By Eve Glazier, M.D., and Elizabeth Ko, M.D.

Andrews McMeel Syndication

Dear Doctors: I work in a big shop where we make custom furniture. My wife thinks it puts me at risk of COPD and insists I should use a mask. Is she right? I thought COPD was something that happens to smokers. Plus, wearing a mask isn’t very comfortable.

Dear Reader: COPD is short for chronic obstructive pulmonary disease. It’s an umbrella term for a group of diseases in which damage to the tissues of the lungs, along with inflammation, obstruct the airways and make breathing difficult.

Symptoms include shortness of breath, a persistent cough, difficulty taking a deep breath, wheezing, excess mucus and a feeling of tightness in the lungs and chest. Because the airways of someone with COPD are obstructed, they can’t get enough oxygen. This causes an oxygen deficit in tissues throughout the body, which results in weakness, fatigue and a loss of stamina.

The two most common conditions associated with COPD are chronic bronchitis and emphysema. In chronic bronchitis, the lining of the bronchial tubes, which carry air to and from the tiny air sacs of the lungs, become inflamed. This causes excess mucus production and a chronic cough. It also puts the person at increased risk of having repeated respiratory infections. In emphysema, those tiny air sacs, known as alveoli, become permanently damaged. This leads to the oxygen deficit and resulting fatigue and breathing difficulties that we discussed earlier.

Smoking is a primary cause of COPD; The condition develops in response to repeated and long-term exposure to irritating gases and fine particulates, both of which smoking delivers in abundance. however, COPD can be an industrial hazard as well. People who work in occupations as varied as construction, mining, agriculture, welding, brick laying, stonemasonry, textiles, painting, and hair and nail care can all be at risk. When workers in these professions are also smokers, their chance of developing COPD goes up.

Occupational health data show that your own work in a carpentry shop, which exposes you to an environment that is not kind to the lungs, does put you at risk of developing COPD. The act of cutting, carving and sanding wood creates fine, airborne particulates that can damage the lungs and impair their ability to function. So can the fumes and gases emitted by the paints, stains, shellacs and solvents typically used in making furniture.

Even in a well-ventilated shop, particulates and gases will remain in the air. Long-term exposure to these can irritate, inflame and even damage delicate lung tissues, which can eventually lead to COPD.

COPD is a progressive disease. That means it gets worse with the passage of time. Although there is no known cure, it can be managed with medications and changes to behavior. Fortunately, you can significantly lower your own risk of developing this condition with one easy step: Always wear a high-quality, well-fitted mask while at work. It may be a bit uncomfortable, but to protect your lungs, it’s a small price to pay.

Send your questions to [email protected].

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Dear Doctors: I work in a big shop where we make custom furniture. My wife thinks it puts me at risk of COPD and insists I should use a mask. Is she right? I thought COPD was something that happens to smokers. Plus, wearing a mask isn't very comfortable.

Dear Reader: COPD is short for chronic obstructive pulmonary disease. It's an umbrella term for a group of diseases in which damage to the tissues of the lungs, along with inflammation, obstruct the airways and make it difficult to breathe.

Symptoms include shortness of breath, a persistent cough, difficulty taking a deep breath, wheezing, excess mucus and a feeling of tightness in the lungs and chest. Because the airways of someone with COPD are obstructed, they can't get enough oxygen. This causes an oxygen deficit in tissues throughout the body, which results in weakness, fatigue and a loss of stamina.

The two most common conditions associated with COPD are chronic bronchitis and emphysema. In chronic bronchitis, the lining of the bronchial tubes, which carry air to and from the tiny air sacs of the lungs, become inflamed. This causes excess mucus production and a chronic cough. It also puts the person at increased risk of having repeated respiratory infections. In emphysema, those tiny air sacs, known as alveoli, become permanently damaged. This leads to the oxygen deficit and resulting fatigue and breathing difficulties that we discussed earlier.

You're correct that smoking is a primary cause of COPD. The condition develops in response to repeated and long-term exposure to irritating gases and fine particulates, both of which smoking delivers in abundance. However, COPD can be an industrial hazard as well. People who work in occupations as varied as construction, mining, agriculture, welding, brick laying, stonemasonry, textiles, painting, and hair and nail care can all be at risk. When workers in these professions are also smokers, their chance of developing COPD goes up.

Occupational health data show that your own work in a carpentry shop, which exposes you to an environment that is not kind to the lungs, does put you at risk of developing COPD. The act of cutting, carving and sanding wood creates fine, airborne particulates that can damage the lungs and impair their ability to function. So can the fumes and gases emitted by the paints, stains, shellacs and solvents typically used in making furniture.

Even in a well-ventilated shop, particulates and gases will remain in the air. Long-term exposure to these can irritate, inflame and even damage delicate lung tissues, which can eventually lead to COPD.

COPD is a progressive disease. That means it gets worse with the passage of time. Although there is no known cure, it can be managed with medications and changes to behavior. Fortunately, you can significantly lower your own risk of developing this condition with one easy step: Always wear a high-quality, well-fitted mask while at work. It may be a bit uncomfortable, but to protect your lungs, it's a small price to pay.

(Send your questions to [email protected], or write: Ask the Doctors, c/o UCLA Health Sciences Media Relations, 10960 Wilshire Blvd., Suite 1955, Los Angeles, CA, 90024. Owing to the volume of mail, personal replies cannot be provided.)

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How We Can Help

Samaritan’s Pulmonary Rehabilitation programs are designed to help people who have been diagnosed with asthma, COPD (chronic bronchitis, emphysema), bronchiectasis, fibrotic or interstitial diseases of the lung. Our staff of pulmonary rehab experts work together to develop specialized programs for you that combine exercise and education. Patients can attend up to 36 one-hour sessions per year, depending on their needs.

Education is a critical component to the Pulmonary Rehabilitation program. Patients will learn about:

  • Managing your symptoms and decreasing your problems with breathing.
  • Improving your physical condition and other factors impacting lung health.
  • Nutrition and weight loss.
  • Different lung diseases and the anatomy and physiology of the lungs.

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The global landscape of respiratory health is undergoing a significant transformation, with the Asthma and COPD Drugs Market emerging as a crucial player in combating chronic pulmonary conditions. Valued at $32,988.7 million in 2020, this market is projected to soar to $52,049.54 million by 2030, marking a notable CAGR of 4.64% from 2021 to 2030.

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Asthma, a chronic inflammatory lung disorder, and Chronic Obstructive Pulmonary Disease (COPD), characterized by irreversible airflow limitation, collectively pose a substantial burden on global health. Asthma, often triggered by allergies and environmental factors, manifests as recurrent wheezing, breathlessness, and chest tightness. COPD, primarily linked to tobacco smoking and occupational hazards, presents as a complex interplay of emphysema and chronic bronchitis.

Diagnosis of these conditions relies on a combination of physical examination and specialized tests such as X-rays and sputum analysis. Treatment modalities encompass a range of medications including inhaled corticosteroids, bronchodilators, and combination therapies tailored to manage acute exacerbations and provide long-term symptom control.

The burgeoning prevalence of asthma and COPD, as evidenced by WHO estimates indicating 262 million asthma cases and 46,1000 associated deaths in 2019, propels the growth of this market. Similarly, data from the American Lung Association highlighting 99 million adults with chronic bronchitis and 2 million with emphysema in the US alone in 2018 underscore the pressing need for effective therapeutic interventions.

Significant strides in respiratory disease management and the introduction of innovative pharmaceuticals further buoy market expansion. For instance, AstraZeneca's recent EU approval for 'Trixeo Aerosphere' for COPD maintenance treatment exemplifies the industry's commitment to addressing unmet clinical needs.

However, the market's trajectory is not without challenges. The exorbitant costs associated with asthma treatment serve as a barrier to access, inhibiting market growth during the forecast period.

Segmentation of the Asthma and COPD Drugs Market based on disease, medication class, and region offers valuable insights into market dynamics. While the asthma segment currently dominates due to rising patient numbers, the COPD segment is poised for robust growth fueled by therapeutic advancements.

Among medication classes, combination drugs lead the pack owing to their efficacy and convenience, although inhaled corticosteroids are expected to witness substantial growth driven by therapeutic innovations.

Geographically, North America commands the lion's share of the market, attributed to the high prevalence of asthma, established manufacturing infrastructure, and pervasive tobacco smoking habits. Nonetheless, Asia-Pacific emerges as a hotspot for market expansion, driven by burgeoning healthcare infrastructure and a burgeoning population.

Stakeholders stand to gain manifold from a comprehensive analysis of the Asthma and COPD Drugs Market, leveraging insights to identify investment opportunities and navigate strategic business decisions. Additionally, a thorough examination of key players and their growth strategies illuminates the competitive landscape, aiding stakeholders in charting their course amidst evolving market dynamics.

The Asthma and COPD Drugs Market presents a promising avenue for stakeholders amidst a backdrop of escalating respiratory health challenges. With innovative therapies, expanding markets, and strategic insights, stakeholders are poised to drive meaningful impact in the global fight against asthma and COPD.

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David Correa

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Allied Market Research (AMR) is a full-service market research and business-consulting wing of Allied Analytics LLP based in Portland, Oregon. Allied Market Research provides global enterprises as well as medium and small businesses with unmatched quality of "Market Research Reports" and "Business Intelligence Solutions." AMR has a targeted view to provide business insights and consulting to assist its clients to make strategic business decisions and achieve sustainable growth in their respective market domain.

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Consumer Medicine Information (CMI) summary

The full CMI on the next page has more details. If you are worried about using this medicine,
speak to your doctor or pharmacist.

1. Why am I using Symbicort Rapihaler?

Symbicort Rapihaler contains two active ingredients in one inhaler: budesonide and
formoterol (eformoterol) fumarate dihydrate. Symbicort Rapihaler is used for treatment
of asthma in adults and adolescents (12 years and over) or Chronic Obstructive Pulmonary
Disease (COPD) in adults (18 years and over).

2. What should I know before I use Symbicort Rapihaler?

Do not use if you have ever had an allergic reaction to any medicine containing budesonide
or formoterol, or any of the ingredients listed at the end of the CMI.
Talk to your doctor if you have any other medical conditions, take any other medicines,
or are pregnant or plan to become pregnant or are breastfeeding.


For more information, see Section 2. What should I know before I use Symbicort Rapihaler? in the full CMI.

3. What if I am taking other medicines?

4. How do I use Symbicort Rapihaler?

Symbicort Rapihaler should be inhaled into your lungs through the mouth.

Follow all directions given to you by your doctor or pharmacist.

5. What should I know while using Symbicort Rapihaler?

Things you should do

If you have an Asthma Action Plan agreed with your doctor, follow it closely at all
times.

Have your reliever medicine available at all times. As advised by your doctor, this
may be your Symbicort Rapihaler (50/3 or 100/3) or another reliever medicine.

Rinse your mouth out with water after taking your daily morning and/or evening dose
of Symbicort Rapihaler and spit this out.

Remind any doctor, dentist or pharmacist you visit that you are using Symbicort Rapihaler.

Things you should not do

Do not stop using this medicine suddenly without checking with your doctor

Driving or using machines

Symbicort Rapihaler may cause dizziness, light-headedness, tiredness or drowsiness
in some people when they first start using it.

Looking after your medicine

Keep your Symbicort Rapihaler in a cool dry place where the temperature stays below
30oC, with the cover firmly in place.

Dispose your Symbicort Rapihaler 3 months after removal from the foil pouch.

6. Are there any side effects?

All medicines can have side effects. If you do experience any side effects, most of
them are minor and temporary. These include sore, yellowish, raised patches in the
mouth (thrush), hoarse voice, unpleasant taste in your mouth, pounding heart, headache,
trembling or muscle cramps. However, some side effects may need medical attention.
These include severe allergic reactions such as difficulty breathing, swelling of
the face, lips or tongue, severe rash or pneumonia (lung infection), signs include
fever or chills, increased phlegm or a change in colour, increased cough or difficulties
breathing. Serious side effects are rare.
For more information, including what to do if you have any side effects, see Section
6. Are there any side effects? in the full CMI.

Active ingredient(s):
budesonide / formoterol (eformoterol) fumarate dihydrate

Full Consumer Medicine Information (CMI)

This leaflet provides important information about using Symbicort Rapihaler. You should also speak to your doctor or pharmacist if you would like further information
or if you have any concerns or questions about using Symbicort Rapihaler.

Where to find information in this leaflet:

1. Why am I using Symbicort Rapihaler?

Symbicort Rapihaler is a pressurised metered dose inhaler (pMDI) or puffer. It contains
two active ingredients in one inhaler: budesonide and formoterol (as formoterol fumarate
dihydrate, which was previously known as eformoterol fumarate dihydrate).

Budesonide belongs to a group of medicines called corticosteroids. Budesonide acts
directly on your airways to reduce inflammation.

Formoterol belongs to a group of medicines called beta-2-agonists. Formoterol opens
up the airways to help you breathe more easily.

The medicine inside Symbicort Rapihaler is inhaled into the lungs for the treatment
of asthma in adults and adolescents (12 years and over) or Chronic Obstructive Pulmonary
Disease (COPD) in adults (18 years and over).

Asthma

Asthma is a disease where the airways of the lungs become narrow and inflamed (swollen),
making it difficult to breathe. This may for example be due to exercise, or exposure
to allergens (e.g. an allergy to house dust mites, smoke or air pollution), or other
things that irritate your lungs.

The budesonide in Symbicort Rapihaler helps to improve your condition and to prevent
asthma attacks from occurring.

The formoterol in Symbicort Rapihaler helps you breathe more easily.

Some people can take Symbicort Rapihaler when they need it – they use Symbicort Rapihaler
as an anti-inflammatory reliever to treat their symptoms when their asthma gets worse
and to help prevent asthma attacks, or to help prevent symptoms from happening (eg
before exercise or exposure to other triggers such as allergens).

