18 degrees Celsius for about 15 minutes and then turned off the pump. Cooling the patient’s body allows the brain to survive brief periods without blood flow. Once the surgical team gets as far down into the pulmonary arteries as possible, they turn the bypass pump back on. After the remaining portions of the clot were removed, they warmed Michelle’s body back to normal.

    Once the clot in the lung was removed, Imielski removed the clots in Michelle’s heart.

    Unique surgical program

    According to Imielski, pulmonary thromboembolectomy is an established procedure. However, only about 12 centers in the U.S. perform the surgery.

    “Most medical programs don't train surgeons on this procedure,” notes Imielski. “Most surgeons in the U.S. who do this procedure were trained directly or indirectly through Dr. Michael Madani, cardiothoracic surgeon with the University of California San Diego. I was lucky enough that one of my mentors at Northwestern University trained with him, so I was able to learn his technique.”

    In addition, there are few programs established to evaluate patients with chronic thromboembolism pulmonary hypertension. Most primary care doctors are unfamiliar with the condition and its treatment.

    A chronic thromboembolism pulmonary hypertension program requires close collaboration between experts in CT surgery and pulmonary medicine. Additionally, the surgery can only be performed at experienced centers with advanced technologies, such as extracorporeal membrane oxygenation (ECMO), which are needed to manage rare but potentially known complications of the procedure. Wake Forest Baptist offers the collaboration and supportive technologies required to provide safe, effective cardiothoracic surgery.

    Confidence in care

    “I went to the right hospital at the right time,” says Michelle. “They knew what it was and came up with a plan of action immediately. I’m thankful this great hospital is located just five minutes from home and in the same city as my family.”

    Michelle also felt confident in Imielski’s ability to deliver a positive outcome.

    “He made me feel very comfortable with the procedure,” Michelle says. “He explained his background and training and helped me understand everything involved.”

    Michelle says the nurses, especially those in the ICU, were fantastic.

    “It’s a lot to process and go through,” Michelle says, “They were kind, understanding and supportive. They were willing to sit and listen to me express my feelings.”

    Results and recovery

    Following surgery, Michelle’s pulmonary artery pressure dropped by half and back into the normal range, leaving her feeling great from the moment she woke up. Her shortness of breath was gone. She just needed time to recover from open-heart surgery.

    Michelle spent about five days in the hospital, followed by continued rest at home. Imielski encouraged her to walk every day to foster healing. She was unable to do any heavy lifting or driving for the first month of her recovery. During the second month, she was allowed to slowly resume her normal activities.

    Back to normal and breathing easy

    Nine months after surgery, Michelle’s life has returned to normal. She’s able to walk around and teach in the classroom with ease. She can keep up with her young daughter without struggling to breathe.

    Michelle takes a low-dose blood thinner to maintain her health. Her care team is trying to figure out why she developed the blood clots. Her pregnancy in 2020, case of COVID-19 in 2021 and years of taking the birth control pill may have created the “perfect storm” for forming blood clots.

    Michelle is looking forward to supporting her family’s fundraiser for the American Lung Association’s Fight For Air Climb in the spring. This event promotes lung disease awareness and involves climbing stairs with friends and family in a fun, positive atmosphere.

    “When you do the stair climb, you support people with lung disease who are fighting for every breath,” says Michelle. “I know firsthand what it’s like to struggle to breathe, so I’m glad I feel well enough to support those still struggling.” 

    Learn more about cardiothoracic surgery at Wake Forest Baptist.

    Source link

    Do you know about pulmonary rehabilitation? Maybe you’ve participated in a few sessions or you have a loved one who did. I didn’t know about these programs until after I was diagnosed with pulmonary hypertension (PH). I also didn’t fully appreciate the hurdles that prevent some people from accessing this valuable care.

    Pulmonary rehab is a “supervised exercise program” meant to strengthen muscles and boost the quality of life for people with lung-related chronic illnesses and diseases, including many with PH. Participating in a 12-week program was one of several items on my post-diagnosis to-do list, after I was discharged from the hospital in March 2016. If I couldn’t return to my semi-regular running, this program sounded like the next best thing to springboard into some physical activity again.

    My initial excitement dissipated quickly. Little did I know that pulmonary rehabilitation programs were rare in their own way.

