• Tuberculosis and Respiratory Diseases
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• v.79 no.1
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• pp.5-13
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• 2016

Chronic obstructive pulmonary disease (COPD) is a chronic and progressive inflammatory disease of the airways and lungs that results in limitations of continuous airflow and is caused by exposure to noxious gasses and particles. A major cause of morbidity and mortality in adults, COPD is a complex disease pathologically mediated by many inflammatory pathways. Macrophages, neutrophils, dendritic cells, and CD8+ T-lymphocytes are the key inflammatory cells involved in COPD. Recently, the non-coding small RNA, micro-RNA, have also been intensively investigated and evidence suggest that it plays a role in the pathogenesis of COPD. Here, we discuss the accumulated evidence that has since revealed the role of each inflammatory cell and their involvement in the immunopathogenesis of COPD. Mechanisms of steroid resistance in COPD will also be briefly discussed.

• Tuberculosis and Respiratory Diseases
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• v.85 no.3
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• pp.221-226
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• 2022

Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation due to chronic airway inflammation and destruction of the alveolar structure from persistent exposure to oxidative stress. The body has various antioxidant mechanisms for efficiently coping with such oxidative stress. The nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element (ARE) is a representative system. Dysregulation of the Nrf2-ARE pathway is responsible for the development and promotion of COPD. Furthermore, COPD severity is also closely related to this pathway. There has been a clinical impetus to use Nrf2 for diagnostic and therapeutic purposes. Therefore, in this work, we systematically reviewed the clinical significance of Nrf2 in COPD patients, and discuss the value of Nrf2 as a potential COPD biomarker.

• 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.

• Tuberculosis and Respiratory Diseases
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• v.80 no.4
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• pp.317-324
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• 2017

Small airway disease (SAD) has been recognized for many years as a central feature of chronic obstructive pulmonary disease (COPD). Histopathology studies have shown that the narrowing and destruction of small airways in COPD combined with inflammatory cell infiltration in the submucosa increases the severity of the disease. SAD is present in the early stages of COPD and becomes more widespread over time as the disease progresses to more severe COPD. The development of inhalers containing extra-fine particles allows the small airways to be pharmacologically targeted. Recent clinical trials have shown the efficacy of extra-fine triple therapy that targets the small airways in patients with COPD. This article reviews the importance and treatment of SAD in COPD.

• Sleep Medicine and Psychophysiology
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• v.27 no.1
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• pp.8-15
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• 2020

Sleep disorder in chronic obstructive pulmonary disease (COPD) is common and typically is associated with oxygen desaturation. The mechanisms of desaturation include hypoventilation and ventilation to perfusion mismatch. Despite the importance of sleep in patients with COPD, this topic is under-assessed in clinical practice. Impaired sleep quality is associated with more severe COPD and may contribute to worse clinical outcomes. Recent data have indicated that specific respiratory management of patients with COPD and sleep disordered breathing improves clinical outcomes. Clinicians managing patients with COPD should pay attention to and actively manage symptoms of comorbid sleep disorders. Management of sleep-related problems in COPD should particularly focus on minimizing sleep disturbance.

• 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.

• 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.

• Tuberculosis and Respiratory Diseases
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• v.71 no.1
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• pp.1-7
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• 2011

Many findings suggest that chronic obstructive pulmonary disease (COPD) imposes an enormous burden on patients, health-care professionals and society. COPD contributes to morbidity and mortality and to a significant use of health-care resources. In spite of a higher prevalence of COPD in Korea, the result of COPD treatment is not effective. The purpose of this article was to review recent advances in the study of COPD in Korea with the aim of improving effective management. This review highlights articles pertaining to the following topics; prevalence, assessment of COPD, risk factors for hospitalization, co-morbid diseases, phenotypes, and treatment issues.

• Korean Journal of Radiology
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• v.21 no.9
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• pp.1104-1113
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• 2020

Objective: To assess the regional ventilation in patients with asthma-chronic obstructive pulmonary disease (COPD) overlap syndrome (ACOS) using xenon-ventilation dual-energy CT (DECT), and to compare it to that in patients with COPD. Materials and Methods: Twenty-one patients with ACOS and 46 patients with COPD underwent xenon-ventilation DECT. The ventilation abnormalities were visually determined to be 1) peripheral wedge/diffuse defect, 2) diffuse heterogeneous defect, 3) lobar/segmental/subsegmental defect, and 4) no defect on xenon-ventilation maps. Emphysema index (EI), airway wall thickness (Pi10), and mean ventilation values in the whole lung, peripheral lung, and central lung areas were quantified and compared between the two groups using the Student's t test. Results: Most patients with ACOS showed the peripheral wedge/diffuse defect (n = 14, 66.7%), whereas patients with COPD commonly showed the diffuse heterogeneous defect and lobar/segmental/subsegmental defect (n = 21, 45.7% and n = 20, 43.5%, respectively). The prevalence of ventilation defect patterns showed significant intergroup differences (p < 0.001). The quantified ventilation values in the peripheral lung areas were significantly lower in patients with ACOS than in patients with COPD (p = 0.045). The quantified Pi10 was significantly higher in patients with ACOS than in patients with COPD (p = 0.041); however, EI was not significantly different between the two groups. Conclusion: The ventilation abnormalities on the visual and quantitative assessments of xenon-ventilation DECT differed between patients with ACOS and patients with COPD. Xenon-ventilation DECT may demonstrate the different physiologic changes of pulmonary ventilation in patients with ACOS and COPD.

• The Journal of Internal Korean Medicine
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• v.32 no.2
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• pp.203-216
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• 2011

Objectives : This study was conducted to evaluate the protective effects of bee venom on lipopolysaccharide (LPS)-induced chronic obstructive pulmonary disease (COPD). Methods : In this study, LPS was administrated to Balb/c mice to induce a disease that resembles COPD. 2 hr prior to LPS administration, mice were treated with bee venom via an intraperitoneal injection. Total cell number and neutrophils number in bronchoalveolar lavage fluid were counted and pro-inflammatory cytokines were also measured. For histologic analysis, periodic acid Schiff (PAS) and hematoxylin and eosin (H&E) stains were evaluated. Proliferating cell nuclear antigens (PCNA) were also assessed by immunohistochemistry. Results : On 7 days after LPS stimulation, influx of neutrophils significantly decreased in the bee venom group, compared with the COPD group. In addition, TNF-a and IL-6 levels decreased in bee venom group. Histological results also demonstrated the attenuation effect of bee venom on LPS-induced lung inflammation. Conclusions : These data suggest that bee venom has protective effects on LPS-induced lung inflammation. Therefore, bee venom may represent a novel therapeutic agent for lung inflammation and in particular for COPD.