Some people need to take Symbicort Rapihaler every day – they use their Symbicort
Rapihaler as a daily maintenance preventer to help maintain control of their asthma
symptoms and help prevent asthma attacks.

Chronic Obstructive Pulmonary Disease (COPD)

COPD (which includes chronic bronchitis and emphysema) is a long-term lung disease.
There is often permanent narrowing and persistent inflammation of the airways. Symptoms
may include difficulty in breathing (breathlessness or wheezing), coughing and increased
sputum (phlegm).

Symbicort Rapihaler when used as prescribed will help to control your COPD symptoms
(ie breathing difficulties).

2. What should I know before I use Symbicort Rapihaler

Warnings

Do not use Symbicort Rapihaler if:

you are allergic to any medicine containing budesonide or formoterol, or any of the
ingredients listed at the end of this leaflet. Always check the ingredients to make
sure you can use this medicine.

Check with your doctor if you:

have any allergies to any other medicines or foods.

have, or have had, any of the following medical conditions, as it may not be safe
for you to take Symbicort Rapihaler:

thyroid problems

diabetes

heart problems

liver problems

tuberculosis (TB)

low levels of potassium in the blood.

currently have an infection. If you take Symbicort Rapihaler while you have an infection,
the medicine may hide some of the signs of an infection. This may make you think,
mistakenly, that you are better or that it is not serious.

have any other medical conditions.

have any questions about how you should be using your Symbicort Rapihaler.

During treatment, you may be at risk of developing certain side effects. It is important
you understand these risks and how to monitor for them. See additional information
under Section 6. Are there any side effects?

Pregnancy and breastfeeding

Check with your doctor if you are pregnant or intend to become pregnant.

Talk to your doctor if you are breastfeeding or intend to breastfeed.

Your doctor will discuss the possible risks and benefits of using Symbicort Rapihaler
during pregnancy and while breastfeeding.

Children

Do not give Symbicort Rapihaler to a child under 12 years, unless directed to by the
child’s doctor.

Symbicort Rapihaler is not recommended for use in children under 12 years.

Asthma Action Plan

If you have asthma, ask your doctor or pharmacist if you have any questions about
your Asthma Action Plan.

Your healthcare professional should give you a personal Asthma Action Plan to help
manage your asthma. This plan will include what medicines to take as a reliever when
you have symptoms or sudden attacks of asthma, medicines you can take to prevent symptoms
from occurring (eg prior to exercise or allergen exposure) and if you need to take
daily maintenance medicines to help control your asthma. It will also provide advice
on when to seek urgent medical attention such as when your asthma suddenly worsens
or worsens over a period of time.

It is important that you discuss with your doctor both your exposure to triggers and
how often your exercise, as these could impact how your doctor prescribes your Symbicort
Rapihaler.

3. What if I am taking other medicines?

Some medicines may interfere with Symbicort Rapihaler and affect how it works. These
include:

medicines used to treat heart problems or high blood pressure such as beta-blockers,
diuretics and antiarrhythmics (disopyramide, procainamide and quinidine)

medicines used to treat glaucoma such as beta-blockers

medicines used to treat depression or other mood/mental disorders such as tricyclic
antidepressants, monoamine oxidase inhibitors and phenothiazines

medicines used to treat hayfever, coughs, colds and runny nose such as antihistamines

medicines used to treat fungal infections (eg ketoconazole)

xanthine derivatives (eg theophylline) which are a class of medicines used to treat
asthma and COPD

medicines used to treat Addison’s disease (when there is inadequate production of
a natural steroid hormone by the adrenal gland) or another condition where there is
too much salt lose in the urine (eg fludrocortisone)

These medicines may be affected by Symbicort Rapihaler or may affect how well it works.
You may need different amounts of your medicine, or you may need to use different
medicines. Your doctor or pharmacist will advise you.

Check with your doctor or pharmacist if you are not sure about what medicines, vitamins
or supplements you are taking and if these affect Symbicort Rapihaler.

Your doctor and pharmacist have more information on medicines to be careful with or
avoid while using Symbicort Rapihaler.

4. How do I use Symbicort Rapihaler?

How to use your Rapihaler

Follow all directions given to you by your doctor or pharmacist carefully.

They may differ from the information contained in this leaflet.

Each pack of Symbicort Rapihaler contains an instruction for use leaflet that tells
you the correct way to use it. Please read this carefully.

If you are not sure how to use the Rapihaler, ask your doctor or pharmacist to show
you how.

How much to take

Asthma (Adults and children 12 years and over)

Your healthcare professional should give you a personal Asthma Action Plan to help
manage your asthma. This plan will include what medicines to take as a reliever when
you have symptoms or sudden attacks of asthma, medicines you take prevent symptoms
from occurring (eg prior to exercise or allergen exposure) and if you need to take
daily maintenance medicines to help control your asthma.

It is important that you discuss with your doctor both your exposure to triggers and
how often you exercise, as these could impact how your doctor prescribes your Symbicort
Rapihaler.

Your doctor may have prescribed Symbicort Rapihaler for you to use as:

an anti-inflammatory reliever medicine only,

both an anti-inflammatory reliever and daily maintenance preventer medicine or,

as a daily maintenance preventer only, where another medicine is use as a reliever.

If your asthma has been under control for some time, your doctor may tell you to take
less inhalations of Symbicort Rapihaler, prescribe you a lower strength of Symbicort
Rapihaler or recommended that you use Symbicort Rapihaler in a different way.

If you are using more inhalations of your reliever medicine or you are wheezing or
breathless more than usual tell your doctor as your asthma may be getting worse.

Ask your doctor if you have any questions about how you should be using your Symbicort
Rapihaler.

Anti-inflammatory reliever only (Symbicort Rapihaler 100/3)

For patients aged 12 years and over, Symbicort Rapihaler 100/3 can be used to treat
asthma symptoms when they happen and to help stop asthma symptoms from happening (eg
just before exercise or before you get exposed to other triggers).

If you get asthma symptoms, take 2 inhalations and wait a few minutes. If you do not
feel better, take 2 more inhalations.

Your doctor will tell you how many inhalations to take before exercising or exposure
to other triggers to help stop symptoms from happening.

Do not use more than 12 inhalations on a single occasion or more than 24 inhalations
in any day. If your symptoms continue to worsen over 3 days, despite using additional
inhalations, tell your doctor.

Have your Symbicort Rapihaler reliever with you at all times.

Anti-inflammatory reliever plus maintenance therapy (Symbicort Rapihaler 50/3 and
100/3)

For patients aged 12 years and over, Symbicort Rapihaler 50/3 and 100/3 can be used
to treat asthma symptoms when they happen. Symbicort Rapihaler 100/3 can also be used
to help stop asthma symptoms from happening (eg just before exercise or before you
get exposed to other triggers).

If you get asthma symptoms, take 2 inhalations of Symbicort Rapihaler 50/3 or 100/3
and wait a few minutes. If you do not feel better, take 2 more inhalations.

Your doctor will tell you how many inhalations of Symbicort Rapihaler 100/3 to take
before exercising or exposure to other triggers to help stop symptoms from happening.

Have your Symbicort Rapihaler 50/3 or 100/3 reliever with you at all times.

You also need to take your Symbicort Rapihaler (50/3 or 100/3) daily as your maintenance
preventer. The usual maintenance dose is 4 inhalations per day (given either as 2
inhalations in the morning and evening or as 4 inhalations in either the morning or
evening). Your doctor may prescribe a maintenance dose of Symbicort Rapihaler 100/3,
4 inhalations twice a day.

Do not use more than 12 inhalations on a single occasion or more than 24 inhalations
of Symbicort Rapihaler (as needed and daily dose) in any day. If your symptoms continue
to worsen over 3 days, despite using additional inhalations, tell your doctor.

NOTE: Symbicort Rapihaler 200/6 is not recommended to be used as anti-inflammatory
reliever medicine.

Daily fixed dose maintenance therapy (Symbicort Rapihaler 50/3, 100/3 and 200/6)

For patients aged 12 years and over, Symbicort Rapihaler 50/3, 100/3 and 200/6 can
be used as a daily fixed-dose maintenance preventer.

The usual dose of Symbicort Rapihaler 50/3 and 100/3 is 2 or 4 inhalations twice a
day. Do not take more than 8 inhalations a day.

The usual dose of Symbicort Rapihaler 200/6 is 2 inhalations twice a day. Do not take
more than 4 inhalations a day.

Symbicort Rapihaler 200/6 can also be given as a higher dose in patients aged 18 years
and over. The usual dose is 4 inhalations twice a day. Do not take more than 8 inhalations
per day.

Have your separate reliever with you at all times.

COPD (Adults)

The usual dose (also maximum recommended dose) is 2 inhalations of Symbicort Rapihaler
200/6 twice a day.

Your doctor should tell you the best way to manage your symptoms and any flare ups.
This may include additional medicines (such as reliever medicines) to use when you
have sudden attacks of breathlessness.

If you are using more inhalations of your reliever medicine or you are wheezing or
breathless more than usual tell your doctor.

If your COPD gets worse, your doctor may give you some additional medicines (such
as oral corticosteroids or antibiotics).

How long to use your Symbicort Rapihaler

If your doctor has told you to take Symbicort Rapihaler daily, it is important that
you use it every day even if you feel well.

Symbicort Rapihaler helps control your asthma or COPD but does not cure it.

Keep using it for as long as your doctor tells you to. Do not stop using it unless
your doctor tells you to.

If you forget to use Symbicort Rapihaler

If you miss a dose of Symbicort Rapihaler, take your dose as soon as you remember.

Do not use a double dose to make up for the dose that you missed.

This may increase the chance of you getting an unwanted side effect.

If you are using Symbicort Rapihaler as a reliever medicine, consult your doctor on
the correct use of the product.

If you are not sure what to do, ask your doctor or pharmacist.

If you have trouble remembering to use your medicine, ask your pharmacist for some
hints.

If you use too much Symbicort Rapihaler

If you think that you have used too much Symbicort Rapihaler, you may need urgent
medical attention.

You should immediately:

phone the Poisons Information Centre
(by calling
13 11 26), or

contact your doctor, or

go to the Emergency Department at your nearest hospital.

You should do this even if there are no signs of discomfort or poisoning.

If you use too much Symbicort Rapihaler, you may feel sick or vomit, have a fast or
irregular heartbeat, a headache, tremble, feel shaky, agitated, anxious, tense, restless,
excited or be unable to sleep.

5. What should I know while using Symbicort Rapihaler?

Things you should do

If you have an Asthma Action Plan that you have agreed with your doctor, follow it
closely at all times
.

Keep using Symbicort Rapihaler for as long as your doctor tells you to, even if you
are feeling well.

See your doctor regularly to make sure that your asthma or COPD is not getting worse.

Have your reliever medicine available at all times. As advised by your doctor, this may be your Symbicort Rapihaler (50/3 or 100/3) or
another reliever medicine.

If you become pregnant while using Symbicort Rapihaler, tell your doctor.

Rinse your mouth out with water after taking your daily morning and/or evening dose
of Symbicort Rapihaler and spit this out.
If you don’t rinse your mouth, you are more likely to develop thrush in your mouth.
You do not have to rinse mouth if you have to take occasional doses of Symbicort Rapihaler
for relief of asthma symptoms (ie as an anti-inflammatory reliever).

Call your doctor straight away if you:

are taking Symbicort Rapihaler for COPD and you notice any signs of pneumonia (infection
of the lung). Signs include fever or chills, increased phlegm/sputum production or
change in colour, increased cough or increased breathing difficulties. Pneumonia is
a serious medical condition and will require urgent medical attention.

Remind any doctor, dentist or pharmacist you visit that you are using Symbicort Rapihaler.

Things you should not do

Do not stop using this medicine suddenly without checking with your doctor.

Do not take any other medicines for your asthma or COPD without checking with your
doctor.

Do not give Symbicort Rapihaler to anyone else, even if they have the same condition
as you.

Do not use Symbicort Rapihaler to treat any other complaints unless your doctor tells
you to.

Driving or using machines

Be careful before you drive or use any machines or tools until you know how Symbicort
Rapihaler affects you.

Symbicort Rapihaler may cause dizziness, light-headedness, tiredness or drowsiness
in some people when they first start using it.

Looking after your medicine

Follow the instructions in the carton on how to take care of your medicine properly.

Storage

Keep your Symbicort Rapihaler in a cool dry place where the temperature stays below
30oC.

Always replace the mouthpiece cover after using Symbicort Rapihaler.

Discard Symbicort Rapihaler within 3 months after removal from the foil pouch.

Store it in a cool dry place away from moisture, heat or sunlight; for example, do
not store it:

in the bathroom or near a sink, or

in the car or on window sills.

Keep it where young children cannot reach it.

WARNING

The canister in Symbicort Rapihaler contains a pressurised liquid. Do not expose to
temperatures higher than 50oC. Do not pierce the canister. The canister should not be broken, punctured or burnt,
even when it seems empty.

Cleaning

The Rapihaler mouthpiece must be wiped with a clean dry cloth/tissue and must never
get wet.

Full instructions on the right way to use and clean Symbicort Rapihaler are inside
each pack.

Getting rid of any unwanted medicine

Since some medicine may remain inside your Symbicort Rapihaler you should always return
it to your pharmacist for disposal including:

when you have taken all your doses and the dose counter is on zero (‘0’ – see instructions
in the pack), or

3 months after removal from the foil pouch, or

it is damaged or past its expiry date, or

your doctor/pharmacist has told you to stop using it.

6. Are there any side effects?

All medicines can have side effects. If you do experience any side effects, most of
them are minor and temporary. However, some side effects may need medical attention.

Tell your doctor or pharmacist as soon as possible if you do not feel well while you
are using Symbicort Rapihaler.

If you get any side effects, do not stop using Symbicort Rapihaler without first talking
to your doctor or pharmacist.

