Respiratory Disease Smoking-Related Disease

name	description	evidence
Chronic Bronchitis	Inflammation of the bronchial tubes leading to increased mucus production and chronic cough.	TRUNCATED
Emphysema	Damage to the alveoli resulting in shortness of breath and reduced surface area for gas exchange.	TRUNCATED

0

population

Global

percentage

11.7

evidence

reference	supports	snippet	explanation
PMID:35261410	NO_EVIDENCE	The estimated pooled prevalence of COPD was 11.1% (95% confidence interval, CI: 7.4-14.8%), using the Global Initiative for Chronic Obstructive Lung Disease fixed criteria and 8.0% (95% CI: 5.6-10.4%) using the lower limit of normal criteria.	The study provides prevalence data for specific regions (e.g., South Asia) but does not mention a global prevalence rate of 11.7%.
PMID:37461046	NO_EVIDENCE	Though disease burden of silicosis has been on a decline in general from 1990 to 2019, which shows a promising prospect but cannot be ignored.	This study focuses on the global incidence, prevalence, and disease burden of silicosis, not COPD.
PMID:26525374	NO_EVIDENCE	Current epidemiologic practice evaluates COPD based on self-reported symptoms of chronic bronchitis, self-reported physician-diagnosed COPD, spirometry confirmed airflow obstruction, or emphysema diagnosed by volumetric computed chest tomography (CT).	The abstract discusses epidemiologic practices for diagnosing COPD but does not provide global prevalence data.

0

phase

Onset

evidence

reference	supports	snippet	explanation
PMID:26154786	PARTIAL	Among 657 persons who had an FEV1 of less than 80% of the predicted value before 40 years of age, 174 (26%) had COPD after 22 years of observation, whereas among 2207 persons who had a baseline FEV1 of at least 80% of the predicted value before 40 years of age, 158 (7%) had COPD after 22 years of observation.	The literature suggests that COPD can develop in individuals with low FEV1 before the age of 40. While this supports the idea that COPD typically begins in individuals over 40, it also indicates that it can start earlier in some cases.
PMID:19934351	SUPPORT	There is growing evidence of higher prevalence of chronic obstructive pulmonary disease (COPD) in the elderly. Age-associated changes in the structure and function of the lung may increase a pathogenetic susceptibility to COPD.	This reference supports the statement that COPD typically begins in individuals over the age of 40, particularly due to age-associated changes in lung structure and function.

notes

Typically begins in individuals over the age of 40.

0

name

Airflow Limitation

description

Obstruction of airflow due to inflammation, mucus build-up, and remodeling of the airways.

cell_types

• Epithelial Cell

evidence

reference	supports	snippet	explanation
PMID:15325838	SUPPORT	Processes contributing to obstruction in the small conducting airways include disruption of the epithelial barrier, interference with mucociliary clearance apparatus, accumulation of inflammatory mucous exudates in the small airway lumen, and infiltration of the airway walls by inflammatory cells.	This study outlines how epithelial barrier disruption, mucus accumulation, and airway remodeling contribute to airflow obstruction in COPD.
PMID:23204254	SUPPORT	Chronic bronchitis (CB) is caused by overproduction and hypersecretion of mucus by goblet cells, leading to worsening airflow obstruction by luminal obstruction of small airways, epithelial remodeling, and alteration of airway surface tension predisposing to collapse.	This study describes how mucus build-up and epithelial remodeling lead to airflow obstruction in COPD.
PMID:36108172	PARTIAL	Phenotypic alterations in the lung epithelium have been widely implicated in chronic obstructive pulmonary disease (COPD) pathogenesis, but the precise mechanisms orchestrating this persistent inflammatory process remain unknown.	This study notes the involvement of epithelial cells in COPD but states that mechanisms remain unknown, partially supporting the role of epithelial cells in airflow obstruction.
PMID:38625125	SUPPORT	Chronic exposure to environmental hazards causes airway epithelial dysfunction, primarily impaired physical barriers, immune dysfunction, and repair or regeneration. Impairment of airway epithelial function subsequently leads to exaggerated airway inflammation and remodeling, the main features of chronic obstructive pulmonary disease (COPD).	This study supports the statement by highlighting the role of epithelial dysfunction, inflammation, and remodeling in COPD pathophysiology.

