• Title/Summary/Keyword: Chronic obstructive pulmonary diseases

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Study Design and Outcomes of Korean Obstructive Lung Disease (KOLD) Cohort Study

  • Park, Tai Sun;Lee, Jae Seung;Seo, Joon Beom;Hong, Yoonki;Yoo, Jung-Wan;Kang, Byung Ju;Lee, Sei Won;Oh, Yeon-Mok;Lee, Sang-Do
    • Tuberculosis and Respiratory Diseases
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    • v.76 no.4
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    • pp.169-174
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    • 2014
  • Background: The Korean Obstructive Lung Disease (KOLD) Cohort Study is a prospective longitudinal study of patients with chronic obstructive pulmonary disease (COPD), asthma, or other unclassified obstructive lung diseases. It was designed to develop new classification models and biomarkers that predict clinically relevant outcomes for patients with obstructive lung diseases. Methods: Patients over 18 years old who have chronic respiratory symptoms and airflow limitations or bronchial hyper-responsiveness were enrolled at 17 centers in South Korea. After a baseline visit, the subjects were followed up every 3 months for various assessments. Results: From June 2005 to October 2013, a total of 477 subjects (433 [91%] males; 381 [80%] diagnosed with COPD) were enrolled. Analyses of the KOLD Cohort Study identified distinct phenotypes in patients with COPD, and predictors of therapeutic responses and exacerbations as well as the factors related to pulmonary hypertension in COPD. In addition, several genotypes were associated with radiological phenotypes and therapeutic responses among Korean COPD patients. Conclusion: The KOLD Cohort Study is one of the leading long-term prospective longitudinal studies investigating heterogeneity of the COPD and is expected to provide new insights for pathogenesis and the long-term progression of COPD.

Chronic Obstructive Pulmonary Disease: Respiratory Review of 2014

  • Lee, Young-Min
    • 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.

Role of AMP-Activated Protein Kinase (AMPK) in Smoking-Induced Lung Inflammation and Emphysema

  • Lee, Jae Seung;Park, Sun Joo;Cho, You Sook;Huh, Jin Won;Oh, Yeon-Mok;Lee, Sang-Do
    • Tuberculosis and Respiratory Diseases
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    • v.78 no.1
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    • pp.8-17
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    • 2015
  • Background: AMP-activated protein kinase (AMPK) not only functions as an intracellular energy sensor and regulator, but is also a general sensor of oxidative stress. Furthermore, there is recent evidence that it participates in limiting acute inflammatory reactions, apoptosis and cellular senescence. Thus, it may oppose the development of chronic obstructive pulmonary disease. Methods: To investigate the role of AMPK in cigarette smoke-induced lung inflammation and emphysema we first compared cigarette smoking and polyinosinic-polycytidylic acid [poly(I:C)]-induced lung inflammation and emphysema in $AMPK{\alpha}1$-deficient ($AMPK{\alpha}1$-HT) mice and wild-type mice of the same genetic background. We then investigated the role of AMPK in the induction of interleukin-8 (IL-8) by cigarette smoke extract (CSE) in A549 cells. Results: Cigarette smoking and poly(I:C)-induced lung inflammation and emphysema were elevated in $AMPK{\alpha}1$-HT compared to wild-type mice. CSE increased AMPK activation in a CSE concentration- and time-dependent manner. 5-Aminoimidazole-4-carboxamide-1-${\beta}$-4-ribofuranoside (AICAR), an AMPK activator, decreased CSE-induced IL-8 production while Compound C, an AMPK inhibitor, increased it, as did pretreatment with an $AMPK{\alpha}1$-specific small interfering RNA. Conclusion: $AMPK{\alpha}1$-deficient mice have increased susceptibility to lung inflammation and emphysema when exposed to cigarette smoke, and AMPK appears to reduce lung inflammation and emphysema by lowering IL-8 production.

Cause of Death in COPD Patients of a Referral Hospital (만성폐쇄성폐질환 환자 사망 원인 - 한 3차 병원 연구)

  • Kim, Beom Jun;Hong, Sang Bum;Shim, Tae Sun;Lim, Chae Man;Lee, Sang Do;Koh, Younsuck;Kim, Woo Sung;Kim, Dong-Soon;Kim, Won Dong;Oh, Yeon-Mok
    • Tuberculosis and Respiratory Diseases
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    • v.60 no.5
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    • pp.510-515
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    • 2006
  • Background : Although 17% of Korean adults over the age of 45 years have chronic obstructive pulmonary disease (COPD), there is only limited data on the cause of death in COPD patients in Korea. Therefore, this retrospective study was performed to examine the cause of death in COPD patients at a referral hospital in Korea. Methods : The medical records of 28 deceased patients diagnosed as COPD in Asan Medical Center from January to December 2003 were reviewed patients had died in Asan Medical Center and 16 patients had died outside the hospital. The Korean National Statistical Office confirmed 88 deceased patients out of 1,078 patients diagnosed as COPD in Asan Medical Center in 2003. After excluding those with tuberculous destroyed lung, bronchiectasis, and lung cancer, 28 COPD patients were evaluated. Results : The causes of death were pulmonary disease including pneumonia in 16 patients (57%), cardiac disease in 5 patients (18%), sudden death in 3 patients (11%), and other causes in 4 patients (14%). The cause of death was pulmonary disease in 83% (10 out of 12 patients) and 38% (6 out of 16 patients) of patients who died in Asan Medical Center and outside the center, respectively (P=0.05). The cause of death was pulmonary disease in 43% of patients with $FEV_1$ more than 50 % of the predicted value and in 55% of patients with $FEV_1$ less than 50 % of the predicted value (P=0.89). Conclusion : Pulmonary disease is the leading cause of death in COPD patients in Korea.