See the information below and, if you need to, ask your doctor or pharmacist if you
have any further questions about side effects.

Less serious side effects

Less serious side effects

What to do

Mouth/throat-related:

sore, yellowish, raised patches in the mouth (thrush)

hoarse voice

irritation of the tongue and mouth

coughing

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Honge Li,1,* Raorao Wang,1,* Xueyan Wei,1,* Chunyan Zhang,1 Wenhui Pei,1 Xuhui Zhang,2 Zhen Yang,1 Zhi Li,3 Yuhuan Zhang,1 Yanli Shi,1 Yunchao Wang,4 Xinhua Wang1

1Institute of Public Health, Gansu University of Chinese Medicine, Lanzhou, Gansu, People’s Republic of China; 2Department of Respiratory Medicine, Affiliated Hospital of Gansu University of Chinese Medicine, Lanzhou, Gansu, People’s Republic of China; 3The State Key Laboratory of Respiratory Disease, The First Affiliated Hospital, Institute of Public Health, Guangzhou Medical University, Guangzhou, Guangdong, People’s Republic of China; 4Institute of Basic Medicine, Gansu University of Chinese Medicine, Lanzhou, Gansu, People’s Republic of China

Correspondence: Yunchao Wang, Institute of Basic Medicine, Gansu University of Chinese Medicine, Lanzhou, Gansu, 730000, People’s Republic of China, Tel +86 18609404912, Email [email protected] Xinhua Wang, Institute of Public Health, Gansu University of Chinese Medicine, Lanzhou, Gansu, 730000, People’s Republic of China, Tel +86 13893602359, Email [email protected]

Background: Chronic obstructive pulmonary disease (COPD) is a chronic respiratory ailment influenced by a blend of genetic and environmental factors. Inflammatory response and an imbalance in oxidative-antioxidant mechanisms constitute the primary pathogenesis of COPD. Glutathione S-transferase P1(GSTP1) plays a pivotal role as an antioxidant enzyme in regulating oxidative-antioxidant responses in the pulmonary system. The activation of the NOD-like receptor thermal protein domain (NLRP3) inflammatory vesicle can trigger an inflammatory response. Several investigations have implicated GSTP1 and NLRP3 in the progression of COPD; nonetheless, there remains debate regarding this mechanism.
Methods: Employing a case-control study design, 312 individuals diagnosed with COPD and 314 healthy controls were recruited from Gansu Province to evaluate the correlation between GSTP1 (rs4147581C>G and rs1695A>G) and NLRP3 (rs3806265T>C and rs10754558G>C) polymorphisms and the susceptibility to COPD.
Results: The presence of the GSTP1 rs4147581G allele substantially elevated the susceptibility to COPD (CGvs.CC:OR=3.11,95% CI=1.961– 4.935, P< 0.001;GGvs.CC:OR=2.065,95% CI=1.273– 3.350, P=0.003; CG+GGvs.CC:OR=2.594,95% CI=1.718– 3.916, P< 0.001). Similarly, the NLRP3rs3806265T allele significantly increased the susceptibility to COPD (TC:TT:OR=0.432,95% CI=0.296– 0.630; TC+CCvs.TT:OR=2.132,95% CI=1.479– 3.074, P< 0.001). However, no statistically significant association was discerned between the rs1695A>G and rs10754558G>C polymorphisms and COPD susceptibility (P> 0.05).
Conclusion: In summary, this study ascertained that the GSTP1 rs4147581C>G polymorphism is associated with increased COPD susceptibility, with the G allele elevating the risk of COPD. Similarly, the NLRP3 rs3806265T>C polymorphism is linked to elevated COPD susceptibility, with the T allele heightening the risk of COPD.

Introduction

Chronic obstructive pulmonary disease (COPD) is a heterogeneous lung condition characterized by persistent respiratory symptoms and airflow limitation due to airway and/or respiratory disease, accompanied by dyspnea, cough, and sputum production.1–6 The global prevalence of COPD is 10.3%, with the prevalence among Chinese adults aged 40 years and older reaching as high as 13.6%, making it the third leading cause of death in the country.

The causes of COPD are complex, and its development is strongly associated with both genetic and environmental factors.7–9 Familial aggregation of COPD indicates the significant role of genetic factors in its development. Studies have indicated that only 10% to 20% of smokers eventually develop COPD, while 25% of COPD patients have never smoked.10–13 This suggests that COPD results from the interplay between genetic and environmental factors.14 Although the pathogenesis of COPD remains unclear, inflammation, protease-antiprotease imbalance, and oxidative-antioxidant imbalance are believed to be the primary mechanisms. Recently, Confalonieri et al propose to also include the concept of “structural changes due to failed regeneration by the distal airways progenitor cells” into the new definition of COPD “structural changes due to failed regeneration by the distal airways progenitor cells”.15 In recent years, several genetic polymorphisms have been linked to COPD development, including polymorphisms in glutathione S-transferase and inflammation-related genes.16,17

Glutathione S-transferase P1 (GSTP1) is a vital antioxidant enzyme highly expressed in the lungs.18,19 The GSTP1 gene, located on chromosome 11q13, has multiple single-nucleotide mutation sites.20 Polymorphisms at these mutant loci may impact their antioxidant function, leading to an oxidative-antioxidant imbalance that could induce COPD. Currently, there is controversy regarding the association between GSTP1 polymorphisms and COPD. While Yan and Ishii found an association, Yim and Yang’s study did not support a correlation between the two.21–26

The early immune response in the lungs against harmful stimuli is primarily mediated by inflammasomes, intracellular polyprotein complexes that recognize signals of injury and pathogens. NOD-like receptor thermal protein domain-associated protein 3 (NLRP3) is a crucial member of the inflammasome responsible for recognizing these signals.27 Mutations in the NLRP3 gene locus may result in abnormal inflammasome activation, leading to an excessive inflammatory response and exacerbating lung tissue damage.28–31 Faner et al and Eltom et al discovered that the rs35829419 mutation at the NLRP3 locus in lung tissues of COPD patients affects interactions with other proteins, further intensifying the inflammatory response and the release of inflammatory mediators.32,33 NLRP3 is also genetically polymorphic and has been linked to the development of several inflammatory diseases. However, although there are fewer studies on NLRP3 polymorphisms and COPD.34,35

In summary, COPD poses a heavy disease burden worldwide due to its high prevalence and mortality. However, the causes of COPD are complex, and its pathogenesis and causes have not been fully elucidated. Currently, it is mainly believed that the development of COPD is related to genes and environmental factors, and gene polymorphisms are also believed to be involved in many aspects of the pathogenesis of COPD. However, there is controversy at home and abroad about the association of GSTP1 gene polymorphisms with the risk of COPD and there are fewer studies on the association of NLRP3 gene polymorphisms with the risk of COPD. COPD is also less studied. Therefore, we conducted a case-control study in Gansu Province, including 312 COPD patients and 314 healthy controls, and used molecular epidemiological methods and real-time fluorescence quantitative PCR to analyse the association between GSTP1 and NLRP3 gene polymorphisms and COPD, with a view to providing theoretical basis for the early prevention programme and treatment of COPD-susceptible population.

Methods

Study Population

Between January 2020 and November 2022, we conducted a case-control study at the Affiliated Hospital of Gansu University of Traditional Chinese Medicine involving 312 COPD patients and 314 healthy controls from both rural and urban natural population cohorts in Gansu, the cases were mainly included in stable COPD patients with stable or mild symptoms such as cough, sputum, and shortness of breath. Our aim was to evaluate the association of GSTP1 (rs4147581C>G and rs1695A>G) and NLRP3 (rs3806265T>C and rs10754558G>C) polymorphisms in relation to COPD susceptibility.

Diagnostic Criteria and Pulmonary Function Tests for COPD

In accordance with the COPD Global Initiative for 2023, COPD is considered diagnosed when there are risk factors associated with dyspnea, cough, sputum production, and smoking, and the ratio of Forced Expiratory Volume in 1 second (FEV1) to Forced Vital Capacity (FVC), measured after a half-hour inhalation of 400 µg of salbutamol, falls below 70%. Pulmonary function tests were conducted using an EasyOne spirometer (NDD Medizintechnik AG, Switzerland) following the manufacturer’s instructions.36

Single Nucleotide Polymorphism (SNP) Selection and Genotyping

We identified potential risk SNPs by consulting the dbSNP database (www.ncbi.nlm.nih.gov/SNP) with the following selection criteria: SNPs located within the upper and lower 2000 bp of GSTP1 and NLRP3, Minor Allele Frequencies (MAFs) exceeding 0.05 in the Chinese population, and low linkage disequilibrium (LD, r2<0.8). Finally, we selected rs4147581C>G, rs1695A>G, rs3806265T>C, and rs10754558G>C for further analysis.

DNA extraction from collected peripheral blood samples was carried out using Tiangen Biochemical’s Blood Genomic DNA Extraction System Kit (DP349). Genotyping was performed using the TaqMan-MGB probe method. To ensure the reliability of PCR reactions, a negative control was included on each plate, and 10% of the samples were randomly selected for repeat testing.

Fluorescence-Based Quantitative PCR Technique

Mix configuration: Prepare PCR reaction mixture with Takara Premix Ex Taq™ (Probe qPCR) kit and vortex oscillation for 15 sec to mix the mixture well. Add sample: Standard DNA sample to 30 ng /μ l, add 18.5 μL PCR reaction mixture to 384 / 96 well plate, add l.5 μ l DNA template to 384 / 96 well plate, seal with sealing plate film and place at low speed, he centrifuwas centrifuged at 2000rpm for 2min. PCR amplification reaction: Place 384 / 96 well plate into 7900 HT quantitative PCR instrument / StepOnePlus quantitative PCR instrument and perform the following steps: Pre read → predenaturation 95°C 10min → denaturation 95°C 15s + annealing extension 60°C 1min (Repeat: 40 cycles) → 60°C 1min → Post read.

Methods of Statistical Analysis

Measurement data are presented as mean±standard deviation (X±SD), and count data are expressed as percentages (%). For group comparisons involving both categorical and continuous data, we employed χ2 tests and t-tests as appropriate.

In examining the association between genetic polymorphisms and COPD susceptibility, we utilized a multifactorial logistic regression model to calculate the odds ratio (OR) and its 95% confidence interval (CI). This analysis was adjusted for potential confounders such as age, gender, and smoking status. We conducted stratified analysis and interaction analysis for each stratum under each factor to assess the association between genotype and COPD risk. The Breslow-Day test was employed to evaluate heterogeneity between strata, with a significance level set at P<0.05. Statistical analysis was performed using SPSS version 25.0.

Results

Demographic Characteristics

Table 1 presents the demographic characteristics of our case-control study, including 312 COPD patients and 314 healthy controls in Gansu Province. Significant disparities in age, smoking status were observed between the two groups, with both demonstrating statistical significance (both P<0.05).

Table 1 Basic Demographic Characteristics of the Study Population

Association Analysis of SNPs in the GSTP1 and NLRP3 Genes with the Risk of COPD

As depicted in Table 2, the GSTP1 rs4147581 G allele markedly elevated the risk of COPD within the Gansu Province, China population (CGvs.CC:OR=3.11,95% CI=1.961–4.935, P<0.001;GGvs.CC:OR=2.065,95% CI=1.273–3.350, P=0.003;CG+GGvs.CC:OR=2.594,95% CI=1.718–3.916, P<0.001). In contrast, the GSTP1 rs1695A allele did not demonstrate a significant association with COPD risk. Nevertheless, logistic regression analysis, adjusting for age, gender, smoking, and BMI, revealed that the GSTP1 rs1695A>G allele was linked to an increased COPD risk within the Gansu Province, China population (AG:AA: adjusted Odds Ratio (OR)=2.495, 95% CI=1.558–3.996;AG+GGvs.AA: adjusted Odds Ratio (OR)=2.619, 95% CI=1.428–3.294, both P<0.001).

Table 2 Association of SNPs in GSTP1 and NLRP3 with COPD Susceptibility

The NLRP3 rs3806265T allele was also associated with COPD risk within the Gansu Province, China population (TC:TT: OR=0.432,95% CI=0.296–0.630; TC+CCvs.TT: OR=2.132, 95% CI=1.479–3.074, both P<0.001). Conversely, no significant association was detected between rs10754558G>C and the prevalence of COPD.

Stratified Analysis and Interaction Analysis of SNPs and Risk of COPD

Stratification and Interaction Analysis of GSTP1 rs4147581C>G and COPD Prevalence Risk

Table 3 presents the findings from the stratification and interaction analysis. Rs4147581C>G in the dominant model, when comparing the CC genotype to the GG/GC genotype, we observed variations in COPD risk across different strata defined by age, sex, and smoking history. Notably, there was no homogeneity between the strata (P<0.05). In the population aged over 60 years, the CC genotype (GG+GCvs.CC: OR=11.176,95% CI = 5.709–21.879) significantly increased the risk of COPD. Similarly, in the male population (GG+GCvs.CC: OR=22.784,95% CI=6.883–75.418), in individuals with a smoking history (GG+GCvs.CC: OR=24.429,95% CI=5.389–110.737), and in those without a smoking history (GG+GCvs.CC: OR=1.979,95% CI=1.327–2.950), the CC genotype was associated with an elevated risk of COPD. Furthermore, in individuals without a smoking history (GG+GCvs.CC: OR=1.327–2.950), the CC genotype exhibited an increased risk of COPD. Regarding BMI, marital status, alcohol consumption, and a history of previous diseases, we observed homogeneity between strata (P>0.05). In these strata, the CC genotype in the dominant model was associated with an increased risk of COPD: BMI (GG+GCvs.CC: OR=2.862,95% CI=1.968–4.162), marital status (GG+GCvs.CC: OR=2.950, 95% CI=2.031–4.286), alcohol consumption (GG+GCvs.CC: OR=3.046,95% CI=2.090–4.439), and a history of previous illnesses(GG+GCvs.CC: OR=2.898,95% CI=1.997–4.205).The results of multiplicative interaction analysis demonstrated that age and sex exhibited significant interactions with the genetic variation of rs4147581C>G, with a statistically significant difference observed between the case and control groups (P<0.05).