    Recommended Reading

    Banner image for

    A respiratory program coordinator reached out to begin the approval process required to get on a waiting list for an available spot. Were these prescribed exercise programs competitive? Was this wait like the stories I’d heard from friends who have to enter lotteries to get their kids into the best preschool or kindergarten? Apparently. In fact, after I was slow to respond to an email at one point during this process, the slot meant for me went to another patient.

    What gives with the rehab exclusivity?

    A month and a half later, on a hot day before Memorial Day weekend, I took the Washington, D.C. area Metro to a second Metro line to get to the bus that would drop me off across the street from a hospital in Maryland, all to reach my first session. I wasn’t sure what to expect going into this experience. I didn’t love the commute, and I certainly didn’t expect to be sweaty from exerting so much energy before arriving for an appointment to exercise to gain strength as part of managing life with a chronic and rare lung disease.

    My pulmonary rehabilitation program took place on the lower level of the hospital, in a room filled with various exercise machines and other workout paraphernalia. A quick scan of my surroundings confirmed that I was the youngest patient there by at least two decades, and back then I was in my early 30s. A respiratory nurse took my heart rate and oxygen saturation numbers before walking me through the stations of the exercise program.

    Each session included the use of two conditioning machines, free weights, and a treadmill for walking. My amount of time on the treadmill would increase as I built up muscle strength and endurance and moved through the program. I was expected to walk for 30 minutes by the 20th session!

    After a few weeks, I opened up and befriended some of the regular respiratory nurses who staffed the program. When I mentioned my commuting struggles, the nurses reinforced the limited number of spots in their program and the larger challenge to meet patient demand because of the few pulmonary rehab programs in the region.

    A large underserved population

    While I could commiserate with them at the time, in reality I was in a much better position, living in an urban area, than others in the U.S. who face barriers to this care.

    A recent PH News article, “Pulmonary rehab sites more than an hour away for US rural residents,” calls attention to a new study about the broader lack of access when it comes to these rehabilitation programs. The article states, “More than 14 million people — mostly living in rural and sparsely populated areas in the country’s western and midwestern regions — need to travel more than one hour to reach the nearest program.”

    Traveling for appointments can be a burden for those of us living with PH or other chronic illnesses, because of mobility issues, medical equipment, or symptoms such as fatigue or shortness of breath. If my commute had been even farther, I’m not sure I would’ve regularly attended my three-times-a-week sessions, despite how beneficial the exercises are to my health and lung condition.

    After my care team suggested I consider another regimen of pulmonary rehab this year, I was inspired to raise awareness about this barrier to care as part of the broader advocacy efforts for Rare Disease Day, on Feb. 29. Given how “transformative” pulmonary rehabilitation can be for people with PH and those across chronic illness and disease communities, access issues shouldn’t make it seem like such a rare luxury.

    Follow me on X (formerly Twitter): @mnaple.


    Note: Pulmonary Hypertension News is strictly a news and information website about the disease. It does not provide medical advice, diagnosis, or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. The opinions expressed in this column are not those of Pulmonary Hypertension News or its parent company, BioNews, and are intended to spark discussion about issues pertaining to pulmonary hypertension.



    Source link

    The hormone vasopressin may help improve oxygen levels and blood flow in newborns with acute pulmonary hypertension who fail to respond to treatment with inhaled nitric oxide, a study suggests.

    About two-thirds of newborns treated with vasopressin in the study, however, developed hyponatremia (a low level of sodium in the blood), suggesting the need for careful monitoring of sodium status during infusion of the hormone.

    The study, “Vasopressin in newborns with refractory acute pulmonary hypertension,” was published in the journal Pediatric Research.

    Recommended Reading

    An illustration showing two people looking with love at a newborn.

    Pressure in lungs normally drops to allow newborns to breathe

    When a baby is born and takes a first breath, the pressure in the lungs falls to adapt to breathing outside of the mother’s womb. This allows blood to travel to the lungs to get oxygen and deliver it to the rest of the body.

    In babies with acute pulmonary hypertension, or persistent pulmonary hypertension of the newborn (PPHN), the pressure in the lungs stays high. As a result, there is a limit on how much oxygen reaches the body’s organs, including the brain, heart, and kidneys.

    Treatment usually involves breathing support in combination with inhaled nitric oxide, a molecule that causes blood vessels to widen and blood pressure to drop. However, not all newborns respond in the same way to inhaled nitric oxide.