1

name

Chronic Inflammation

description

Persistent irritation from inhaled substances like cigarette smoke leads to airway and alveolar inflammation.

cell_types

• Neutrophil
• Macrophage
• T-lymphocyte

evidence

reference	supports	snippet	explanation
PMID:17305517	SUPPORT	Neutrophils and macrophages have been implicated in this process; they release proteolytic enzymes and generate oxidants, which cause tissue damage, as well as cytokines and chemokines, which can potentiate inflammation and trigger an immune response.	The literature describes the involvement of neutrophils, macrophages, and T-lymphocytes in the inflammatory process associated with COPD, supporting the notion of persistent irritation and chronic inflammation.
PMID:24507838	SUPPORT	This inflammation is characterized by increased numbers of alveolar macrophages, neutrophils, and T lymphocytes, which are recruited from the circulation.	This article further substantiates the involvement of these cell types (neutrophils, macrophages, and T-lymphocytes) in the pathophysiology of COPD, linking them to chronic inflammation.
PMID:38035712	SUPPORT	In this study, we found that neutrophilic phenotype (NP, 58.0%) was the most common airway inflammation phenotype in patients with COPD, followed by mixed granulocytic phenotype (MGP, 32.6%).	The study indicates that neutrophils are predominant in COPD, supporting the statement about chronic inflammation.
PMID:38891820	SUPPORT	Recent multiomics-based evidence suggests that the plasticity of alveolar macrophages contributes to the onset and progression of COPD through the coordinated modulation of numerous transcription factors.	The article highlights the role of macrophages in the pathogenesis and progression of COPD, thus supporting the statement.
PMID:11993785	PARTIAL	The characteristic changes in the central airways include inflammatory cellular infiltration into the airway wall and mucous gland enlargement.	This reference provides a broader overview of the pathological changes in COPD, mentioning inflammatory cells but not specifically detailing the involvement of neutrophils, macrophages, and T-lymphocytes.

2

name

Airway Remodeling

description

Structural changes in the airway due to chronic inflammation, including fibrosis and increased airway thickness.

cell_types

• Smooth Muscle Cell

evidence

reference	supports	snippet	explanation
PMID:20500603	SUPPORT	Moreover, airway remodelling occurs not only in asthma but also in several pulmonary disorders such as chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis and systemic sclerosis.	The statement aligns with the mentioned literature which notes airway remodeling as part of chronic obstructive pulmonary disease.
PMID:30257694	SUPPORT	Multiple dysfunctions of ASM contribute to modulating airway responses to stimuli, remodeling, and fibrosis, as well as influence the compliance of lungs.	The statement is supported as this literature highlights the role of airway smooth muscle cells in airway remodeling and fibrosis in COPD.
PMID:15347849	SUPPORT	Increases in airway smooth muscle mass occur in large airways of severe asthmatics and in small airways of patients with COPD.	The literature supports the statement by confirming the involvement of smooth muscle cells and structural changes in the airways in COPD.

3

name

Alveolar Destruction

description

Breakdown of alveolar walls, leading to reduced surface area for gas exchange and loss of lung elasticity.

cell_types

• Alveolar Macrophage

evidence

reference	supports	snippet	explanation
PMID:11993785	PARTIAL	In the lung parenchyma, emphysema defined as alveolar destruction and airspace enlargement is present.	While the reference supports alveolar destruction as part of COPD's pathophysiology, it does not mention alveolar macrophages specifically.
PMID:29433833	PARTIAL	In inflammatory lung diseases such as chronic obstructive pulmonary disease (COPD), despite their increased numbers, macrophages demonstrate significantly reduced phagocytic capacity of bacteria and apoptotic cells.	The macrophages' role in the pathophysiology of COPD is discussed, focusing on their reduced phagocytic capacity rather than direct alveolar destruction.
PMID:32493486	PARTIAL	External insults like smoke and pollution can disturb surfactant homeostasis and result in either surfactant insufficiency or accumulation. But disruption of surfactant homeostasis is also observed in many chronic adult diseases, including chronic obstructive pulmonary disease (COPD).	The role of alveolar macrophages (responsible for the degradation of surfactant) in the development of COPD is mentioned, but no direct link to alveolar destruction.
PMID:24707174	PARTIAL	There are eight types of EMPs which are defined by the presence of different endothelial markers on the cell membrane: vascular endothelial-cadherin; platelet endothelial cell adhesion molecule; melanoma cell adhesion molecule; E-selectin; CD51; CD105; von Willebrand factor; and CD143 EMPs.	The reference discusses endothelial injury and microparticles in COPD, which may indirectly relate to alveolar destruction, but does not directly address it or the role of alveolar macrophages.