Table 3 Stratification Analysis and Interaction Analysis Between GSTP1 rs4147581C>G and COPD Susceptibility

Stratification and Interaction Analysis of NLRP3 rs3806265 T>C and COPD Prevalence Risk

The results of the stratification and interaction analysis are presented in Table 4. In the dominant model, rs3806265T>C, compared to the TT genotype, displayed variations in strata involving marital status and smoking. Notably, a lack of homogeneity between strata (P<0.05) was evident in the married population (TC+CCvs.TT: OR=2.816,95% CI=1.979–4.008), and the population with a smoking history (TC+CCvs.TT: OR=7.130,95% CI=3.291–15.451), and those without a smoking history (TC+CCvs.TT: OR=1.673,95% CI=1.156–2.421) increased the risk of COPD. In the dominant model, when stratified by TC/CC genotypes compared to TT genotypes, and across various strata, including age, sex, BMI, alcohol consumption, and history of previous diseases, we observed homogeneity between these strata (P>0.05). In each of these strata, the TC/CC genotypes were associated with an increased risk of COPD: age (TC+CCvs.TT:OR=2.088,95% CI=1.469–2.968), sex(TC+CCvs.TT:OR=2.268,95% CI=1.619–3.176), BMI(TC+CCvs.TT: OR=2.432,95% CI=1.743–3.392), alcohol consumption (TC+CC vs.TT: OR=2.339,95% CI=1.683–3.251), and history of previous illness (TC+CCvs.TT: OR=2.336,95% CI=1.680–3.247). Furthermore, the results of the multiplicative interaction analysis revealed that the interaction between smoking and alcohol consumption, in relation to the genetic variation in rs3806265 T>C, exhibited a statistically significant difference between the case and control groups (P<0.05).

Table 4 Stratified Analysis and Interaction Analysis Between NLRP3 rs380626 T>C and COPD Susceptibility

Analysis of the Relationship Between COPD Severity and SNPs

A total of 110 COPD patients with complete pulmonary function indicators and stable stage were selected from the case group. The severity of COPD was divided into four levels according to the percentage of the expected value of forced pulmonary capacity in the first second. Among them, the predicted value of FEV1 ≥ 80% was mild, and the predicted value of 50% ≤ FEV1 < 80% was moderate. 30% ≤FEV1 < 50% is expected to be severe, and FEV1 < 30% is expected to be extremely severe. The correlation between GSTP1 (rs4147581C>G and rs1695A>G) and NLRP3 (rs3806265T>C and rs10754558G>C) and COPD severity was analyzed. As shown in Table 5, the group of cases with complete lung function was analysed by chi-square test, and it was found that rs4147581C>G, rs1695A>G, rs3806265T>C, and rs10754558G>C were unassociated with the severity of COPD.

Table 5 Analysis of the Relationship Between COPD Severity and SNPs

Discussion

Gene polymorphisms are thought to be involved in several aspects of COPD pathogenesis, and the association between polymorphisms in the GSTP1 gene and the risk of COPD is controversial both nationally and internationally, and there have been fewer studies on polymorphisms in the NLRP3 gene and COPD. To elucidate the role of GSTP1 and NLRP3 polymorphisms in COPD development, our study examined the relationship between two SNPs in the GSTP1 gene (rs4147581C>G, rs1695A>G) and two SNPs in the NLRP3 gene (rs3806265T>C, rs10754558G>C) and COPD risk in the Gansu population, China. Notably, GSTP1 rs4147581C>G allele exhibited an elevated COPD risk, with CG and GG genotypes demonstrating higher susceptibility compared to the rs4147581CC genotype within the age>60 years, male, smoking population (P<0.05). Furthermore, the NLRP3 rs3806265T>C allele was linked to an increased COPD risk, with the TT genotype displaying a higher prevalence in the married and smoking populations (P<0.05) compared to the rs3806265TC/CC genotype. And neither rs4147581 nor rs3806265 was associated with COPD severity.

GSTP1, a member of the GST enzyme family, serves various physiological functions.37 GSTs have been reported to participate in antioxidant processes within the body.38 Among the GSTs, GSTP1 and its close association with oxidative stress and inflammatory responses in COPD are notable GSTP1 polymorphisms contribute to an imbalance in oxidative-oxidative processes, affecting the ability to counter oxidative stress and other lung disease-associated biological mechanisms. This, in turn, impacts COPD development and severity.39 Additionally, GSTP1 plays a protective role against airway cell damage induced by smoking. Consequently, the association between GSTP1 and COPD has garnered increased attention. NLRP3 protein primarily resides in cells, serving to detect in vivo danger signals, thus, promoting the release of inflammatory factors such as IL-1β and IL-18.40 NLRP3 plays a crucial role in macrophage and neutrophil migration and aggregation, as well as in oxidative stress generation.41 Inhibition of NLRP3 inflammatory vesicles indirectly mitigates the inflammatory effects of IL-1β and IL-18, presenting an ideal target for COPD treatment.

In this study, we selected two SNPs from the GSTP1 gene (rs4147581C>G and rs1695A>G) and two from the NLRP3 gene (rs3806265T>C and rs10754558G>C) for investigation. Online tools such as NCBI, Ensembl, and SNP info Web Server were used to obtain information on the location and function of these SNPs. The GSTP1 gene, located on chromosome 11q13, spans approximately 3 kb with 7 exons.42 Specifically, rs4147581C>G, positioned at Chr11: 67584114, has demonstrated significant associations with survival in patients with hepatocellular carcinoma, where its mutant genotype reduces the risk of death in these patients.43–46 Meanwhile, rs1695A>G at Chr11: 67585218 has shown associations with conditions such as cervical cancer, asthma, cyclophosphamide efficacy, and adverse effects. The NLRP3 gene, situated on chromosome 1q44, extends over approximately 40 kb.47,48 Within this gene, rs3806265T>C, located at Chr1: 247423034, has been linked to multiple sclerosis, juvenile systemic lupus erythematosus, and myasthenia gravis in recent studies.49–51 Similarly, rs10754558G>C at Chr1: 247448734 has been reported to be associated with rheumatoid arthritis, chronic kidney disease, psoriasis, and others.

Our study findings indicate an association between the GSTP1 rs4147581C>G variant and the risk of developing COPD. Patients with the CG/GG genotype exhibited a higher incidence of COPD compared to those with the CC genotype. GSTP1 functions as a detoxifying enzyme involved in intracellular oxidative stress responses and the removal of toxic metabolites.52 The rs4147581C>G variant may lead to reduced activity and function of the GSTP1 enzyme, diminishing its capacity to bind and eliminate toxicants and harmful metabolites. This can result in intracellular toxicant accumulation, increased oxidative stress, and exacerbated inflammatory responses, thereby elevating the risk of cardiovascular diseases like coronary artery disease, hypertension, and myocardial infarction.

Furthermore, we found an association between the NLRP3 rs3806265T>C variant and the risk of developing COPD, with a higher prevalence of the TT genotype compared to the TC/CC genotype.53 NLRP3 rs3806265 may play a pivotal role in inflammatory injury in COPD. The variant could lead to aberrant NLRP3 protein function, impacting the abnormal activation of inflammatory vesicles and deviating inflammatory signaling pathways. This, in turn, increases intracellular stress levels and contributes to the development and exacerbation of inflammatory diseases.

In this study, we investigated the role of GSTP1rs4147581C>G and NLRP3rs3806265T>C variants as risk factors for chronic obstructive pulmonary disease (COPD). Our findings provide a new way to predict and prevent COPD.54 In addition, studies by Yadav et al in North Indian populations found that GST gene polymorphisms can be used as susceptibility biomarkers for COPD, which also provides support for our study.55 The study of the effect of IL5RA variants on COPD in a Chinese population by Li et al provides new evidence to further our understanding of the genetic susceptibility to COPD. This study reveals an association between IL5RA gene variants and COPD, which could help us better predict and prevent COPD.56 The study of Castro et al on the influence of gene polymorphism on the severity of silicosis provides us with a new perspective. The study, conducted in silicon-exposed Brazilian workers, explored the effect of genetic polymorphisms on the severity of silicosis, providing useful information for the prevention and treatment of lung disease.57 Finally, Cheng et al ‘s study that circular RNA-SNPs may increase susceptibility to silicosis provides new clues to our understanding of genetic susceptibility to silicosis. The study, conducted in a Chinese population, identified a novel circular RNA-SNP that may increase susceptibility to lung lesions. Taken together, these studies provide valuable information for our understanding of the genetic susceptibility to COPD and lung-related diseases, which can help us better prevent and treat these diseases. In future studies, we will continue to explore the role of these gene variants in COPD, with a view to providing more guidance for clinical diagnosis and treatment.

This study explored the genetic role of GSTP1 and NLRP3 genes in the risk of developing COPD using a case-control design in Gansu Province. The results showed that genetic polymorphisms in these genes were correlated with the occurrence of COPD in Gansu Province. However, this study has its limitations. Firstly, the sample size is limited, and further validation with an expanded sample size is necessary. Secondly, the study subjects were sourced from specific hospitals, potentially introducing selection bias. Thirdly, there might be recall bias in the collection of past information during the questionnaire survey. Lastly, as this study is a case-control design, establishing the temporal sequence of genetic polymorphisms and COPD is challenging. Future research should consider cohort and experimental studies to further validate these findings.

Conclusion

In conclusion, GSTP1 rs4147581C>G allele exhibited an elevated COPD risk, with CG and GG genotypes demonstrating higher susceptibility compared to the rs4147581CC genotype within the age>60 years, male, smoking population. Furthermore, the NLRP3 rs3806265T>C allele was linked to an increased COPD risk, with the TT genotype displaying a higher prevalence in the married and smoking populations compared to the rs3806265TC/CC genotype.

Abbreviations

COPD, chronic obstructive pulmonary disease; GSTP1, Glutathione S-transferase P1; NLRP3, NOD-like receptor thermal protein domain associated protein 3; LD, Linkage disequilibrium; GWAS, genome-wide association analysis; SNPs, the single nucleotide polymorphisms; FEV1, forced expiratory volume in 1 second; FVC, forced vital capacity; MAFs, the minor allele frequencies; PCR, TaqMan real-time polymerase chain reaction.

Acknowledgment

We thank the Institute of Public Health, Gansu University of Traditional Chinese Medicine. We thank the researchers in our laboratory for their guidance on experimental techniques.

Author Contributions

All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Funding

This study was supported by the following grants: National Key Research and Development Project of China 2017YFC0907202 (Xinhua Wang); National Natural Science Foundation of China (82260889) (Xuhui Zhang); Central Guided Local Science and Technology Development Funds Project No.22ZY1QA003(Xinhua Wang); 2022 Gansu Province Higher Education Institutions Industry Support Program Project No.2022CYZC-53(Xinhua Wang).

Disclosure

The authors report no conflicts of interest in this work.

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15. Confalonieri M, Braga L, Salton F, et al. Chronic obstructive pulmonary disease definition: is it time to incorporate the concept of failure of lung regeneration? Am J Respir Crit Care Med. 2023;207(3):366–367. doi:10.1164/rccm.202208-1508LE

16. Zhou H, Yang J, Li D, et al. Association of IREB2 and CHRNA3/5 polymorphisms with COPD and COPD-related phenotypes in a Chinese Han population. J Human Gene. 2012;57:738–746. doi:10.1038/jhg.2012.104

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19. Zuntar I, Petlevski R, Dodig S, et al. GSTP1, GSTM1 and GSTT1 genetic polymorphisms and total serum GST concentration in stable male COPD. Acta Pharm. 2014;64:117–129. doi:10.2478/acph-2014-0003

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24. Yang L, Li X, Tong X, et al. Association between glutathione S-transferase P1 Ile (105) Val gene polymorphism and chronic obstructive pulmonary disease: a meta-analysis based on seventeen case-control studies. Meta Gene. 2015;6:59–64. doi:10.1016/j.mgene.2015.08.007

25. Yang Q, Huang W, Yin D, et al. EPHX1 and GSTP1 polymorphisms are associated with COPD risk: a systematic review and meta-analysis. Front Genetics. 2023;14:1128985. doi:10.3389/fgene.2023.1128985

26. Du Y, Zhang H, Xu Y, et al. Association among genetic polymorphisms of GSTP1, HO-1, and SOD-3 and chronic obstructive pulmonary disease susceptibility. Int J Chronic Obstr. 2019;14:2081–2088. doi:10.2147/COPD.S213364

27. Mo R, Li J, Chen Y, et al. lncRNA GAS5 promotes pyroptosis in COPD by functioning as a ceRNA to regulate the miR-223-3p/NLRP3 axis. Molecul Med Rep. 2022;26:219. doi:10.3892/mmr.2022.12735

28. Faner R, Sobradillo P, Noguera A, et al. The inflammasome pathway in stable COPD and acute exacerbations. ERJ Open Res. 2016;2:2. doi:10.1183/23120541.00002-2016

29. Eltom S, Stevenson CS, Rastrick J, et al. P2X7 receptor and caspase 1 activation are central to airway inflammation observed after exposure to tobacco smoke. PLoS One. 2011;6:e24097. doi:10.1371/journal.pone.0024097

30. Mahalanobish S, Dutta S, Saha S, et al. Melatonin induced suppression of ER stress and mitochondrial dysfunction inhibited NLRP3 inflammasome activation in COPD mice. Food and Chemical Toxicology. 2020;144:111588.