    Vasopressin regulates blood pressure by fine-tuning the balance of sodium and body fluids. Previous reports have suggested vasopressin may ease symptoms in newborns with difficult-to-treat acute pulmonary hypertension.

    Now, a team of researchers in Canada looked at the safety of add-on vasopressin and its effectiveness in newborns younger than 1 month who experienced acute pulmonary hypertension but failed to respond to inhaled nitric oxide.

    Recommended Reading

    Banner image for

    Study included 25 newborns who started on vasopressin days after birth

    The study included 25 newborns (14 girls, 11 boys) who were started on vasopressin at a median age of 2 days. Eleven were preterm babies, meaning they were born before 37 weeks of pregnancy. Pulmonary hypertension developed right after birth in 23 newborns, and after the first week of life in two.

    Vasopressin was started due to low levels of oxygen (32%), cardiovascular compromise (8%), or both (60%). Cardiovascular compromise occurs when the heart in unable to pump enough blood to the rest of the body.

    The hormone was infused continuously at a median dose of 0.3 micro-units per kilogram of body weight per minute via a central line, which usually goes all the way up to a vein near or just inside the heart. The infusion was given for a median of 72 hours (three days).

    After 12 hours of treatment with vasopressin, the median oxygenation index, a measure of how much breathing support is needed to maintain a healthy oxygen level, dropped from 28.4 to 14.4, indicating an improvement. After 24 hours, it had further dropped to 12.5.

    The fraction of inspired oxygen, which refers to the concentration of oxygen in the gas mixture supplied by a ventilator, decreased from 0.91 to 0.5 after 12 and 24 hours post-treatment with vasopressin.

    “One of the key observations in our study was the improvement in oxygenation indices after twelve and twenty-hours of vasopressin infusion,” the researchers wrote, noting the observation is in line with previous reports.

    At the same time, the mean blood pressure increased from 41 millimeters of mercury before to 51 post-treatment at 12 and 24 hours, indicating an improvement of blood flow.

    Before treatment, the median level of sodium in the blood was 135 millimoles per liter (mmol/L). During treatment with vasopressin, however, 17 (68%) newborns experienced an episode of hyponatremia, as sodium reached a level lower than 130 mmol/L.

    Recommended Reading

    An illustration showing two people looking with love at a newborn.

    Call for monitoring of sodium levels for newborns receiving vasopressin

    While hyponatremia did not appear to result in any damage to the liver or kidneys, “careful monitoring of serum sodium levels are warranted in newborns who are receiving vasopressin infusion,” the researchers wrote.

    None of the newborns required extracorporeal membrane oxygenation, a type of support wherein part of the patient’s blood is diverted through an artificial lung for gas exchange (oxygenation and removal of carbon dioxide ) and then returning it to the patient. Nine newborns (36%) died, including six due to their initial diagnosis and three following a decision to redirect care.

    “The use of vasopressin may be associated with improvement in oxygenation and hemodynamic [blood flow] status of neonatal patients” with acute pulmonary hypertension that failed to respond to initial therapy, the researchers concluded.

    “However, larger, prospective studies [conducted over time] are needed to validate these findings and establish optimal treatment protocols for [acute pulmonary hypertension] in neonates,” they wrote.

    Source link

    Breathing Easier: New Research Supports Preterm Birth Survivors: Chronic lung disease is an unfortunate yet common ailment for people born preterm, however Curtin University research is working towards a better outcome for this group, regardless of their age.

    The project, known as FINGERPRINT, has been awarded nearly $2 million over five years from the Medical Research Future Fund.

    The research team will use sophisticated machine learning approaches to better understand the different types of lung disease affecting more than half of people born preterm, to create more effective treatments and better predict those at risk of developing such lung conditions.

    Preterm lung disease has features of asthma and chronic obstructive pulmonary disease (COPD) and is often managed with similar treatments, as there is no evidence-based guidance on how to treat preterm respiratory disease specifically.

    The FINGERPRINT project aims to address this by distinguishing the different types of preterm lung disease to develop phenotypes — or ‘fingerprints’ ؙ— which are individual identifiers which will allow researchers to develop targeted, personalised treatments for the person living with the disease.