0

category

Respiratory

name

Dyspnea

frequency

VERY_FREQUENT

diagnostic

True

evidence

reference	supports	snippet	explanation
PMID:28277858	SUPPORT	Indeed, it is an important symptom in chronic obstructive pulmonary disease (COPD), where it is associated with limited physical activity, increased anxiety and depression, decreased health-related quality of life (HRQoL), and reduced survival.	The literature supports that dyspnea is a common symptom in COPD and is frequently observed in patients, confirming its categorization as a respiratory phenotype with diagnostic importance.
PMID:35698999	SUPPORT	Dyspnoea and pain are symptoms of chronic obstructive pulmonary disease (COPD)... The pooled prevalence of pain and dyspnoea was 44% (95% confidence interval (CI) 35%-52%) and 91% (95% CI 87%-94%) respectively.	This study highlights the high prevalence of dyspnea in patients with COPD, further supporting its status as a very frequent respiratory phenotype.
PMID:34972922	SUPPORT	Attempts to connect the products of the analysis of the EBC with the clinical manifestations of COPD such as dyspnea are scarce. Up to date research has shown a positive correlation between the elevated levels of some markers of EBC such as H(2)O(2) and 8-isoprostane and dyspnea, while others present ambiguous results.	The correlation between dyspnea and COPD is reinforced by the positive association found with certain markers in exhaled breath condensate.

1

category

Respiratory

name

Chronic Cough

frequency

VERY_FREQUENT

diagnostic

True

evidence

reference	supports	snippet	explanation
PMID:29881269	SUPPORT	Compared with patients without chronic cough, those with chronic cough exhibited a lower forced expiratory volume in 1 second (% predicted) and diffusing capacity of the lungs for carbon monoxide (% predicted), more frequent AECOPD, more severe dyspnea, and worse QoL.	The study identifies chronic cough as a common and significant phenotype in COPD patients, indicating its very frequent occurrence and diagnostic importance.
PMID:31740261	SUPPORT	COPD is now widely accepted as a heterogeneous condition with multiple phenotypes and endotypes. This review will discuss the old and new concepts for the different types of COPD phenotypes.	The statement mentions the heterogeneity of COPD with multiple phenotypes, which could include phenotypes like chronic cough.

2

category

Respiratory

name

Sputum Production

frequency

VERY_FREQUENT

evidence

reference	supports	snippet	explanation
PMID:22753831	SUPPORT	Chronic cough and sputum production: a clinical COPD phenotype?	The title of the article itself suggests that sputum production is recognized as a phenotype of COPD.
PMID:23204254	SUPPORT	Chronic bronchitis (CB) is a common but variable phenomenon in chronic obstructive pulmonary disease (COPD).	Chronic bronchitis, which involves overproduction and hypersecretion of mucus, is described as a common phenomenon in COPD, indicating sputum production is a frequent COPD phenotype.

name	presence	evidence	notes	context
Arterial Blood Gases	Altered	TRUNCATED	May show hypoxemia and hypercapnia.	None
C-Reactive Protein (CRP)	Elevated	TRUNCATED	None	General inflammation and exacerbations.