31. Zhang MY, Jiang YX, Yang YC, et al. Cigarette smoke extract induces pyroptosis in human bronchial epithelial cells through the ROS/NLRP3/caspase-1 pathway. Life Sci. 2021;269:119090. doi:10.1016/j.lfs.2021.119090

32. Cheng L, Yin R, Yang S, et al. Rs4612666 Polymorphism of the NLRP3 gene is associated with the occurrence of large artery atherosclerotic ischemic strokes and microembolic signals. Biomed Res. Int. 2018;2018:6345805. doi:10.1155/2018/6345805

33. Zhou D, Wang X, Chen T, et al. The NLRP3 rs10754558 polymorphism is associated with the occurrence and prognosis of coronary artery disease in the Chinese han population. Biomed Res. Int. 2016;2016:3185397. doi:10.1155/2016/3185397

34. Sui J, Li H, Fang Y, et al. NLRP1 gene polymorphism influences gene transcription and is a risk factor for rheumatoid arthritis in han Chinese. Arthritis Rheum. 2012;64:647–654. doi:10.1002/art.33370

35. Von Herrmann KM, Salas LA, Martinez EM, et al. NLRP3 expression in mesencephalic neurons and characterization of a rare NLRP3 polymorphism associated with decreased risk of Parkinson’s disease. NPJ Parkinson’s Dis. 2018;4:24. doi:10.1038/s41531-018-0061-5

36. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease (2023 report). Avaliable from: goldcopd.org/2023-gold-report-2/. Accessed February 7, 2024.

37. Gattás GJ, Kato M, Soares-Vieira JA, et al. Ethnicity and glutathione S-transferase (GSTM1/GSTT1) polymorphisms in a Brazilian population. Braz J Med Biol Res. 2004;37:451–458. doi:10.1590/s0100-879x2004000400002

38. Tomaki M, Sugiura H, Koarai A, et al. Decreased expression of antioxidant enzymes and increased expression of chemokines in COPD lung. Pulmon Pharmacol Ther. 2007;20:596–605. doi:10.1016/j.pupt.2006.06.006

39. Ishii T, Matsuse T, Igarashi H, et al. Tobacco smoke reduces viability in human lung fibroblasts: protective effect of glutathione S-transferase P1. Am J Physiol Lung Cell Mol Physiol. 2001;280:L1189–L1195. doi:10.1152/ajplung.2001.280.6.L1189

40. Guo P, Li R, Piao TH, et al. Pathological mechanism and targeted drugs of COPD. Int J Chronic Obstr. 2022;17:1565–1575. doi:10.2147/COPD.S366126

41. Chen X, Liu G, Yuan Y, et al. NEK7 interacts with NLRP3 to modulate the pyroptosis in inflammatory bowel disease via NF-κB signaling. Cell Death Dis. 2019;10:906. doi:10.1038/s41419-019-2157-1

42. Wang Z, Qu K, Niu W, et al. Glutathione S-transferase P1 gene rs4147581 polymorphism predicts overall survival of patients with hepatocellular carcinoma: evidence from an enlarged study. Tumour Biol. 2016;37:943–952. doi:10.1007/s13277-015-3871-7

43. Phuthong S, Settheetham-Ishida W, Natphopsuk S, et al. Genetic Polymorphism of the Glutathione S-transferase Pi 1 (GSTP1) and susceptibility to cervical cancer in human papilloma virus infected Northeastern Thai Women. Asian Pac J Cancer Prev. 2018;19:381–385. doi:10.22034/APJCP.2018.19.2.381

44. Mukhammadiyeva GF, Bakirov AB, Karimov DO, et al. Analysis of the GSTP1 rs1695 polymorphism association with the development of asthma and phenotypic manifestations. J Asthma. 2022;59:1065–1069. doi:10.1080/02770903.2021.1910295

45. Dasgupta RK, Adamson PJ, Davies FE, et al. Polymorphic variation in GSTP1 modulates outcome following therapy for multiple myeloma. Blood. 2003;102:2345–2350. doi:10.1182/blood-2003-02-0444

46. Zhong S, Huang M, Yang X, et al. Relationship of glutathione S-transferase genotypes with side-effects of pulsed cyclophosphamide therapy in patients with systemic lupus erythematosus. Br. J. Clin. Pharmacol. 2006;62:457–472. doi:10.1111/j.1365-2125.2006.02690.x

47. Imani D, Azimi A, Salehi Z, et al. Association of nod-like receptor protein-3 single nucleotide gene polymorphisms and expression with the susceptibility to relapsing-remitting multiple sclerosis. Int J Immunogene. 2018;45:329–336. doi:10.1111/iji.12401

48. Agah E, Nafissi S, Saleh F, et al. Investigating the possible association between NLRP3 gene polymorphisms and myasthenia gravis. Muscle and Nerve. 2021;63:730–736. doi:10.1002/mus.27193

49. Cheng L, Liang X, Qian L, et al. NLRP3 gene polymorphisms and expression in rheumatoid arthritis. Exp Ther Med. 2021;22:1110.

50. La Russa A, Lofaro D, Montesanto A, et al. Association between NLRP3 rs10754558 and CARD8 rs2043211 variants and susceptibility to chronic kidney disease. Int J Mol Sci. 2023;24:1110. doi:10.3892/etm.2021.10544

51. Dawood A, Shehata W. Evaluation of NLRP3 (rs10754558) and PTPN22 (1858C/T) (rs2476601) functional polymorphisms in psoriasis susceptibility in Egypt. Appl Clin Gene. 2021;14:331–339. doi:10.2147/TACG.S319065

52. Qu K, Liu SS, Wang ZX, et al. Polymorphisms of glutathione S-transferase genes and survival of resected hepatocellular carcinoma patients. World J Gastroenterol. 2015;21:4310–4322. doi:10.3748/wjg.v21.i14.4310

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57. Cheng Z, Zhang Y, Zhao R, et al. A novel circRNA-SNP may increase susceptibility to silicosis. Ecotoxicol Environ Saf. 2022;242:113855. doi:10.1016/j.ecoenv.2022.113855

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Emphysema Treatment Global Market Report 2024

Emphysema Treatment Global Market Report 2024

"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 Emphysema Treatment 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 emphysema treatment market size has grown strongly in recent years. It will grow from $4.96 billion in 2023 to $5.29 billion in 2024 at a compound annual growth rate (CAGR) of 6.5%. The growth in the historic period can be attributed to smoking epidemic impact, advancements in medications, pulmonary rehabilitation programs, improved diagnostic tools, awareness and education..

The emphysema treatment market size is expected to see strong growth in the next few years. It will grow to $6.85 billion in 2028 at a compound annual growth rate (CAGR) of 6.7%. The growth in the forecast period can be attributed to aging population trends, customized treatment approaches, expanded access to therapies, focus on symptom management, collaborative healthcare models.. Major trends in the forecast period include exploration of gene therapies, patient education and empowerment, integration of artificial intelligence (ai), increased accessibility to treatment, long-acting medications development..

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Market Segmentation:

The emphysema treatment market covered in this report is segmented -

1) By Treatment: Smoking Cessation, Bronchodilators, Steroids, Leukotriene Modifiers, Supplemental Oxygen, Antibiotics, Gene Therapy, Surgery Transplant, Other Treatments

2) By Distribution Channel: Online Providers, Drug Stores and Retail Pharmacies, Hospital Pharmacies

3) By End-User: Clinics, Surgical Centre, Other End-Users

Major Driver - Surging Cases Of Chronic Obstructive Pulmonary Disease (COPD) To Drive Market Growth

The rise in the prevalence of chronic obstructive pulmonary disease (COPD) cases is expected to propel the growth of the emphysema treatment market going forward. Chronic obstructive pulmonary disease (COPD) is a set of disorders that cause airflow obstruction and breathing difficulties, including emphysema and chronic bronchitis. Emphysema therapies are essential in reducing the advancement of Chronic Obstructive Pulmonary Disease (COPD) as they focus on treating symptoms, restoring lung function, and delaying disease progression. For instance, in September 2021, according to the study released by the Forum of International Respiratory Societies, a Switzerland-based respiratory health advocacy organization, an estimated 200 million people have COPD in 2021, with around 3.2 million dying each year, making it the third-leading cause of mortality globally. Therefore, the rise in the prevalence of chronic obstructive pulmonary disease (COPD) cases drives the emphysema treatment market.

Competitive Landscape:

Major companies operating in the emphysema treatment market report are AstraZeneca PLC, Teva Pharmaceutical Industries Ltd., Novartis AG, GlaxoSmithKline PLC, Hikma Pharmaceuticals PLC, Boehringer Ingelheim GmbH, Mylan N.V., Pfizer Inc., Orion Oyj, Verona Pharma PLC, Pulmonx Corporation, Bioxyne Limited, Intrexon Corporation, iCure Pharmaceuticals Inc., Kamada Ltd., Emphasys Medical Inc., Halozyme Therapeutics Inc., Mariposa Health Limited, Uptake Technologies Inc., British Technology Group International , Astellas Pharma Inc., Respinova Ltd, Gala Therapeutics Inc., Pulmatrix Inc., Broncus Medical Inc., Holaira Inc., PneumRx Inc., Spiration Inc., Aeris Therapeutics Inc., CSA Medical Inc., Olympus Corporation

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www.thebusinessresearchcompany.com/report/emphysema-treatment-global-market-report

Top Trend - Minimally Invasive Procedures Transforming The Market

Major companies operating in the emphysema market are developing minimally invasive procedures for emphysema patients to gain a competitive edge in the market. Minimally invasive procedures refer to medical interventions or surgical techniques that are performed with minimal disruption to the body's normal structures. For instance, in January 2022, Adena Health System, a US-based healthcare company, launched the Zephyr Valve surgery. It is a minimally invasive procedure that offers an alternative to conventional lung volume reduction surgery for individuals experiencing lung hyperinflation, a common issue in emphysema and COPD. This innovative approach involves placing small, one-way Zephyr Valves in the airways of the lungs via a bronchoscope. These valves facilitate the release of trapped air, preventing further accumulation, and allowing healthier lung areas to expand, thereby improving breathing.

The Table Of Content For The Market Report Include:

1. Executive Summary

2. Emphysema Treatment Market Characteristics

3. Emphysema Treatment Market Trends And Strategies

4. Emphysema Treatment Market - Macro Economic Scenario

5. Emphysema Treatment Market Size And Growth

…..

27. Emphysema Treatment Market Competitor Landscape And Company Profiles

28. Key Mergers And Acquisitions

29. Future Outlook and Potential Analysis

30. Appendix

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This release was published on openPR.



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In a world where cigarette smoke is as much a part of the skyline as the buildings themselves, a groundbreaking study emerges from the labs of the University of Alabama at Birmingham (UAB), casting a new shadow on the already darkened reputation of smoking. This comprehensive research unveils a sinister link between cadmium, a common component in batteries, found in cigarette smoke, and the exacerbation of chronic obstructive pulmonary disease (COPD), a condition that has long plagued millions globally.

The Unseen Enemy in Smoke

While the air we breathe might appear clear, the truth is far more opaque, especially for the 1 billion smokers worldwide. Cigarette smoke, a cocktail of over 600 ingredients transforming into more than 7,000 chemicals upon combustion, contains an array of substances harmful to human health. Among these, cadmium, in even low doses, has been pinpointed by the UAB study as a significant contributor to lung injury and the progression of COPD, a disease that encompasses chronic bronchitis and emphysema, leading to the blockage of airflow and making breathing difficult.

A Closer Look at the Culprits: Cadmium and ANO1

The UAB researchers took a deep dive into the cellular level, focusing on how cadmium affects lung epithelial cells. Their findings spotlight the role of a chloride channel gene known as ANO1 and microRNA-381 in the lung tissue samples and airway epithelial cells of both non-smokers and smokers with COPD. The study's revelations are profound: smokers exhibited increased expression of ANO1 in their airway epithelial cells, a pattern similarly observed in normal human airway epithelial cells exposed to low doses of cadmium. The implications of these findings are significant, suggesting that the deleterious effects of cadmium on the lungs are mediated through the dysregulation of microRNA-381, leading to the upregulation of ANO1.

Hope on the Horizon: Therapeutic Possibilities

Perhaps the most significant silver lining to emerge from this cloud of smoke is the potential for new therapeutic targets. The study's exploration into the synthetic inhibition of microRNA-381, which resulted in increased ANO1 expression, alongside the use of a microRNA-381-mimic that decreased ANO1 expression, lays the groundwork for innovative treatments. These findings not only enhance our understanding of the molecular mechanisms underpinning cadmium-induced lung injury but also open the door to novel strategies aimed at mitigating the damage wrought by cigarette smoke.

As the curtain falls on this enlightening journey through the microscopic battlefields within smokers' lungs, the message is clear: the impact of cigarette smoke extends far beyond the visible cloud exhaled after a puff. With over 480,000 deaths annually in the US attributed to smoking, and 30% of cancer-related deaths linked to this habit, the UAB study serves as a crucial reminder of the unseen dangers lurking within each cigarette. The road to recovery for those affected by COPD and the quest for effective treatments continues, underscored by the hope that research such as this paves the way for a future where the air is not only clearer but safer for all to breathe.



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Discover insights into the Global Metered Dose Inhaler Devices Market, projected to grow at a high CAGR during 2024-2031. Advancements in technology, rising investments in R&D, and increasing prevalence of respiratory disorders such as asthma and COPD are key drivers.

Industry Overview 

Metered Dose Inhaler Devices Market is estimated to grow at a high CAGR during the forecast period 2024-2031 

A metered-dose inhaler (MDI) is a pressurized inhaler that delivers medication using a propellant spray. It is widely useful for people with respiratory disorders like asthma, chronic obstructive pulmonary disease (COPD), chronic bronchitis, and emphysema. 

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Market Trends 

The market for metered dose inhalers is poised for growth, propelled by the increasing adoption of breathing-actuated inhalers and substantial investments in research and development. 