    Study lead Associate Professor Shannon Simpson, from Curtin School of Allied Health and Telethon Kids Institute, said this individualised approach was vital in identifying appropriate and tailored treatment options for a vulnerable group of people.

    “People born preterm can have a range of lung symptoms throughout their lives,” she said.

    “For example, they are five times more likely to be diagnosed with asthma, are over-represented in adults with COPD or pulmonary hypertension and we have even recently seen the first case reports of lung transplant in young adults who were born pre-term.

    “We believe phenotype traits of lung disease will be “expressed” to varying degrees between individuals born significantly preterm, which can be targeted to develop personalised treatments.”

    Another key aspect of the study is helping to predict which babies born preterm will develop lung disease later in life.

    Most research on predicting those at risk of long-term respiratory outcomes after preterm birth has, to date, focused on bronchopulmonary dysplasia (BPD), which is determined by the degree of respiratory support a baby requires while they are in a neonatal intensive care unit.

    However, Associate Professor Simpson said many other factors other than BPD in babies are likely to predict a person’s risk of respiratory health issues developing later in life.

    “Many people born preterm who never developed BPD are now recognised to be at risk of future lung disease,” she said.

    “Various studies have shown survivors of preterm birth often have multiple disease phenotypes unique to them occurring simultaneously and changing over time, with some likely interacting with one another — which all hampers the ability to describe an individual’s disease by a single phenotype.

    “FINGERPRINT will help provide the first step towards developing treatable trait-based precision medicine approaches to what is an emerging health crisis with serious consequences.”

    The study is a collaboration between Curtin and Wal-yan Respiratory Research Centre — a partnership between Telethon Kids Institute, Perth Children’s Hospital and Perth Children’s Hospital Foundation — with contributions from the University of Melbourne, The University of Western Australia, Erasmus University Medical Center and Edith Cowan University.

    Hippocratic Post
    Latest posts by Hippocratic Post (see all)

    Source link

    Vittorio Cecchi Gori is hospitalized in intensive care at the Gemelli Polyclinic in Rome due to respiratory failure. What is that? What is it due to? It is “a pathological condition caused by the inability of the respiratory system to guarantee adequate exchanges of oxygen between the environment and the blood”, with consequent “inability to obtain adequate blood values ​​of oxygen and carbon dioxide”.

    Respiratory failure, what it is and causes

    Respiratory failure “can be acute, when its onset is rapid and sudden, or chronic, when it occurs progressively to stabilize or evolve over time”. There are different causes at the origin, explains Laura Mancino, pulmonologist at the Angelo hospital in Mestre (Venice), in an in-depth analysis on the 'Let's take breath' portal, dedicated to breathing diseases.

    “The most frequent causes of acute respiratory failure are acute pulmonary edema, massive pulmonary embolism, tension pneumothorax, asthmatic crisis, pneumonia causing acute respiratory distress syndrome such as Covid-19 related pneumonia”, i.e. associated with Sars-CoV-2 infection. Precisely due to pulmonary complications from Covid, Cecchi Gori had already been hospitalized at the beginning of 2022. The cause of acute respiratory failure can then be “traumas, intoxications from drugs or toxins”, lists the specialist. “The most common causes of chronic respiratory failure are” instead “chronic lung diseases such as chronic obstructive pulmonary disease (COPD) or interstitial lung diseases (pulmonary fibrosis), neurological diseases such as amyotrophic lateral sclerosis (ALS), obesity syndrome -hypoventilation (or Pickwick syndrome), cystic fibrosis, pulmonary hypertension, congenital or chronic worsening heart diseases”.

    Symptoms

    What are the symptoms? “Common manifestations of respiratory insufficiency are dyspnea, or shortness of breath – describes the pulmonologist – the reduction in oxygen saturation”, which is why Cecchi Gori arrived at Gemelli before having a respiratory crisis that left him led to hospitalization, or even “the use of the accessory muscles of ventilation, but also drowsiness to the point of coma”.

    “Respiratory insufficiency can therefore” determine alterations in the values ​​of oxygen in the blood, but also of carbon dioxide. In the sense of a decrease or, what is much more serious, an increase. This distinction – specifies Mancino – is necessary to keep in mind” when it comes to deciding on treatment.