0

name

Alpha-1 Antitrypsin (AAT)

evidence

reference	supports	snippet	explanation
PMID:32800189	SUPPORT	Alpha-1 antitrypsin deficiency (AATD) was the first genetic risk factor for chronic obstructive pulmonary disease (COPD) described.	The abstract clearly mentions that AATD is a genetic risk factor for COPD, supporting the statement.
PMID:35104244	SUPPORT	Alpha-1 antitrypsin deficiency (AATD) is the most common genetic cause and risk factor for chronic obstructive pulmonary disease.	The text directly supports the statement by identifying AATD as a common genetic cause and risk factor for COPD.
PMID:36630963	SUPPORT	Genetic variation in alpha-1 antitrypsin (AAT) causes AAT deficiency (AATD) through liver aggregation-associated gain-of-toxic pathology and/or insufficient AAT activity in the lung manifesting as chronic obstructive pulmonary disease (COPD).	The abstract highlights that genetic variation in AAT leading to AATD manifests as COPD, thus supporting the statement.

association

Deficiency is a genetic risk factor.

0

name

Smoking

evidence

reference	supports	snippet	explanation
PMID:30810540	SUPPORT	Although cigarette smoking is the major risk factor, only 10-20% of smokers develop COPD.	This clearly identifies smoking as a major risk factor for COPD development.
PMID:31759959	SUPPORT	The observation that COPD is an independent risk factor for cardiovascular disease (CVDs) comes from comparisons between smokers with COPD and smokers without COPD.	This snippet highlights the relationship between smoking, COPD, and other health issues, indirectly supporting smoking as a risk factor for COPD.
PMID:28933915	SUPPORT	The epithelial lining of the airway forms the first barrier against environmental insults, such as inhaled cigarette smoke, which is the primary risk factor for the development of chronic obstructive pulmonary disease (COPD).	Directly states that cigarette smoke is the primary risk factor for COPD development.
PMID:18303418	SUPPORT	Approximately one-quarter of smokers can be affected by clinically significant chronic obstructive pulmonary disease. ... Smokers may reduce their risk of developing chronic obstructive pulmonary disease by physical activity and increase their survival by smoking reduction.	This supports the statement by highlighting the prevalence of COPD among smokers and the role of smoking in disease progression.
PMID:37429033	SUPPORT	Age of Initiating Smoking: An Independent Predictor of Chronic Obstructive Pulmonary Disease in Later Life.	This implies that smoking is a risk factor in the development of COPD.

notes

Primary risk factor for development and progression.

1

name

Air Pollution

evidence

reference	supports	snippet	explanation
PMID:33542053	SUPPORT	Our findings suggest that, when considering total personal exposure to air pollutants, mainly the gaseous pollutants affect COPD patients' health.	This study found that exposure to various air pollutants adversely affects the health of COPD patients, supporting the idea that air pollution exacerbates COPD symptoms.
PMID:25673984	SUPPORT	The major pathogenic factors causing disease include infection and inflammation, protease and antiprotease imbalance, and oxidative stress overwhelming antioxidant defenses.	This reference discusses environmental factors, including pollutants, that contribute to oxidative stress and inflammation in COPD, thus supporting the statement.
PMID:37068517	SUPPORT	Harmful inhaled workplace exposures can contribute to the development of chronic obstructive pulmonary disease (COPD).	This statement supports the environmental influence on COPD, including air pollutants, as a risk factor.
PMID:16916323	SUPPORT	Evidence from epidemiological studies finding consistent associations between air pollution and various outcomes (respiratory symptoms, reduced lung function, chronic bronchitis and mortality), has suggested that outdoor air pollution is a contributing cause of morbidity and mortality.	This reference directly links air pollution to exacerbation and pathogenesis of COPD, supporting the statement.
PMID:27751401	SUPPORT	We focus on the major constituents of air pollutants and their impacts on chronic respiratory diseases.	This review highlights the detrimental effects of air pollution on respiratory health, particularly in the discussion on chronic respiratory diseases such as COPD.

notes

Exposure to pollutants can exacerbate symptoms.