Advancements in technology, coupled with a growing demand for metered dose inhalers, are key factors driving market expansion. Additionally, heightened research and development investments and a rise in chronic respiratory conditions such as asthma, COPD, and chronic bronchitis contribute to this growth. According to the World Health Organization (WHO), nearly 200 million individuals worldwide are affected by chronic obstructive pulmonary disease (COPD). Government organizations' increased funding for chronic disease treatment further accelerates market growth. For example, in the European Union, COPD's direct cost represents about 6% of total health expenditure, constituting approximately 56% of the total respiratory disease costs. 

The adoption of metered dose inhalers is also bolstered by technological advancements. Increasing awareness among individuals about advanced respiratory devices, such as bronchodilator inhalers, which offer advantages over traditional treatments, further drives market expansion. Moreover, rising healthcare expenditures from both governmental and private sectors may lead to increased infrastructure investments, further stimulating the metered dose inhaler market. 

Market growth is further supported by various product launches and research endeavors. For instance, Teva Pharmaceuticals, an affiliate of Teva Pharmaceutical Industries Ltd., announced groundbreaking study findings on May 17, 2022. These findings centered on the usage of short-acting beta agonists (SABA) and their established clinical thresholds, highlighting real-world applications in asthma patients in the U.S. Teva's introduction of the ProAir Digihaler (albuterol sulfate) inhalation powder, a digital inhaler, underscores the industry's commitment to innovation and advancing patient care. 

For Customized Report: www.datamintelligence.com/customize/metered-dose-inhaler-devices-market 

Market Segmentation 

By Product Type 

  • Manually-Actuated Pressurized Inhalers 
  • Breath-Actuated Pressurized Inhalers 

By Medications 

  • Corticosteroids 
  • Bronchodilators 
  • Combination (Corticosteroid & Bronchodilators) 

By Application 

  • Chronic Obstructive Pulmonary Disease (COPD)  
  • Asthma 
  • Emphysema 
  • Chronic Bronchitis 
  • Bronchospasm 
  • Others 

By Distribution Channel 

  • Hospital Pharmacies  
  • Retail Pharmacies 
  • Online Pharmacies 

Market Key Players 

Major players are F. Hoffmann-La Roche, AstraZeneca, GSK plc, Pfizer Inc., Amgen Inc., Novartis AG, Boehringer Ingelheim GmbH, Cipla Inc., Merck & Co. Inc and Teva Pharmaceutical Industries Ltd. 

Trending Reports 

Medical Suction Devices Market 

Tracheostomy Tube Market 

Nebulizers Market 

Inhalation Therapy Nebulizer Market 

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While Chennai grapples with an increasing prevalence of Chronic Obstructive Pulmonary Disease (COPD), experts have noticed a concerning trend among patients: many are not adhering to their COPD treatment plans. These patients’ reluctance to follow prescribed protocols may be attributed to several factors such as lack of awareness and misconceptions about the disease.

COPD encompasses a range of respiratory conditions, including chronic bronchitis and emphysema, that impede airflow and cause breathing difficulties. Recognizable symptoms include chest tightness, fatigue, recurrent respiratory infections, coughing, mucus production, and wheezing. The rise in COPD cases in urban areas, particularly among women, can be attributed to multiple factors, including increased air pollution that exacerbates symptoms and the high incidence of smoking, especially among younger age groups.

To effectively manage COPD, patients must educate themselves on symptom management and adhere strictly to their prescribed treatment plans. It is critical for individuals to understand the correct usage of inhalers and follow their doctors’ recommendations for optimal disease control. Additionally, measures such as wearing masks, getting vaccinated, and minimizing exposure to air pollution are essential for preventing COPD or reducing its severity.

However, pulmonologists in Chennai express concern over the lack of treatment adherence among COPD patients. Dr. Logamurthy, a pulmonologist from ESIC Hospital, emphasizes the need for increased awareness and holistic interventions to address this challenge. Many patients neglect their treatment and fail to attend follow-up visits, contributing to the overall management issue. Furthermore, Dr. Logamurthy highlights the surge in COPD cases observed this year, particularly among adults.

It is crucial to recognize that construction activities and vehicular emissions also significantly contribute to the city’s pollution levels, further worsening respiratory conditions. To effectively manage COPD, it is imperative for healthcare providers and society as a whole to prioritize awareness campaigns that emphasize proper treatment protocols and encourage patients to adhere to their prescribed plans.

In conclusion, the alarming rise in COPD cases in Chennai demands urgent action. Only through a collaborative effort that addresses the lack of treatment adherence, dispels myths, and promotes awareness can the city effectively manage this debilitating respiratory disease.

FAQ:

1. What is COPD?
– COPD stands for Chronic Obstructive Pulmonary Disease, which is a group of respiratory conditions that impede airflow and cause breathing difficulties. It includes chronic bronchitis and emphysema.

2. What are the symptoms of COPD?
– Some common symptoms of COPD include chest tightness, fatigue, recurrent respiratory infections, coughing, mucus production, and wheezing.

3. Why is there an increase in COPD cases in urban areas, particularly among women?
– The increase in COPD cases in urban areas, especially among women, can be attributed to factors such as increased air pollution that exacerbates symptoms and a high incidence of smoking, particularly among younger age groups.

4. How can COPD be effectively managed?
– Effective management of COPD involves educating oneself on symptom management, adhering strictly to prescribed treatment plans, understanding the correct usage of inhalers, following doctors’ recommendations, wearing masks, getting vaccinated, and minimizing exposure to air pollution.

5. Why are pulmonologists in Chennai concerned about treatment adherence among COPD patients?
– Many COPD patients in Chennai neglect their treatment and fail to attend follow-up visits, which is a concern for pulmonologists. This lack of adherence contributes to the overall management issue of COPD.

6. How can construction activities and vehicular emissions worsen COPD?
– Construction activities and vehicular emissions significantly contribute to the pollution levels in Chennai, which can further worsen respiratory conditions, including COPD.

Definitions:

– Chronic Obstructive Pulmonary Disease (COPD): A group of respiratory conditions, including chronic bronchitis and emphysema, that impede airflow and cause breathing difficulties.

– Inhalers: Devices used to deliver medication directly into the lungs to alleviate breathing difficulties and manage respiratory conditions like COPD.

– Pulmonologists: Doctors who specialize in diagnosing and treating conditions related to the respiratory system, including COPD.

Related Links:
COPD Foundation
National Heart, Lung, and Blood Institute – COPD

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Medicines

Consultation Closes 29 Feb

What we’re proposing 

We’re seeking feedback on a proposal to fund three new treatments and widen access to two others, through a provisional agreement with GlaxoSmithKline New Zealand Limited (GSK).

The proposal would result in three new treatments being funded from 1 May 2024:

The proposal would also result in widened access for two currently funded treatments:

The provisional agreement with GSK also includes amendments to the contractual terms for vilanterol with umeclidinium dual therapy inhaler (brand name Anoro Ellipta), currently funded for COPD, dolutegravir (brand name Tivicay) funded for HIV and lamotrigine (brand name Lamictal), used for the treatment of epilepsy and mood disorders.

Consultation closes at 4pm Thursday 29th February. Feedback can be emailed to [email protected]

Niraparib for gynaecological cancers

What would the effect be? 

From 1 May 2024 niraparib capsules (branded as Zejula) would be funded for first-line and second line maintenance treatment of advanced, high-grade, platinum sensitive ovarian, fallopian tube or primary peritoneal cancer, subject to eligibility criteria. Niraparib would be funded for all people who meet eligibility criteria, irrespective of BReast CAncer (BRCA) gene mutational status or homologous recombination deficiency (HRD).

We anticipate that up to 111 people would benefit from niraparib in the first year of funding, increasing to 116 people per year by year 5.

Who we think will be interested

  • People with gynaecological cancers, their whānau, friends and caregivers
  • Healthcare professionals involved in the care of people with gynaecological cancers
  • Te Whatu Ora hospitals and other organisations who deliver services and support for people, and their whānau who are affected by gynaecological cancers
  • People or groups with an interest in treatments for gynaecological cancers
  • Pharmacies and wholesalers
  • Pharmaceutical suppliers of cancer treatments

About gynaecological cancers and niraparib (branded as Zejula)

Gynaecological cancers are a type of cancer that affects the female reproductive system. Ovarian cancer is the second most common gynaecological cancer in New Zealand after endometrial cancer. Around 370 people are diagnosed with ovarian cancer per year. Fallopian tube and primary peritoneal cancer are less common.

Ovarian cancer is associated with poor health outcomes and high mortality. Māori and Pacific people experience higher incidence of ovarian cancer, with worse outcomes compared with non-Māori, non-Pacific people. Pacific people are more likely to be impacted by ovarian cancer compared to other ethnicities.

Niraparib is a targeted oral cancer medicine. It targets a protein found in cells called Poly (ADP-ribose) polymerase (PARP). PARP helps damaged cells to repair themselves. Niraparib stops PARP from repairing cancer cells, so the cancer cells die.

Niraparib is used as a maintenance treatment for people with gynaecological cancers who have responded to chemotherapy. This means that people take it for an extended period after they have received treatment for their cancer to prevent its return. Niraparib has been shown to reduce the likelihood of progression and would likely improve survival in people with these cancers. It is taken at home as a once-daily capsule.

More information about niraparib dosing and administration is available from the Medsafe datasheet.(external link)

Another PARP inhibitor called olaparib is currently funded, however it is funded subject to eligibility criteria(external link) restricting use to people who have a particular gene mutation called a BRCA mutation. The funding of niraparib would not require testing to confirm mutational gene status.

Why we’re proposing this

Niraparib was considered by the Cancer Treatments Advisory Committee (CTAC) in July 2021 [PDF, 533 KB]. Our advisors recommended that niraparib be funded as a first and second line maintenance treatment for three gynaecological cancers irrespective of mutation status with a medium priority.

While consideration was also given to those with BRCA mutated or HRD status, we are proposing to fund niraparib irrespective of mutation status. Our advisors have told us that people without BRCA or HRD mutations are still likely to benefit from this treatment and that this would help improve equitable access to treatment.

Full details of the clinical advice we have received is available from the Application Tracker(external link)

Details about our proposal

Niraparib would be listed in Section B and Part II of Section H of the Pharmaceutical Schedule from 1 May 2024 at the following price and subsidy (ex-manufacturer, excluding GST):

Chemical

Brand

Formulation

Pack size

Proposed price and subsidy

Niraparib

Zejula

Cap 100 mg

56

$8,929.84

Niraparib

Zejula

Cap 100 mg

84

$13,393.50

A confidential rebate would apply to Zejula that would reduce the net price and it would have protection from delisting and subsidy reduction until 30 June 2028.

We’re proposing that community pharmacies are able to claim wastage for any capsules that are not dispensed.

Niraparib would be listed in Section B of the Pharmaceutical Schedule subject to the following eligibility criteria:

Special Authority for Subsidy

Initial application from any relevant practitioner. Approvals valid for 6 months for applications meeting the following criteria:

All of the following:

  1. Patient has advanced high-grade serous* epithelial ovarian, fallopian tube, or primary peritoneal cancer; and
  2. Patient has received one line** of previous treatment with platinum-based chemotherapy; and
  3. Patient has experienced a partial or complete response to the previous treatment with platinum-based chemotherapy; and
  4. Patient has not previously received funded treatment with a PARP inhibitor; and
  5. Treatment will be commenced within 12 weeks of the patient’s last dose of the immediately preceding platinum-based regimen; and
  6. Treatment to be administered as maintenance treatment; and
  7. Treatment not to be administered in combination with other chemotherapy.

Renewal from any relevant practitioner. Approvals valid for 6 months for applications meeting the following criteria:

All of the following:

Notes:

* “high-grade serous” includes tumours with high-grade serous features or a high-grade serous component.

**A line of chemotherapy treatment is considered to comprise a known standard therapeutic chemotherapy regimen and supportive treatments.

Similar eligibility criteria would also apply in Part II of Section H of the Pharmaceutical Schedule.  

Fluticasone furoate with umeclidinium and vilanterol for chronic obstructive pulmonary disease (COPD)

What would the effect be?

From 1 May 2024 the single inhaler triple-therapy (inhaled corticosteroid/long-acting muscarinic antagonist/long-acting beta agonist [ICS/LAMA/LABA]), fluticasone furoate with umeclidinium and vilanterol inhaler (branded as Trelegy Ellipta) would be funded for the treatment of moderate to severe chronic obstructive pulmonary disease (COPD).

We estimate that around 15,000 people would benefit from this inhaler in the first year of funding, and that this would increase to over 30,000 people after five years.

People can already receive the ICS/LABA/LAMA combination therapy from more than one inhaler. Funding this triple therapy combination in a single inhaler would mean people only need to use one inhaler instead of two or three. We expect this to reduce barriers for people to access treatment for their COPD.

Who we think will be interested

  • People with COPD, their whānau and friends
  • Healthcare professionals involved in the care of people with COPD
  • Te Whatu Ora hospitals and other organisations who deliver services and support for people with COPD
  • People or groups with an interest in treatments for COPD
  • Pharmacies and wholesalers
  • Pharmaceutical suppliers of respiratory treatments

About COPD and fluticasone furoate/umeclidinium/vilanterol (branded as Trelegy Ellipta)

COPD is a common lung disease that causes breathing problems. It is also known as emphysema and chronic bronchitis. COPD results from a blockage or damage to the lungs that causes restricted airflow, coughing, wheezing, breathing problems, and tiredness. Medicines for COPD work by opening and reducing swelling in the airways.

COPD is estimated to affect 15% of all New Zealanders aged over 45 years. It is the fourth leading cause of death in New Zealand behind cancer, heart disease and stroke. COPD is permanent, disabling and frequently progressive.

