• Tuberculosis and Respiratory Diseases
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• v.77 no.4
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• pp.155-160
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• 2014

Chronic obstructive pulmonary disease (COPD) is characterized by a diverse array of pulmonary and nonpulmonary manifestations, but our understanding of COPD pathogenesis and the factors that influence its heterogeneity in disease presentation is poor. Despite this heterogeneity, treatment algorithms are primarily driven by a single measurement, forced expiratory volume in 1 second ($FEV_1$) as a percentage of its predicted value ($FEV_1%$). In 2011, a major shift in Global Initiative for Chronic Obstructive Lung Disease (GOLD) treatment recommendations was proposed that stratifies patients with COPD on the basis of symptoms and exacerbation history. This article reviews the work reported in 2013 that enlightens our understanding of COPD with respect to COPD classification systems, phenotype, biomarker, exacerbation, and management for patients with COPD.

• Tuberculosis and Respiratory Diseases
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• v.76 no.2
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• pp.53-58
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• 2014

Chronic obstructive pulmonary disease (COPD) is a common airway disease that has considerable impact on disease burdens and mortality rates. A large number of articles on COPD are published within the last few years. Many aspects on COPD ranging from risk factors to management have continued to be fertile fields of investigation. This review summarizes 6 clinical articles with regards to the risk factors, phenotype, assessment, exacerbation, management and prognosis of patients with COPD which were being published last year in major medical journals.

• Tuberculosis and Respiratory Diseases
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• v.79 no.4
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• pp.207-213
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• 2016

Chronic obstructive pulmonary disease (COPD) encompasses several clinical syndromes, most notably emphysema and chronic bronchitis. Most of the current treatments fail to attenuate severity and progression of the disease, thereby requiring better mechanistic understandings of pathogenesis to develop disease-modifying therapeutics. A number of theories on COPD pathogenesis have been promulgated wherein an increase in protease burden from chronic inflammation, exaggerated production of reactive oxygen species and the resulting oxidant injury, or superfluous cell death responses caused by enhanced cellular injury/damage were proposed as the culprit. These hypotheses are not mutually exclusive and together likely represent the multifaceted biological processes involved in COPD pathogenesis. Recent studies demonstrate that mitochondria are involved in innate immune signaling that plays important roles in cigarette smoke-induced inflammasome activation, pulmonary inflammation and tissue remodeling responses. These responses are reviewed herein and synthesized into a view of COPD pathogenesis whereby mitochondria play a central role.

• Tuberculosis and Respiratory Diseases
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• v.85 no.4
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• pp.289-301
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• 2022

Chronic obstructive pulmonary disease (COPD) is a chronic airway inflammation characterized by fixed airflow limitation and chronic respiratory symptoms, such as cough, sputum, and dyspnea. COPD is a progressive disease characterized by a decline in lung function. During the natural course of the disease, acute deterioration of symptoms leading to hospital visits can occur and influence further disease progression and subsequent exacerbation. Moreover, COPD is not only restricted to pulmonary manifestations but can present with other systemic diseases as comorbidities or systemic manifestations, including lung cancer, cardiovascular disease, pulmonary hypertension, sarcopenia, and metabolic abnormalities. These pulmonary and extrapulmonary conditions lead to the aggravation of dyspnea, physical inactivity, decreased exercise capacity, functional decline, reduced quality of life, and increased mortality. In addition, pneumonia, which is attributed to both COPD itself and an adverse effect of treatment (especially the use of inhaled and/or systemic steroids), can occur and lead to further deterioration in the prognosis of COPD. This review summarizes the long-term outcomes of patients with COPD. In addition, recent studies on the prediction of adverse outcomes are summarized in the last part of the review.

• Tuberculosis and Respiratory Diseases
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• v.59 no.1
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• pp.5-13
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• 2005

Chronic obstructive pulmonary disease (COPD) is a chronic progressive disease, characterized by irreversible airflow limitation, with a partially reversible component. The pathological abnormalities of COPD are associated with lung inflammation, imbalances of proteinase and antiproteinase, and oxidative stress, which are induced by noxious particles and gases in susceptible individuals. The physiological changes of COPD are mucus hypersecretion, ciliary dysfunction, airflow limitation, pulmonary hyperinflation, gas exchange abnormalities, pulmonary hypertension, cor pulmonale and systemic effects. The airflow limitation principally results from an increase in the resistance of the small conducting airways and a decrease in pulmonary elastic recoil due to emphysematous lung destruction. This article provides a general overview of the pathophysiology of COPD.

• Tuberculosis and Respiratory Diseases
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• v.87 no.3
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• pp.221-233
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• 2024

The 2023 Global Initiative for Chronic Obstructive Lung Disease (GOLD) revised the definition of chronic obstructive pulmonary disease (COPD) to broadly include a variety of etiologies. A new taxonomy, composed of etiotypes, aims to highlight the heterogeneity in causes and pathogenesis of COPD, allowing more personalized management strategies and emphasizing the need for targeted research to understand and manage COPD better. However, controversy arises with including some diseases under the umbrella term of COPD, as their clinical presentations and treatments differ from classical COPD, which is smoking-related. COPD due to infection (COPD-I) and COPD due to environmental exposure (COPD-P) are classifications within the new taxonomy. Some disease entities in these categories show distinct clinical features and may not benefit from conventional COPD treatments, raising questions about their classification as COPD subtypes. There is also controversy regarding whether bronchiectasis with airflow limitations should be classified as an etiotype of COPD. This article discusses controversial issues associated with the proposed etiotypes for COPD in terms of COPD-I, COPD-P, and bronchiectasis. While the updated COPD definition by GOLD 2023 is a major step towards recognizing the disease's complexity, it also raises questions about the classification of related respiratory conditions. This highlights the need for further research to improve our understanding and approach to COPD management.