2

name

Occupational Dust and Chemicals

evidence

reference	supports	snippet	explanation
PMID:11964759	SUPPORT	occupational exposure to dusts, chemicals and gases will be considered an established, or supported by good evidence, risk factor for chronic obstructive pulmonary disease	The abstract confirms that occupational exposure to dusts, chemicals, and gases is a well-supported risk factor for chronic obstructive pulmonary disease.
PMID:20535848	SUPPORT	Lung function loss associated with occupational dust exposure in metal smelting	This study provides evidence of lung function loss due to occupational dust exposure, supporting the assertion that long-term exposure to such environmental factors increases the risk of chronic obstructive pulmonary disease.
PMID:23361196	SUPPORT	Recent studies have recognized the contribution of workplace exposures to chronic lung diseases, in particular chronic obstructive pulmonary disease (COPD)	The abstract discusses the recognized contribution of workplace exposures, including textile dust, to chronic obstructive pulmonary disease.
PMID:24278358	SUPPORT	Occupational inhalative exposure to bg-dust was associated with a statistically significant decreased FEV1 and FEV1/FVC revealing airway obstruction consistent with COPD	The meta-analysis presented indicates a significant association between occupational exposure to inorganic dust and the development of chronic obstructive pulmonary disease.
PMID:35409627	SUPPORT	Pesticides in general and especially organophosphate and carbamate insecticides... showed an association, and cadmium (Cd), chromium (Cr and CrVI), arsenic (As), and diisocyanates, a possible association with COPD	The scoping review identifies several environmental substances, including chemicals associated with occupational exposure, that have a strong or possible association with chronic obstructive pulmonary disease.

notes

Long-term exposure increases risk.

0

name

Smoking Cessation

description

Stopping smoking to slow disease progression and improve outcomes.

evidence

reference	supports	snippet	explanation
PMID:25496790	SUPPORT	Stopping smoking reduces the risk of developing COPD and is an essential treatment for this inflammatory disease. Smoking cessation decreases the prevalence of respiratory symptoms, number of hospitalizations, and decline in FEV1, as well as exacerbation frequency and overall mortality.	The reference clearly states that smoking cessation is essential in reducing various harmful outcomes related to COPD.
PMID:19811377	SUPPORT	Smoking cessation and lung volume reduction surgery would both qualify as disease-modifying interventions.	The reference identifies smoking cessation as a disease-modifying intervention, which indicates its importance in slowing disease progression and thus improving outcomes.
PMID:11935838	SUPPORT	The most important intervention is smoking cessation.	The reference emphasizes that smoking cessation is the most important intervention to minimize the impact of COPD.
PMID:27576232	SUPPORT	Smoking cessation is the only intervention shown to slow disease progression.	The reference clearly supports the claim that smoking cessation can slow disease progression and improve outcomes for COPD patients.

1

name

Bronchodilators

description

Medications that relax muscles of the airways to improve airflow (e.g., beta-agonists, anticholinergics).

evidence

reference	supports	snippet	explanation
PMID:29794201	SUPPORT	Bronchodilator therapy can often decrease symptoms of air-flow obstruction by relaxing airway smooth muscle (bronchodilation), decreasing dyspnea, and improving quality of life.	The reference discusses how bronchodilator therapy relaxes airway smooth muscle, which improves airflow in obstructive lung diseases like COPD.
PMID:27576232	SUPPORT	Long-acting beta2-agonists and long-acting muscarinic antagonists are first-line treatments for patients with persistently symptomatic COPD with an FEV1 of 80% or less of predicted.	This reference identifies bronchodilators, specifically long-acting beta2-agonists and muscarinic antagonists, as key treatments for COPD by improving airflow.
PMID:28757318	SUPPORT	Combination long-acting inhaled bronchodilators are central to the management of patients with moderate to very severe chronic obstructive pulmonary disease.	This reference confirms that bronchodilators, such as long-acting beta2 agonists and long-acting muscarinic antagonists, are used to manage COPD symptoms by improving pulmonary function.