Respiratory health (Romaha Ora) is one of Pharmac’s Māori health areas of focus (Hauora Arotahi). The health burden of COPD is one of the most significant sources of healthcare disparity in New Zealand. Māori and Pacific peoples are more likely to experience and are more severely impacted by COPD compared to other ethnicities. Amongst New Zealanders aged 50 – 64 years, Māori are approximately five times more likely to die from COPD-related causes than non-Māori and are affected by COPD up to 20 years earlier. Māori and Pacific peoples are three to four times more likely to be admitted to hospital for COPD than people in other ethnic groups in New Zealand. *

COPD is more frequent in communities with higher levels of deprivation and higher smoking rates, over 85% of cases of COPD are estimated to be caused by inhalation of tobacco smoke.**

(*) Best Practice Advocacy Centre New Zealand (BPAC). Available from: bpac.org.nz

(**) The Asthma Foundation. COPD in New Zealand. Available from: www.asthmafoundation.org.nz

Trelegy Ellipta is a combination of three medicines in a single inhaler.

  • Fluticasone furoate reduces inflammation and swelling the lungs.
  • Umeclidinium is a bronchodilator that keeps airways open by blocking the tightening of smooth muscle around the airways.
  • Vilanterol is also a bronchodilator that opens airways by relaxing the muscles around the airways in the lungs.

These three chemicals (fluticasone furoate, umeclidinium and vilanterol) and other types of ICS/LAMA/LABA medicines are administered by use of either a single or dual Inhaler. Trelegy Ellipta would be the first funded single inhaler, triple-therapy in New Zealand for COPD.

More information about fluticasone furoate with umeclidinium and vilanterol dosing and administration is available from the Medsafe datasheet(external link).

While fluticasone furoate/umeclidinium/vilanterol is Medsafe approved for the treatment of asthma as well as COPD Pharmac is yet to receive a funding application for this indication. 

Why we’re proposing this

The single inhaler triple-therapy, fluticasone furoate with umeclidinium and vilanterol was considered by the Pharmacology and Therapeutics Advisory Committee (PTAC) in May 2019 and by the Respiratory Advisory Committee in October 2020. PTAC and the Respiratory Advisory Committee both recommended that it be funded only if it was cost-neutral to the pricing of the same components received from multiple inhalers (fluticasone furoate/vilanterol trifenatate 100/25mg [Breo Ellipta] in combination with umeclidinium 62.5mg [Incruse Ellipta]), within the context of treatment of respiratory disease.

In summary, the advice we received was that there was equivalent benefit from multiple inhaler triple therapy to that of triple therapy from a single inhaler. The Committees considered there are, however suitability benefits from combining the treatment in a single inhaler. This may include better adherence to treatment, easier to use regimen (once daily), and reduced chances of errors when administering compared to triple therapy from multiple inhalers.

Funding a triple therapy single inhaler may also be equity enhancing by reducing barriers for people to access treatment with multiple single inhalers. The need to dispose of less inhalers and use less propellant could also reduce the impact on the environment.

Full details about the clinical advice we have received, and its status over time, is available in the Application Tracker(external link).

The application has been ranked on our Options for Investment list since June 2019. We are pleased to have now reached a provisional commercial agreement with the supplier to progress it.

Details about our proposal

Chemical

Brand

Formulation

Pack size

Proposed price and subsidy

Fluticasone furoate with umeclidinium and vilanterol

Trelegy Ellipta

100/62.5/25

Powder for inhalation fluticasone furoate 100 mcg with umeclidinium 62.5 mcg and vilanterol 25 mcg

1 inhaler - OP

(30 doses per inhaler)

$104.24

A confidential rebate would apply to Trelegy Ellipta that would reduce the net price and it would have protection from delisting and subsidy reduction until 30 June 2028.

Trelegy Ellipta would be listed in Section B of the Pharmaceutical schedule subject to the following eligibility criteria:

Special Authority for Subsidy

Initial application from any relevant practitioner. Approvals valid without further renewal unless notified for applications meeting the following criteria:

All of the following

Similar eligibility criteria would also apply in Part II of Section H of the Pharmaceutical Schedule.  

Dolutegravir with lamivudine for treatment of Human Immunodeficiency Virus (HIV)

What would the effect be?

From 1 May 2024 dolutegravir with lamivudine combination tablets (branded as Dovato) would be funded for people with HIV, subject to the existing eligibility criteria(external link) for HIV treatments.

We anticipate that 885 people would use Dovato in place of their current HIV treatment regimens or initiate treatment for HIV using Dovato, increasing to 1,950 people after 5 years. 

Who we think will be interested 

  • People living with HIV, their whānau, friends and caregivers
  • Healthcare professionals involved in the care of people with HIV
  • Te Whatu Ora hospitals and other organisations who deliver services and support for people, and their whānau who are affected by HIV
  • People or groups with an interest in treatments for HIV
  • Pharmacies and wholesalers 

About HIV and dolutegravir with lamivudine (branded as Dovato)

Human immunodeficiency virus (HIV) is a virus that attacks the body’s immune system. If HIV is not treated, it can lead to AIDS (acquired immunodeficiency syndrome). Once a person is diagnosed with HIV, it stays in their system for life – as there is no cure available. However, with treatment people living with HIV can live long, healthy lives.

In New Zealand, inequities in HIV outcomes have been clearly identified. Gay, bisexual and other men who have sex with men (MSM) are the most disproportionately affected by HIV and are 348 times more likely to be diagnosed with HIV than the heterosexual population. There are further and intersecting inequities within this population group. Māori and Pacific gay, bisexual and other MSM are no more likely to be living with HIV than non-Māori gay, bisexual and other MSM, however, they are more than twice as likely to be diagnosed late and present with advanced HIV. *

(*) Saxton et al 2022(external link); pubmed.ncbi.nlm.nih.gov/34479989/(external link)

Dovato is a tablet which is a combination of two antiretroviral medicines, dolutegravir and lamivudine. Antiretrovirals work by stopping the virus replicating in the body, allowing the immune system to repair itself and preventing further damage. However, if treatment is interrupted the virus will return.

Both medicines which make up Dovato are currently funded for treatment of HIV as separate tablets which are each taken 1-2 times per day. Dovato combines the two medicines into a single, once per day HIV treatment.

More information about dosing and administration of dolutegravir with lamivudine for HIV infection is available from the Medsafe datasheet(external link). 

Why we’re proposing this 

The dolutegravir/lamivudine combination tablet, Dovato, was considered by the Anti-infective Advisory Committee in September 2022. The Committee recommended it be funded only if cost-neutral to the cost of other funded HIV medicine regimens.

Our clinical advisors have told us that Dovato is clinically equivalent to currently funded treatment regimens, but that it would be more convenient for people than receiving multi-tablet treatment regimens and it may help people better manage their HIV over time.

Advocacy groups for people living with HIV have highlighted that a crucial part of improving the lives of people living with HIV is reducing the stigma associated with the disease. Simplifying treatment as much as possible to allow people to receive effective treatment with minimal impact on their day to day lives would contribute to this endeavour.

Full details about the clinical advice we have received, and its status over time, is available in the Application Tracker(external link).

The application has been ranked on our Options for Investment list since January 2024. We are pleased to have now reached a provisional commercial agreement with the supplier to progress it.

Details about our proposal 

Dolutegravir with lamivudine would be listed in Section B and Part II of Section H of the Pharmaceutical Schedule from 1 May 2024 at the following price and subsidy (ex-manufacturer, excluding GST):

Chemical

Brand

Formulation

Pack size

Proposed price and subsidy

Dolutegravir with lamivudine

Dovato 50/300

Tab dolutegravir 50 mg with lamivudine 300 mg

30

$1,090.00

A confidential rebate would apply to Dovato that would reduce the net price and it would have protection from delisting and subsidy reduction until 30 June 2028.

Dovato would be listed in section B subject to the existing antiretrovirals eligibility criteria(external link) and in Part II of Section H.

Mepolizumab for treatment of relapsed or refractory eosinophilic granulomatosis with polyangiitis (EGPA)

What would the effect be?

From 1 May 2024 access to mepolizumab (branded as Nucala) would be widened to include people with eosinophilic granulomatosis with polyangiitis (EGPA), a rare condition severely affecting small blood vessels.

We expect up to 15 people in New Zealand would be able to receive mepolizumab for EGPA in the first year increasing to 23 by year 5.

Who we think will be interested

  • People with EGPA, their whānau and friends
  • Healthcare professionals involved in the care of people with EGPA
  • Te Whatu Ora hospitals and other organisations who deliver services and support for people with EGPA
  • People or groups with an interest in treatments for EGPA
  • Pharmacies and wholesalers
  • Pharmaceutical suppliers of respiratory treatments

About EGPA and mepolizumab (branded as Nucala)

EGPA is a rare disease, formerly called Churg-Strauss syndrome. It is a form of vasculitis, characterised by inflammation of the blood vessels, which can restrict blood flow and damage vital organs and tissues.

We are unsure of the relative incidence and outcomes of EGPA on Māori and Pacific peoples.

Mepolizumab, currently funded for the treatment of severe eosinophilic asthma is a monoclonal antibody against a protein called interleukin-5 (IL-5). By blocking the action of IL-5 mepolizumab helps reduce the activity of specialised white blood cells called eosinophils.  

Mepolizumab is Medsafe approved for treatment to manage symptoms in patients aged 18 years and older that have EGPA. It is available as prefilled pen and is administered by subcutaneous injection every 4 weeks at a dose of 300 mg per 4 weeks. More information about dosing and administration of mepolizumab for EGPA is available from the Medsafe datasheet(external link).

Why we’re proposing this

Mepolizumab for the treatment of eosinophilic granulomatosis with polyangiitis (EGPA) was considered by the Respiratory Advisory Committee in April 2022. The Committee recommended it be funded with a high priority. Our clinical advisors told us there is a high health need for those people with relapsed or refractory EGPA. There is strong evidence of a benefit in using mepolizumab to sustain remission, in turn improving symptom-related quality of life, reducing the risk of organ damage and improve survival.

Full details about the clinical advice we have received, and its status over time, is available in the Application Tracker(external link).

Details about our proposal 

The eligibility criteria(external link) for mepolizumab (Nucala) inj 100 mg prefilled pen in Section B of the Pharmaceutical Schedule would be amended from 1 May 2024 to include the following indication:

Special Authority for Subsidy

Initial application – (eosinophilic granulomatosis with polyangiitis) from any relevant specialist or any relevant practitioner on the recommendation of a relevant specialist. Approvals valid for 12 months for applications meeting the following criteria:

All of the following:

  1. The patient has eosinophilic granulomatosis with polyangiitis; and
  2. The patient has trialled and not received adequate benefit from at least one of the following: azathioprine, cyclophosphamide, leflunomide, methotrexate, mycophenolate, or rituximab at maximum tolerated dose for at least three months (unless contraindicated to all); and
  3. Either:

Renewal application – (eosinophilic granulomatosis with polyangiitis) from any relevant specialist or any relevant practitioner on the recommendation of a relevant specialist.  Approvals valid for 12 months where patient has no evidence of clinical disease progression.

Similar eligibility criteria would also apply in Part II of Section H of the Pharmaceutical Schedule. 

Recombinant varicella zoster virus vaccine for the prevention of shingles in immunocompromised people

What would the effect be? 

From 1 July 2024 access to the recombinant varicella zoster virus vaccine (branded as Shingrix) for the prevention of shingles would be widened to include immunocompromised people 18 years or older with the following illnesses:

  • People who are pre- or post- haematopoietic stem cell transplant
  • People who have had a solid organ transplant
  • People with haematological malignancies
  • People living with poorly controlled HIV infection
  • People who are planned to or are receiving disease modifying anti-rheumatic drugs (DMARDs) for:
    • systemic lupus erythematosus
    • polymyalgia rheumatica
    • rheumatoid arthritis
  • People with end stage kidney disease (CKD 4 or 5)
  • People with primary immunodeficiency

There would be no other changes to age eligibility criteria for Shingrix at this time, meaning that it would remain funded for all other people aged 65 years.

We expect approximately 15,000 immunocompromised people would benefit from the shingles vaccine in the first two years as a result of this proposal and another 2000 people every year after that to a total of 21,000 after 5 years.

Who we think will be interested

  • Immunocompromised people, their whānau and friends
  • Healthcare professionals involved in the delivery of vaccines and the care of immunocompromised people
  • Te Whatu Ora hospitals and other organisations who deliver services and support for immunocompromised people
  • People or groups with an interest in treatments for Shingles
  • Pharmacies and wholesalers
  • Suppliers of vaccines

About shingles and recombinant varicella zoster virus vaccine (branded as Shingrix)

Herpes zoster, commonly known as shingles, is a painful blistering rash caused by the same virus that causes chickenpox. Anyone who has previously had chickenpox may subsequently develop shingles or post-herpetic neuralgia (prolonged nerve pain in the rash area) from reactivation of the virus later in life. Shingles is more common and more severe in people with poor immunity and the elderly.

One in every three people can expect to suffer at least one attack of shingles in their lifetime. Particularly for older people, shingles and post-herpetic neuralgia can be very painful, prolonged and debilitating and may affect their ability to carry out simple daily activities, such as dressing and bathing.

Shingrix is a recombinant vaccine indicated for the prevention of herpes zoster (shingles) and post-herpetic neuralgia. Recombinant vaccines use small proteins from of the virus or bacteria they are intended to protect against instead of the whole live attenuated or inactivated organisms in some vaccines.

More information about Shingrix is available from the Medsafe datasheet(external link).

Zoster vaccine (Shingrix) is currently funded for people who are 65 years of age. Shingrix requires two doses given 6 months apart. Both doses are funded if the person being vaccinated is 65 when they receive their first dose.

Why we’re proposing this

The Immunisation Advisory Committee considered Shingrix for people who are immunocompromised at its May 2022 and November 2023 meetings (November 2023 record not yet published). Our clinical advisors have told us that the Shingrix vaccine is a safe and effective treatment for preventing shingles and recommended that access should be widened to specific groups of immunocompromised people. They have told us that people who are immunocompromised are at much greater risk of shingles and its complications. They also told us that Shingrix is much better at preventing the complications of shingles than the current antiviral treatments available once the disease has begun.