    “When the partial pressure of oxygen in the blood falls below 55 mmHg – explains the expert – then it is necessary to treat respiratory failure”. We begin with the administration of oxygen through simple nasal cannulas, if the oxygen requirement is low, then moving on to special masks, up to high flow oxygen therapy through nasocannulae if the oxygen requirement is very high. “These measures are useful in correcting respiratory failure defined as hypoxemic and normocapnic, i.e. with normal carbon dioxide values”.

    However, “some pathologies (the most common is COPD) are characterized not only by low oxygen values ​​but also by high carbon dioxide values” or hypercarbia. The accumulation of carbon dioxide in the blood “initially manifests itself with hyper-reactivity and agitation, and then leads to a reduction in the state of consciousness (the patient appears drowsy), up to coma”. In this case the administration of oxygen is not enough, the pulmonologist points out, in fact it must be controlled because “the excess would lead to a further increase in carbon dioxide. It will therefore be necessary to reduce the carbon dioxide values ​​using non-invasive ventilation devices (patient in sub-intensive or home therapy) and in the most serious cases invasive (patient intubated in intensive care or tracheotomised)”.

    Read also

    Source link

    Chronic lung disease is an unfortunate yet common ailment for people born preterm, however Curtin University research is working towards a better outcome for this group, regardless of their age.

    The project, known as FINGERPRINT, has been awarded nearly $2 million over five years from the Medical Research Future Fund.

    The research team will use sophisticated machine learning approaches to better understand the different types of lung disease affecting more than half of people born preterm, to create more effective treatments and better predict those at risk of developing such lung conditions.

    Preterm lung disease has features of asthma and chronic obstructive pulmonary disease (COPD) and is often managed with similar treatments, as there is no evidence-based guidance on how to treat preterm respiratory disease specifically.

    The FINGERPRINT project aims to address this by distinguishing the different types of preterm lung disease to develop phenotypes - or 'fingerprints' ؙ- which are individual identifiers which will allow researchers to develop targeted, personalised treatments for the person living with the disease.

    Study lead Associate Professor Shannon Simpson, from Curtin School of Allied Health and Telethon Kids Institute, said this individualised approach was vital in identifying appropriate and tailored treatment options for a vulnerable group of people.

    "People born preterm can have a range of lung symptoms throughout their lives," she said.

    "For example, they are five times more likely to be diagnosed with asthma, are over-represented in adults with COPD or pulmonary hypertension and we have even recently seen the first case reports of lung transplant in young adults who were born pre-term.

    "We believe phenotype traits of lung disease will be "expressed" to varying degrees between individuals born significantly preterm, which can be targeted to develop personalised treatments."

    Another key aspect of the study is helping to predict which babies born preterm will develop lung disease later in life.

    Most research on predicting those at risk of long-term respiratory outcomes after preterm birth has, to date, focused on bronchopulmonary dysplasia (BPD), which is determined by the degree of respiratory support a baby requires while they are in a neonatal intensive care unit.

    However, Associate Professor Simpson said many other factors other than BPD in babies are likely to predict a person's risk of respiratory health issues developing later in life.

    "Many people born preterm who never developed BPD are now recognised to be at risk of future lung disease," she said.

    "Various studies have shown survivors of preterm birth often have multiple disease phenotypes unique to them occurring simultaneously and changing over time, with some likely interacting with one another - which all hampers the ability to describe an individual's disease by a single phenotype.

    "FINGERPRINT will help provide the first step towards developing treatable trait-based precision medicine approaches to what is an emerging health crisis with serious consequences."

    The study is a collaboration between Curtin and Wal-yan Respiratory Research Centre - a partnership between Telethon Kids Institute, Perth Children's Hospital and Perth Children's Hospital Foundation - with contributions from the University of Melbourne, The University of Western Australia, Erasmus University Medical Center and Edith Cowan University.

    /Public Release. This material from the originating organization/author(s) might be of the point-in-time nature, and edited for clarity, style and length. Mirage.News does not take institutional positions or sides, and all views, positions, and conclusions expressed herein are solely those of the author(s).View in full here.

    Source link

    Access to pulmonary rehabilitation programs for people with pulmonary hypertension (PH) and other chronic respiratory conditions is considerably more difficult for those living in rural U.S. regions than in urban areas, scientists report.