2

name

Inhaled Corticosteroids

description

Reduce airway inflammation and frequency of exacerbations.

evidence

reference	supports	snippet	explanation
PMID:20102305	PARTIAL	Short-term treatment with ICS improves lung function and quality of life; in addition, several studies with longer follow-up have shown less decline over time in quality of life, and fewer exacerbations. By contrast, long-term studies have been unable to show substantial improvement in the decline of lung function in COPD.	While ICS do help reduce the frequency of exacerbations and improve quality of life, the evidence on their effectiveness in reducing airway inflammation specifically is more nuanced.
PMID:37348121	PARTIAL	Current pharmacologic strategies, including first- and second-line therapies such as long-acting beta(2)-agonists, long-acting muscarinic antagonists, inhaled corticosteroids, phosphodiesterase-4 inhibitors, and macrolides, provide relief to patients with COPD. However, many patients remain symptomatic, with persistent symptoms and/or acute exacerbations and progressive lung function loss.	ICS are included in the treatment strategies, and while they help mitigate exacerbations, the snippet suggests that not all patients experience reduced airway inflammation.
PMID:29938633	SUPPORT	The major alteration has been in the section concerning treatment with inhalation medication - now aiming at an easy stepwise up-titration of long-acting medicine as well as a guide of how to down-titrate inhaled corticosteroids.	The guideline update underscores the role of ICS in managing stable COPD, highlighting their long-term use for reducing symptoms and managing exacerbations.
PMID:30846476	SUPPORT	Recent large randomised controlled trials have provided important new information concerning the therapeutic effects of ICSs and long-acting bronchodilators on exacerbations.	The new evidence indicates that ICS are effective in reducing exacerbations, supporting their role in treatment.

3

name

Phosphodiesterase-4 Inhibitors

description

Reduce inflammation and relax airways.

evidence

reference	supports	snippet	explanation
PMID:15699784	SUPPORT	Some of the selective PDE4 inhibitors have demonstrated in vitro and in vivo anti-inflammatory activity on cells commonly linked to airway inflammation in COPD, such as neutrophils.	The reference indicates that selective phosphodiesterase 4 inhibitors show anti-inflammatory activity, supporting the statement about reducing inflammation.
PMID:20649375	SUPPORT	Roflumilast targets inflammatory processes in COPD, with beneficial effects on tobacco-induced lung inflammation, lung fibrosis and remodeling, mucociliary malfunction and oxidative stress.	Roflumilast, a PDE4 inhibitor, targets inflammatory processes, thus supporting the statement.
PMID:34731461	SUPPORT	The orally administered PDE4 inhibitor roflumilast reduces exacerbation rates in the subgroup of chronic obstructive pulmonary disease patients with a history of exacerbations and the presence of chronic bronchitis, but can cause PDE4 related adverse effects due to systemic exposure.	This reference confirms the anti-inflammatory effect of PDE4 inhibitors which aligns with the statement.
PMID:32361678	SUPPORT	Protein kinases have been implicated in mediating inflammatory signals and airway remodeling associated with reduced lung function in chronic pulmonary disease.	This reference supports the role of PDE inhibitors, specifically kinase inhibitors, in reducing inflammation in COPD.
PMID:37707336	SUPPORT	Phosphodiesterase-4, the primary enzyme responsible for cAMP degradation in the majority of immune and inflammatory cells, plays a critical role in the regulation of intracellular cAMP levels.	The inhibition of PDE4 is shown to regulate inflammation, indirectly supporting the statement.

4

name

Oxygen Therapy

description

Long-term oxygen use for patients with severe chronic hypoxemia.

evidence

reference	supports	snippet	explanation
PMID:24461631	SUPPORT	This therapeutic intervention has been shown to increase survival in patients with chronic obstructive pulmonary disease (COPD) and respiratory failure.	The literature supports that long-term oxygen therapy (LTOT) is used to treat patients with COPD who have severe chronic hypoxemia.
PMID:37353334	SUPPORT	Long-term oxygen therapy (LTOT) is a mainstay treatment for patients with severe resting hypoxemia secondary to chronic respiratory conditions including COPD.	This reference specifically mentions LTOT as a primary treatment for patients with severe chronic hypoxemia due to COPD.
PMID:19462352	SUPPORT	Only smoking cessation and long term oxygen therapy (LTOT) improve survival in COPD.	This study confirms that LTOT is a treatment that improves survival in patients with severe COPD and chronic hypoxemia.