People who receive the shingles vaccine have substantially lower rates of shingles and complications from the disease once acquired. As a recombinant vaccine, Shingrix can also be given to immunocompromised people where a live-attenuated vaccine is not suitable. Prevention of shingles cases also reduces the number of consultations required by community health nurses and general practitioners reducing the pressure on front-line healthcare services.

The Committee considered the impact that shingles may have on Māori and Pacific peoples and their whānau may be disproportionally greater compared to non-Māori, non-Pacific peoples due to the well documented barriers experienced by Māori within the healthcare system.

Full details about the clinical advice we have received for this application, and its status over time, is available in the Application Tracker.(external link)

We have received a number of funding applications for wider funding of the shingles vaccine. the status of each application can be viewed on our Application Tracker(external link):

Details about our proposal

The eligibility criteria for varicella zoster vaccine [shingles vaccine] inj 50 mcg per 0.5 ml vial plus vial in Section I(external link) and Part II of Section H of the Pharmaceutical Schedule would be amended as follows (additions in bold and deletions in strikethrough):

VARICELLA ZOSTER VACCINE [SHINGLES VACCINE]

a) Only on a prescription

b) No patient co-payment payable

c)

A) Funded for patients meeting the following criteria:

1) Two doses for all people aged 65 years

Either:

  1. Two doses for all people aged 65 years; or
  2. Two doses for people 18 years of age or older with any of the following:
    1. pre- or post-haematopoietic stem cell transplant; or
    2. solid organ transplant; or
    3. haematological malignancies; or
    4. people living with poorly controlled HIV infection; or
    5. planned or receiving disease modifying anti-rheumatic drugs (DMARDs) for polymyalgia rheumatica, systemic lupus erythematosus or rheumatoid arthritis; or
    6. end stage kidney disease (CKD 4 or 5); or
    7. primary immunodeficiency

B) Contractors will be entitled to claim payment from the Funder for the supply of Varicella zoster vaccine (Shingles vaccine) to patients eligible under the above criteria pursuant to their contract with Te Whatu Ora Health New Zealand for subsidised immunisation, and they may only do so in respect of the Varicella zoster vaccine [Shingles vaccine] listed in the Pharmaceutical Schedule.

C) Contractors may only claim for patient populations within the criteria that are covered by their contract, which may be a sub-set of the population described in paragraph A above.

A confidential rebate would apply to Shingrix that would reduce the net price and it would have protection from delisting and subsidy reduction until 30 June 2027. 

Other contractual changes associated with this proposal

Dolutegravir

Dolutegravir (Tivicay) is funded for the treatment of HIV subject to eligibility criteria(external link). There would be no changes to the list price and subsidy, or current eligibility criteria for Tivicay as part of this proposal.

As part of the proposal, the net price for Tivicay would reduce via confidential rebate from 1 May 2024 and there would be subsidy and delisting protection for Tivicay until 30 April 2027. 

Umeclidinium/vilanterol

Umeclidinium/vilanterol (Anoro Ellipta) is funded for COPD subject to eligibility criteria(external link). There would be no changes to the list price and subsidy, or current eligibility criteria for Anoro Ellipta as part of this proposal.

As part of the proposal, the net price for Anoro would reduce via confidential rebate from 1 May 2024 and there would be subsidy and delisting protection for Anoro until 30 April 2027. 

Lamotrigine

There would be no changes to the list price and subsidy for the 2 mg and 5 mg strengths of lamotrigine (brand name Lamictal). As part of the proposal, the net price for Lamictal would reduce via confidential rebate from 1 May 2024. The net price of other strengths of the Lamictal brand lamotrigine accessed via Pharmac’s exceptional circumstances framework would also reduce via confidential rebate. 

To provide feedback 

Send us an email: [email protected] by 4pm Thursday 29th February

All feedback received before the closing date will be considered by Pharmac’s Board (or its delegate) prior to making a decision on this proposal. 

Your feedback may be shared

Feedback we receive is subject to the Official Information Act 1982 (OIA). Please be aware that we may need to share your feedback, including your identity, in response to an OIA request. This applies to anyone providing feedback, whether they are providing feedback themselves or for an organisation, in a personal or professional capacity.

We can only keep feedback confidential as allowed under the OIA and other related laws. If you want any part of your feedback treated as confidential, you need to tell us. Please let us know if you want to keep part of your feedback confidential, and why. Is it commercially sensitive, confidential or proprietary, or personal information? Clearly state this and tell us which parts of your feedback you want to keep confidential for these reasons. We will consider your request under our OIA requirements.

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A range of reproductive factors, including age when periods first start and an early menopause, are all linked to a heightened risk of COPD—the umbrella term for progressive lung conditions that cause breathing difficulties—finds research published online in the journal Thorax.

Miscarriage, stillbirth, infertility, and having 3 or more children are also associated with a heightened risk of COPD, which includes emphysema and chronic bronchitis, the findings show.

Recent evidence indicates substantial gender  differences in susceptibility to, and severity of, COPD, note the researchers. Women seem to develop severe COPD at younger ages than men. And while smoking is a major risk factor, non-smokers with COPD are more likely to be women, they add.

Previously published studies looking at the potential influence of female hormones on COPD risk have been hampered by methodological flaws, note the researchers. To try and get round these issues, they drew on the International Collaboration for a Life Course Approach to Reproductive Health and Chronic Disease Events (InterLACE) consortium.

This is a collection of 27 observational studies, pooling individual level data from more than 850,000 women in 12 countries.

For the purposes of the current study, the researchers included three groups of women (283,070; average age 54) with data on reproductive factors and COPD: the Australian Longitudinal Study on Women's Health 1946-51 (ALSWH-mid); the UK Biobank; and the Swedish Women's Lifestyle and Health Study (WLH).

In the ALSWH-mid and UK Biobank groups, women were tracked until the end of December 2019. Women in WLH were tracked up to the end of 2010.

Information on reproductive factors was collected at study entry or at subsequent data collection points, along with potentially influential factors: birth year (before or after 1950), ethnicity, educational level, duration of smoking, asthma (never and ever), and weight (BMI).

COPD was retrospectively and prospectively identified through self-report and medical records, which included prescriptions, hospital admissions, emergency care visits, and death registry data.

The women's health was monitored for an average of 11 years. During this time, 10,737 (4%) women developed COPD at an average age of 63. 

Women with COPD were more likely to be older when recruited to their studies, to have fewer than 10 years of formal education, to be obese, to have smoked for at least 10 years, and to have asthma-all risk factors for the condition. Some 53, 205 (16%) women were excluded because of missing data.

Several reproductive factors were associated with the risk of COPD, including age when periods first started; number of children; a history of infertility, miscarriage or stillbirth, especially multiple miscarriages or stillbirths; and age at menopause.

A U-shaped pattern emerged for the age at which periods first started. Those who began menstruating before or at the age of 11 were 17% more likely to develop COPD than those who did so at the age of 13; after the age of 16, the risk was 24% higher.

Women with children were at higher risk of COPD than childless women. Compared with having 2 children, more than 3 was associated with a 34% higher risk, while women with one child were at 18% higher risk.

Women who experienced infertility also had a 13% higher risk of COPD than women who were fertile. 

And among those who had ever been pregnant, a history of miscarriage was associated with a 15% higher risk of COPD, with the risk rising in tandem with the number of miscarriages: 28% higher for 2; and 36% higher for 3 or more.

Similarly, stillbirth was associated with a 42% overall higher risk of COPD, with the risk rising in tandem with the number of stillbirths.

Menopause before the age of 40 was associated with a 69% higher risk, compared with those experiencing it naturally at the age of 50-51, while the risk was 21% lower for those who went through it at or after the age of 54.

This is an observational study, so can't establish cause, and the researchers acknowledge various limitations to their findings, including potentially influential factors. 

For example, they had no detailed information on hormonal contraception and HRT use, and data on parental history of COPD, childhood respiratory infections, secondhand smoking or occupational exposures, weren't available for all 3 of the groups. 

But by way of an explanation for their findings, they suggest that the female hormone estrogen is likely to have a key role in COPD risk in women, because of its various effects on the lung. 

"The overall effect of estrogen might differ depending on the timing," they suggest. "In the early or middle reproductive stage, long or higher accumulated exposure to estrogen would be detrimental to the lung, leading to a higher risk of COPD among women with early menarche or multiple live births. 

"In the later stage, estrogen may be protective, since earlier age at menopause or [ovary removal] (indicates shorter exposure to estrogen) were associated with a higher risk of COPD." 

Other factors, including autoimmune disease, such as type 1 diabetes, and social and environmental factors, such as air pollution, underweight, and socioeconomic deprivation, might also be influential, they add.

Source:

Journal reference:

Liang, C., et al. (2024). Female reproductive histories and the risk of chronic obstructive pulmonary disease. Thorax. doi.org/10.1136/thorax-2023-220388.

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Sydney: The early onset of periods and early menopause can be linked to a heightened risk of Chronic Obstructive Pulmonary Disease (COPD) -- the umbrella term for progressive lung conditions that cause breathing difficulties -- according to a study.

Those who began menstruating before or at the age of 11 were 17 per cent more likely to develop COPD than those who did so at the age of 13; after the age of 16, the risk was 24 per cent higher, said the team from University of Queensland in Australia.

Menopause before the age of 40 was associated with a 69 per cent higher risk compared with those experiencing it naturally at the age of 50-51, while the risk was 21 per cent lower for those who went through it at or after the age of 54, said the team.

Further, the study published in the journal Thorax showed that women with children were at higher risk of COPD than childless women.

Compared with having two children, more than three was associated with a 34 per cent higher risk, while women with one child were at 18 per cent higher risk.

A history of miscarriage was associated with a 15 per cent higher risk of COPD, with the risk rising in tandem with the number of miscarriages: 28 per cent higher for two and 36 per cent higher for three or more.

Stillbirth (42 per cent), infertility (13 per cent) were also associated with a heightened risk of COPD, which includes emphysema and chronic bronchitis.

Women also seem to develop severe COPD at younger ages than men. And while smoking is a major risk factor, non-smokers with COPD are more likely to be women, the study noted.

“This is an observational study, so can't establish the cause,” said the researchers while acknowledging various limitations to their findings, including potentially influential factors like zero information on hormonal contraception and use of hormone replacement therapy.

The researchers believe that the female hormone oestrogen is likely to have a key role in COPD risk in women, because of its various effects on the lung. "The overall effect of oestrogen might differ depending on the timing," they suggest.

"In the early or middle reproductive stage, long or higher accumulated exposure to oestrogen would be detrimental to the lung, leading to a higher risk of COPD among women with early menarche or multiple live births.

"In the later stage, oestrogen may be protective, since earlier age at menopause or ovary removal (indicates shorter exposure to oestrogen) were associated with a higher risk of COPD."

Other factors, including autoimmune diseases, such as type 1 Diabetes, and social and environmental factors, such as air pollution, underweight, and socioeconomic deprivation, might also be influential, they added.

For the study, the team examined a collection of 27 observational studies, pooling individual-level data from more than 850,000 women in 12 countries. The women's health was monitored for an average of 11 years. During this time, 10,737 (4 per cent) women developed COPD at an average age of 63.

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We've all been told that smoking can increase our risk of lung disease. But new research shows that our reproductive hormones may also play a role, particularly if you're a woman.

Chronic obstructive pulmonary disease, or COPD, refers to a group of diseases that cause airflow blockage and other problems related to breathing, including emphysema and chronic bronchitis. According to the U.S. Centers for Disease Control and Prevention, 16 million Americans live with COPD, with significantly more women being affected than men.

Specifically, women tend to develop severe COPD at younger ages than men, and non-smoking related cases of COPD are more likely to be found in women. This has led researchers to believe that female hormones may have some role in the discrepancy but, until recently, previous research into this area has been limited.

However, in a new study, published in the journal Thorax, researchers from the University of Queensland have used 27 observational studies to pool data from more than 850,000 women in 12 countries to examine the potential links between various reproductive factors and the development of COPD.

Period tracker
Stock image. Various reproductive factors have been linked to an increased risk of COPD, including early onset and late onset periods.

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The women's health was monitored for an average of 11 years across all studies, during which 10,737 individuals developed COPD. And these cases appeared to be associated with the women's reproductive health.

To start, the age at which the women had started their periods was a significant predictor of their risk of developing COPD. This followed a U-shaped curve, with both early and late periods coming with an increased risk of COPD. Those who started menstruating at or before the age of 11 were 17 percent more likely to develop COPD, while those who started menstruating after the age of 16 saw a 24 percent higher risk.

Women with children were significantly more likely to develop the disease than those without, as were those who had experienced infertility or miscarriage.

Early-onset menopause (before the age of 40) was also associated with a 69 percent higher risk of COPD compared with those experiencing menopause between 50 and 51. By contrast, those who went through menopause at or after the age of 54 saw a 21 percent lower risk of developing the condition.

"The overall effect of estrogen might differ depending on the timing," the authors write to explain their results. "In the early or middle reproductive stage, long or higher accumulated exposure to estrogen would be detrimental to the lung, leading to a higher risk of COPD among women with early menarche or multiple live births.

"In the later stage, estrogen may be protective, since earlier age at menopause or [ovary removal] (indicates shorter exposure to estrogen) were associated with a higher risk of COPD."

However, while the pool of participants is large, these findings are purely observational and do not prove that estrogen exposure can cause COPD. Moreover, the authors point to various other factors—such as autoimmune disease, air pollution, and being underweight—that could also increase COPD risk.

While more research is needed to confirm these links, the study shines a light on how reproductive histories can affect our overall health, and offers new insights to medical professionals to support women's health.