    Travel longer than 60 minutes affects more than 14 million U.S. residents of rural or underpopulated areas, they found. By racial or ethnic group, distance to a rehab center was a particular barrier for American Indians and Alaskan native peoples.

    “The disparities highlighted in our study underscore the need for innovative solutions to improve access to PR [pulmonary rehabilitation] services for those in underserved areas,” the scientists wrote in their research letter, “Accessibility of Pulmonary Rehabilitation in the US,” published in JAMA Network Open.

    Recommended Reading

    A graphic of the words

    Pulmonary rehabilitation is a key component of PH care

    PH is a chronic and progressive disease associated with high blood pressure in the pulmonary arteries, the blood vessels that supply the lungs. Increased blood pressure in the lungs means that the heart’s right side must work harder to pump blood through the arteries, which may cause heart failure later in life.

    Pulmonary rehabilitation is an essential component of care for people with PH and other chronic respiratory conditions. It is a comprehensive, multidisciplinary program designed to improve their quality of life and overall health. It is known to improve patients’ exercise capacity and to ease shortness of breath (dyspnea), a common PH symptom.

    Such programs typically feature a structured exercise component, monitored by nurses or exercise specialists, and educational sessions to help patients better understand and manage their condition.

    “It has been demonstrated across almost the entirety of pulmonary medicine to improve patient health and patient-reported outcomes,” Peter Kahn, MD, a  pulmonary and critical care fellow at the Yale School of Medicine and one of the report’s two scientists, said in a Yale news release.

    Despite these reported benefits, access to pulmonary rehabilitation services “remains a relevant issue,” particularly for people living in rural areas, they noted.

    Using geographic data sets, U.S. census data, a survey, and computational tools, the scientists evaluated patients’ access to this type of care by measuring travel time to rehabilitation sites.

    “By focusing on travel times instead of geodesic distance, our findings offer a more realistic depiction of the challenges faced by many individuals, particularly those in rural and sparsely populated regions and minoritized racial and ethnic groups,” the investigators wrote. (Geodesic distance is defined as the shortest distance between two points on a curved surface, like that of the Earth.)

    By race or ethnicity, American Indians and Alaskan native groups lack access

    A total of 1,759 sites were identified, with most (84.9%) located in urban areas. Dense urban areas and large cities had shorter travel times, with almost half (47.8%) of Americans living within a 15-minute drive of a rehabilitation center, and another 32.5% within a 30-minute drive.

    However, more than 14 million people — mostly living in rural and sparsely populated areas in the country’s western and midwestern regions — need to travel more than one hour to reach the nearest program. By racial and ethnic grouping, a similar 60-minute or greater travel distance also affected nearly 30% of American Indian and Alaska Native populations.

    Khan noted that traveling long distances can lead patients to abandon treatment, due to existing limitations with walking and other physical activities, as well as the burden of carrying multiple oxygen tanks or battery supplies.

    “While innovative solutions such as virtual PR can help bridge these gaps in the short term, long-term solutions will require collaboration between policy makers and those providing health care to those in underresourced areas,” the scientists wrote.

    Better health insurance coverage for rehabilitation programs also is needed, Kahn added in the news release. Specifically, he mentioned that insurance generally limits the number of rehabilitation sessions a patient can attend, and payments given to the programs themselves fail to cover costs, effectively limiting their number.

    “Insurance payers, both government and private, do not sufficiently reimburse pulmonary rehabilitation programs for the people, equipment, and supplies needed to effectively run them,” Kahn said.

    Source link

    Travel times limit access to pulmonary rehabilitation programs to help people with chronic lung conditions, such as chronic obstructive pulmonary disease (COPD), a U.S. report revealed.

    Data showed about 80% of people live within a 30-minute drive of a rehabilitation site, mostly those who reside within major urban and suburban areas. In contrast, over 14 million people, particularly in the country’s western and midwestern regions, must travel more than an hour to reach a rehabilitation center.

    “The disparities highlighted in our study underscore the need for innovative solutions to improve access to [pulmonary rehabilitation] services for those in underserved areas,” the researchers wrote.

    The research letter, “Accessibility of Pulmonary Rehabilitation in the US,” was published in the journal JAMA Network Open.