• Tuberculosis and Respiratory Diseases
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• v.86 no.2
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• pp.71-81
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• 2023

Chronic obstructive pulmonary disease (COPD) affects close to 400 million people worldwide. COPD is characterized by significant airflow limitation on spirometry. Most patients with COPD are diagnosed in their fifth or sixth decades of life. However, the disease begins much earlier. By the time airflow limitation is detected on spirometry, patients with COPD have lost close to 50% of their small airways. Thus, identification of patients with early COPD, defined as persons with preserved spirometry, who demonstrate pathologic or functional hallmarks of COPD, is essential for disease modification and ultimately disease elimination. This paper provides an up-to-date overview of the current case definition of early COPD, its importance, the novel technologies required for its detection in young adults and future directions in therapeutics for treatment.

• Genomics & Informatics
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• v.17 no.1
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• pp.2.1-2.12
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• 2019

Chronic obstructive pulmonary disease (COPD) is a type of progressive lung disease, featured by airflow obstruction. Recently, a comprehensive analysis of the transcriptome in lung tissue of COPD patients was performed, but the heterogeneity of the sample was not seriously considered in characterizing the mechanistic dysregulation of COPD. Here, we established a new transcriptome analysis pipeline using a deconvolution process to reduce the heterogeneity and clearly identified that these transcriptome data originated from the mild or moderate stage of COPD patients. Differentially expressed or co-expressed genes in the protein interaction subnetworks were linked with mitochondrial dysfunction and the immune response, as expected. Computational protein localization prediction revealed that 19 proteins showing changes in subcellular localization were mostly related to mitochondria, suggesting that mislocalization of mitochondria-targeting proteins plays an important role in COPD pathology. Our extensive evaluation of COPD transcriptome data could provide guidelines for analyzing heterogeneous gene expression profiles and classifying potential candidate genes that are responsible for the pathogenesis of COPD.

• Tuberculosis and Respiratory Diseases
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• v.84 no.3
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• pp.188-199
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• 2021

Background: Chronic obstructive pulmonary disease (COPD) is a common chronic respiratory disease with increased prevalence in the elderly. Telomeres are repetitive DNA sequences found at the end of the chromosome, which progressively shorten as cells divide. Telomere length is known to be a molecular marker of aging. This study aimed to assess the relationship between telomere length and the risk of COPD, lung function, respiratory symptoms, and emphysema index in Chronic Obstructive Pulmonary Disease in Dusty Areas (CODA) cohort. Methods: We extracted DNA from the peripheral blood samples of 446 participants, including 285 COPD patients and 161 control participants. We measured absolute telomere length using quantitative real-time polymerase chain reaction. All participants underwent spirometry and quantitative computed tomography scan. Questionnaires assessing respiratory symptoms and the COPD Assessment Test was filled by all the participants. Results: The mean age of participants at the baseline visit was 72.5±7.1 years. Males accounted for 72% (321 participants) of the all participants. The mean telomere length was lower in the COPD group compared to the non-COPD group (COPD, 16.81±13.90 kb; non-COPD, 21.97±14.43 kb). In COPD patients, 112 (75.7%) were distributed as tertile 1 (shortest), 91 (61.1%) as tertile 2 and 82 (55%) as tertile 3 (longest). We did not find significant associations between telomere length and lung function, exacerbation, airway wall thickness, and emphysema index after adjusting for sex, age, and smoking status. Conclusion: In this study, the relationship between various COPD phenotypes and telomere length was analyzed, but no significant statistical associations were shown.

• Tuberculosis and Respiratory Diseases
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• v.85 no.4
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• pp.302-312
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• 2022

Chronic obstructive pulmonary disease (COPD) is a complex and heterogeneous disease. Not all patients with COPD respond to available drugs. Identifying respondents to therapy is critical to delivering the most appropriate treatment and avoiding unnecessary medication. Recognition of individual patients' dominant characteristics by phenotype is a useful tool to better understand their disease and tailor treatment accordingly. To look for a suitable phenotype, it is important to understand what makes COPD complex and heterogeneous. The pathology of COPD includes small airway disease and/or emphysema. Thus, COPD is not a single disease entity. In addition, there are two types (panlobular and centrilobular) of emphysema in COPD. The coexistence of different pathological subtypes could be the reason for the complexity and heterogeneity of COPD. Thus, it is necessary to look for the phenotype based on the difference in the underlying pathology. Review of the literature has shown that clinical manifestation and therapeutic response to pharmacological therapy are different depending on the presence of computed tomography-defined airway wall thickening in COPD patients. Defining the phenotype of COPD based on the underlying pathology is encouraging as most clinical manifestations can be distinguished by the presence of increased airway wall thickness. Pharmacological therapy has shown significant effect on COPD with airway wall thickening. However, it has limited use in COPD without an airway disease. The phenotype of COPD based on the underlying pathology can be a useful tool to better understand the disease and adjust treatment accordingly.