5

name

Pulmonary Rehabilitation

description

Exercise training, education, and support to improve quality of life and physical conditioning.

evidence

reference	supports	snippet	explanation
PMID:29526182	SUPPORT	PR is an effective and cost-effective therapeutic intervention that improves physical performance ability, shortness of breath, and the quality of life in patients with COPD.	The reference indicates that pulmonary rehabilitation (PR) improves physical performance, shortness of breath, and quality of life in COPD patients, aligning with the statement's description of treatments including exercise training, education, and support.
PMID:34338012	SUPPORT	Exercise improves the physiological and psychological condition of people with chronic obstructive pulmonary disease and should be encouraged, with referral to a pulmonary rehabilitation service if available.	This reference supports the statement's claim by emphasizing the importance of exercise and recommending pulmonary rehabilitation to improve the quality of life and physical conditioning in COPD patients.
PMID:34955635	SUPPORT	The combination of drug therapy with non-drug therapy such as pulmonary rehabilitation training has demonstrated a great potential in reducing the occurrence of complications and delaying the progression of COPD.	This reference supports the statement by highlighting the benefits of pulmonary rehabilitation training, specifically its potential to improve quality of life and physical conditioning in COPD patients.
PMID:24874124	SUPPORT	Pulmonary rehabilitation targets the systemic manifestations of COPD, the causes of which include inactivity, systemic inflammation, hypoxia and corticosteroid treatment.	This reference supports the statement by indicating that pulmonary rehabilitation addresses systemic issues in COPD and implies improvement in quality of life and physical conditioning.
PMID:24507849	SUPPORT	The main objective of pulmonary rehabilitation is to restore muscle function and exercise tolerance, reverse other nonrespiratory consequences of the disease, and help patients to self-manage chronic obstructive pulmonary disease and its exacerbations and symptoms.	This reference supports the statement by detailing the benefits of pulmonary rehabilitation, including exercise training, education, and support, to improve quality of life and physical conditioning.

6

name

Lung Volume Reduction Surgery

description

Surgical removal of damaged lung tissue for severe emphysema.

evidence

reference	supports	snippet	explanation
PMID:22189668	SUPPORT	Surgical approaches include lung transplantation and lung volume reduction and the latter has been shown to improve exercise tolerance, quality of life, and survival in highly selected patients with advanced emphysema.	The literature supports the use of lung volume reduction surgery as a treatment for severe emphysema in chronic obstructive pulmonary disease (COPD) patients.
PMID:33926668	SUPPORT	As symptoms and lung function decline, treatment modalities, such as lung volume reduction surgery, have been used in individuals with chronic obstructive pulmonary disease and upper lobe predominant emphysema.	The literature indicates that lung volume reduction surgery is a treatment used for severe emphysema, a condition associated with COPD.
PMID:31145187	SUPPORT	Mortality benefits to therapy have been demonstrated in only 2 therapeutic interventions to date: long-term use of daily supplemental oxygen and surgical lung volume reduction (LVRS) for upper-lobe-predominant disease in patients with a low baseline exercise capacity.	The statement is supported as the literature suggests that lung volume reduction surgery is an established treatment for upper-lobe-predominant, severe emphysema in COPD patients.

7

name

Lung Transplantation

description

Considered in end-stage COPD with severe impairment.

evidence

reference	supports	snippet	explanation
PMID:17240617	SUPPORT	Lung transplantation is a surgical option for patients who fail optimization of medical treatment for the severe symptoms that result from COPD.	This reference states that lung transplantation is a considered treatment option for patients with severe symptoms resulting from COPD.
PMID:31375190	SUPPORT	End-stage congestive heart failure, chronic obstructive pulmonary disease...palliative principles can guide decision making and symptom management in these disease states.	The reference focuses on end-stage COPD and mentions lung transplantation as a consideration in managing the conditions of patients.
PMID:36050206	SUPPORT	The International Thoracic Organ Transplant Registry...focus on lung transplant recipients with chronic obstructive pulmonary disease.	This source concentrates on lung transplantation for patients with COPD, in line with the statement’s context of it being a treatment for end-stage COPD.
PMID:23248802	SUPPORT	Chronic obstructive pulmonary disease...treated by lung transplantation.	This abstract explicitly mentions the use of lung transplantation for individuals with very severe COPD.