    Recommended Reading

    Main banner for Caroline Gainer's column,

    Pulmonary rehabilitation linked to better outcomes for COPD patients

    COPD is a chronic inflammatory disease of the lungs, marked by airway blockages, wheezing, cough with mucus, and shortness of breath. Various disease treatments have been approved to help patients’ manage, working to ease COPD symptoms.

    Pulmonary rehabilitation is a non-drug therapeutic approach for COPD and other conditions, such as interstitial lung diseases (lung scarring) and pulmonary hypertension. It combines supervised exercise and educational sessions designed to manage the illness better, aiming to improve patients’ overall health and quality of life.

    Such techniques can help with conserving energy, supplemental oxygen therapy, and taking advantage of periods of higher energy.

    “It has been demonstrated across almost the entirety of pulmonary medicine to improve patient health and patient-reported outcomes,” Peter Kahn, MD, a pulmonary and critical care fellow at Yale School of Medicine, in Connecticut, and one of two study authors, said in a university news release. “Through these programs, patients not only gain a more comprehensive understanding of their condition, but also improve their exercise tolerance in a meaningful way.”

    Despite its demonstrated efficacy, access to pulmonary rehabilitation programs across the U.S. remains a problem, the researchers noted.

    The team used large-scale geographic datasets to measure the time it takes to travel to locations that provide pulmonary rehabilitation.

    “Technologies enabling travel time computations at a massive scale are not just innovative but transformative, providing us with nuanced insights,” said Walter Mathis, MD, a psychiatrist and health services researcher at Yale School of Medicine, and the study’s other author.

    Rehabilitation site locations were obtained from the livebetter.org website, data on population and ethnicity came from the American Community Survey 2021, and urbanicity data from the U.S. Census Urban Areas. Minimum travel times were calculated from every census block to the 25 closest sites, with analysis limited to the contiguous 48 states and Washington, D.C.

    For 14 million people, nearest rehab center is over an hour away

    Of the 1,759 pulmonary rehabilitation sites identified, 1,494 (84.9%) were located in urban areas. The shortest travel times to these sites were in densely populated urban areas and major cities, with about half (47.8%) of individuals living within a 15-minute drive. An additional 32.5% live within a 30-minute drive, which includes those in suburban areas.

    Access, however, was limited for people in rural and sparsely populated regions, particularly in the West and Midwest. Travel times often exceeded 30 minutes, with many residents — representing more than 14 million people — needing over an hour to drive to the nearest program location.

    When assessed by race or ethnicity, 26.9% of American Indian and Alaska Native populations lived within a 15-minute drive to a pulmonary rehabilitation program, while 29.7% lived more than an hour away. These disparities differed markedly from other groups, which included Asian, Black, Hispanic, and white populations.

    “Access to programs within a reasonable amount of travel time is key,” Kahn said. “First, many patients with chronic respiratory conditions require oxygen supplementation. Long commutes may mean they have to transport multiple oxygen tanks or battery supplies, which may cause patients to forgo the treatment. Second, because exertional intolerance is a symptom of these diseases, long travel can be incredibly taxing and also serve as a barrier to participation.”

    Researchers suggested that telemedicine and virtual rehabilitation can help bridge these gaps in the short term, but “long-term solutions will require collaboration between policy makers and those providing health care to those in underresourced areas,” they wrote.

    “Insurance payers, both government and private, do not sufficiently reimburse pulmonary rehabilitation programs for the people, equipment, and supplies needed to effectively run them,” Kahn said. “That represents a barrier to offering these programs. Of equal importance, insurance limits how many rehabilitation sessions a patient can attend.”

    He added: “If you’re someone with a chronic respiratory condition like advanced COPD, you really need ongoing therapeutic sessions. But right now, payers limit patients to a small number of lifetime sessions relative to the long-term burden of the disease. And that needs to change.”

    Source link

    By Ernie Mundell HealthDay Reporter

    HealthDay

    WEDNESDAY, Feb. 7, 2024 (HealthDay News) -- Pulmonary rehabilitation can be a lifeline for millions of Americans coping with COPD or other chronic lung ailments.

    However, new research finds that travel time and cost issues put pulmonary rehab programs out of reach for many patients.

    “Access to programs within a reasonable amount of travel time is key,” stressed study lead author Dr. Peter Kahn, a pulmonary and critical care fellow at the Yale School of Medicine.