Chronic Obstructive Pulmonary Disease: Respiratory Review of 2013

  • Kim, Yu-Il
    • 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.

Pulmonary Strongyloidiasis Masquerading as Exacerbation of Chronic Obstructive Pulmonary Disease

  • Pradhan, Gourahari;Behera, Priyadarshini;Panigrahi, Manoj Kumar;Bhuniya, Sourin;Mohapatra, Prasanta Raghab;Turuk, Jyotirmayee;Mohanty, Srujana
    • Tuberculosis and Respiratory Diseases
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    • v.79 no.4
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    • pp.307-311
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    • 2016
  • Pulmonary strongyloidiasis is an uncommon presentation of Strongyloides infection, usually seen in immunocompromised hosts. The manifestations are similar to that of acute exacerbation of chronic obstructive pulmonary disease (COPD). Therefore, the diagnosis of pulmonary strongyloidiasis could be challenging in a COPD patient, unless a high index of suspicion is maintained. Here, we present a case of Strongyloides hyperinfection in a COPD patient mimicking acute exacerbation, who was on chronic steroid therapy.

Effect of the Changing the Lower Limits of Normal and the Interpretative Strategies for Lung Function Tests (폐기능검사 해석에 정상하한치 변화와 새 해석흐름도가 미치는 영향)

  • Ra, Seung Won;Oh, Ji Seon;Hong, Sang-Bum;Shim, Tae Sun;Lim, Chae Man;Koh, Youn Suck;Lee, Sang Do;Kim, Woo Sung;Kim, Dong-Soon;Kim, Won Dong;Oh, Yeon-Mok
    • Tuberculosis and Respiratory Diseases
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    • v.61 no.2
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    • pp.129-136
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    • 2006
  • Background: To interpret lung function tests, it is necessary to determine the lower limits of normal (LLN) and to derive a consensus on the interpretative algorithm. '0.7 of LLN for the $FEV_1$/FVC' was suggested by the COPD International Guideline (GOLD) for defining obstructive disease. A consensus on a new interpretative algorithm was recently achieved by ATS/ERS in 2005. We evaluated the accuracy of '0.7 of LLN for the $FEV_1$/FVC' for diagnosing obstructive diseases, and we also determined the effect of the new algorithm on diagnosing ventilatory defects. Methods: We obtained the age, gender, height, weight, $FEV_1$, FVC, and $FEV_1$/FVC from 7362 subjects who underwent spirometry in 2005 at the Asan Medical Center, Korea. For diagnosing obstructive diseases, the accuracy of '0.7 of LLN for the $FEV_1$/FVC' was evaluated in reference to the $5^{th}$ percentile of the LLN. By applying the new algorithm, we determined how many more subjects should have lung volumes testing performed. Evaluation of 1611 patients who had lung volumes testing performed as well as spirometry during the period showed how many more subjects were diagnosed with obstructive diseases according to the new algorithm. Results: 1) The sensitivity of '0.7 of LLN for the $FEV_1$/FVC' for diagnosing obstructive diseases increased according to age, but the specificity was decreased according to age; the positive predictive value decreased, but the negative predictive value increased. 2) By applying the new algorithm, 34.5% (2540/7362) more subjects should have lung volumes testing performed. 3) By applying the new algorithm, 13% (205/1611) more subjects were diagnosed with obstructive diseases; these subjects corresponded to 30% (205/681) of the subjects who had been diagnosed with restrictive diseases by the old interpretative algorithm. Conclusion: The sensitivity and specificity of '0.7 of LLN for the $FEV_1$/FVC' for diagnosing obstructive diseases changes according to age. By applying the new interpretative algorithm, it was shown that more subjects should have lung volumes testing performed, and there was a higher probability of being diagnosed with obstructive diseases.

A Mitochondrial Perspective of Chronic Obstructive Pulmonary Disease Pathogenesis

  • Kang, Min-Jong;Shadel, Gerald S.
    • 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.

Pulmonary Rehabilitation for Chronic Obstructive Pulmonary Disease: Highly Effective but Often Overlooked

  • Arnold, Michael T.;Dolezal, Brett A.;Cooper, Christopher B.
    • Tuberculosis and Respiratory Diseases
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    • v.83 no.4
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    • pp.257-267
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    • 2020
  • Patients with chronic obstructive pulmonary disease receive a range of treatments including but not limited to inhaled bronchodilators, inhaled and systemic corticosteroids, supplemental oxygen, and pulmonary rehabilitation. Pulmonary rehabilitation is a multidisciplinary intervention that seeks to combine patient education, exercise, and lifestyle changes into a comprehensive program. Programs 6 to 8 weeks in length have been shown to improve health, reduce dyspnea, increase exercise capacity, improve psychological well-being, and reduce healthcare utilization and hospitalization. Although the use of pulmonary rehabilitation is widely supported by the literature, controversy still exists regarding what should be included in the programs. The goal of this review was to summarize the evidence for pulmonary rehabilitation and identify the areas that hold promise in improving its utilization and effectiveness.