    “First, many patients with chronic respiratory conditions require oxygen supplementation," he explained in a Yale news release. "Long commutes may mean they have to transport multiple oxygen tanks or battery supplies, which may cause patients to forgo the treatment. Second, because exertional [exercise] intolerance is a symptom of these diseases, long travel can be incredibly taxing and also serve as a barrier to participation.”

    As the researchers explained, pulmonary rehab programs are often utilized by people with chronic obstructive pulmonary disease (COPD), interstitial lung disease or pulmonary hypertension. 

    These programs have patients meet with skilled health care workers to foster techniques that will make day-to-day life with a respiratory disorder easier. For example, they'll learn strategies to better harness their daily energy or maximize supplemental oxygen therapy.

    All of this "has been demonstrated across almost the entirety of pulmonary medicine to improve patient health and patient-reported outcomes,” Kahn said. "Through these programs, patients not only gain a more comprehensive understanding of their condition, but also improve their exercise tolerance in a meaningful way.” 

    But just how accessible are such programs for patients across the United States?

    In the study, Kahn's group "used massive geographic data sets and computational infrastructure to compute hundreds of millions of travel times" to and from rehab programs.

    The team found that 80% of Americans do live within a half-hour's drive of a facility offering pulmonary rehab.

    But that still leaves 14 million people -- mostly concentrated in the West and Midwest -- who must drive more than an hour to reach a rehab program.

    Kahn's team believes telehealth might be able to help some of these patients, although long-term studies are needed to confirm that.

    Cost can be an impediment to access, too.

    “Insurance payers, both government and private, do not sufficiently reimburse pulmonary rehabilitation programs for the people, equipment and supplies needed to effectively run them,” Kahn said.

    Too often, insurance companies also limit the number of rehab sessions they'll cover for patients, he added.

    “If you’re someone with a chronic respiratory condition like advanced COPD, you really need ongoing therapeutic sessions,” Kahn said. “But right now, payers limit patients to a small number of lifetime sessions relative to the long-term burden of the disease. And that needs to change.”

    SOURCE: Yale University, news release, Feb. 5, 202

    Copyright © 2024 HealthDay. All rights reserved.

    Source link

    Early in 2022, Tamara Coleman started to experience episodes of shortness of breath—she’d never had asthma, but now she’d be in the middle of a conversation and find herself struggling to breathe. Gradually, she noticed other confusing symptoms, including weight gain to the point where her clothes no longer fit and pain that limited her ability to clean her house.

    She had always been healthy and active. At almost 50 years old, she had owned a home daycare, worked with toddlers in a Head Start program, and taken classes in early childhood education. As her own six children started to grow up and leave home, her plan was to work as long as she could and then spend her retirement enjoying her grandchildren.

    Those plans came to a halt in 2018, after surgery for a back injury from a bad fall. That forced her to retire early and confine her work to physically easier temporary positions. But the shortness of breath and other new symptoms were a new problem. In April 2022, with her feet so swollen she could barely put on her shoes, her family took her to the Yale New Haven Hospital emergency department.

    Coleman spent 10 days in the hospital, where she received a surprising diagnosis: chronic thromboembolic pulmonary hypertension (CTEPH), a rare, progressive, potentially fatal condition. It develops when blood clots in the lungs (called pulmonary embolisms) block blood vessels in the heart for an extended period of time.

    “CTEPH is a condition associated with high mortality,” explains Prashanth Vallabhajosyula, MD, MS, a Yale Medicine cardiac surgeon and surgical director of the Yale Aortic Institute, part of the Yale New Haven Health Heart & Vascular Center. “We can give medications to help clear out the clots, but, at times, there is some remnant clot that stays in the arteries in the lungs.” The gold-standard treatment, he says, is a complex open-heart surgery called a pulmonary thromboendarterectomy that only a few surgeons can perform.

    Dr. Vallabhajosyula and his Yale colleagues follow hundreds of patients with the condition, whether they have undergone the surgery or take medication (a comorbidity, or other condition, may make surgery too risky). Some patients have traveled to Yale from other parts of the country to have their CTEPH treated; Coleman lives 12 minutes away.

    How many people have CTEPH? How successful is the surgery—and are there other alternatives? Tamara Coleman, Dr. Vallabhajosyula, and Yale Medicine pulmonary vascular disease specialist Phillip Joseph, MD, talked to us about CTEPH.

    Source link