• Tuberculosis and Respiratory Diseases
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• v.85 no.2
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• pp.122-136
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• 2022

Although chronic obstructive pulmonary disease (COPD) and interstitial lung disease (ILD) have distinct clinical features, both diseases may coexist in a patient because they share similar risk factors such as smoking, male sex, and old age. Patients with both emphysema in upper lung fields and diffuse ILD are diagnosed with combined pulmonary fibrosis and emphysema (CPFE), which causes substantial clinical deterioration. Patients with CPFE have higher mortality compared with patients who have COPD alone, but results have been inconclusive compared with patients who have idiopathic pulmonary fibrosis (IPF). Poor prognostic factors for CPFE include exacerbation, lung cancer, and pulmonary hypertension. The presence of interstitial lung abnormalities, which may be an early or mild form of ILD, is notable among patients with COPD, and is associated with poor prognosis. Various theories have been proposed regarding the pathophysiology of CPFE. Biomarker analyses have implied that this pathophysiology may be more closely associated with IPF development, rather than COPD or emphysema. Patients with CPFE should be advised to quit smoking and undergo routine lung function tests, and pulmonary rehabilitation may be helpful. Various pharmacologic agents and surgical approaches may be beneficial in patients with CPFE, but further studies are needed.

• Korean Journal of Radiology
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• v.22 no.10
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• pp.1719-1729
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• 2021

Objective: Emphysema and small-airway disease are the two major components of chronic obstructive pulmonary disease (COPD). We propose a novel method of quantitative computed tomography (CT) emphysema air-trapping composite (EAtC) mapping to assess each COPD component. We analyzed the potential use of this method for assessing lung function in patients with COPD. Materials and Methods: A total of 584 patients with COPD underwent inspiration and expiration CTs. Using pairwise analysis of inspiration and expiration CTs with non-rigid registration, EAtC mapping classified lung parenchyma into three areas: Normal, functional air trapping (fAT), and emphysema (Emph). We defined fAT as the area with a density change of less than 60 Hounsfield units (HU) between inspiration and expiration CTs among areas with a density less than -856 HU on inspiration CT. The volume fraction of each area was compared with clinical parameters and pulmonary function tests (PFTs). The results were compared with those of parametric response mapping (PRM) analysis. Results: The relative volumes of the EAtC classes differed according to the Global Initiative for Chronic Obstructive Lung Disease stages (p < 0.001). Each class showed moderate correlations with forced expiratory volume in 1 second (FEV₁) and FEV₁/forced vital capacity (FVC) (r = -0.659-0.674, p < 0.001). Both fAT and Emph were significant predictors of FEV₁ and FEV₁/FVC (R² = 0.352 and 0.488, respectively; p < 0.001). fAT was a significant predictor of mean forced expiratory flow between 25% and 75% and residual volume/total vital capacity (R² = 0.264 and 0.233, respectively; p < 0.001), while Emph and age were significant predictors of carbon monoxide diffusing capacity (R² = 0.303; p < 0.001). fAT showed better correlations with PFTs than with small-airway disease on PRM. Conclusion: The proposed quantitative CT EAtC mapping provides comprehensive lung functional information on each disease component of COPD, which may serve as an imaging biomarker of lung function.

• Tuberculosis and Respiratory Diseases
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• v.79 no.3
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• pp.121-126
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• 2016

Lung function reportedly declines with age and that this decline is accelerated during disease progression. However, a recent study showed that the decline might peak in the mild and moderate stage. The prognosis of chronic obstructive pulmonary disease (COPD) can be improved if the disease is diagnosed in its early stages, prior to the peak of decline in lung function. This article reviews recent studies on early COPD and the possibility of applying the U.S. Preventive Services Task Force recommendation 2008 and 2015 for early detection of COPD in Korea.

• 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.80 no.1
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• pp.1-10
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• 2017

Chronic obstructive pulmonary disease (COPD) is a critical condition with high morbidity and mortality. Although several medications are available, there are no definite treatments. However, recent advances in the understanding of stem and progenitor cells in the lung, and molecular changes during re-alveolization after pneumonectomy, have made it possible to envisage the regeneration of damaged lungs. With this background, numerous studies of stem cells and various stimulatory molecules have been undertaken, to try and regenerate destroyed lungs in animal models of COPD. Both the cell and drug therapies show promising results. However, in contrast to the successes in laboratories, no clinical trials have exhibited satisfactory efficacy, although they were generally safe and tolerable. In this article, we review the previous experimental and clinical trials, and summarize the recent advances in lung regeneration therapy for COPD. Furthermore, we discuss the current limitations and future perspectives of this emerging field.

• 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.

• 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.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.61 no.3
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• pp.218-226
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• 2006

Background: The lung volume and diffusing capacity are influenced by ethnicity. However, there are no equations for predicting the normal lung volume in the adult Korean population, and there is only one equation for diffusing capacity. The aim of this study is to select the most suitable reference equation for the Korean population. Method: 30 men and 33 women at Hanyang University Guri Hospital, and 27 men and 34 women at Asan Medical Center in healthy nonsmoking adults were enrolled in this study. The subject's age, gender, height, weight, lung volume by plethysmography, and diffusing capacity by a single breathing method were obtained. The most suitable equation with the lowest sum of residuals between the observed and predicted values for lung volume and diffusing capacity was selected. Result: At Hanyang University Guri Hospital, the equations with the lowest sum of residuals in the total lung capacity were ECSC's equation in males (sum of residual: 0.04 L) and Crapo/Morris's equation (-1.04) in women. At the Asan Medical Center, the equations with the lowest sum of residuals in the total lung capacity were Goldman/Becklake's equation in males (sum of residual: -2.35) and the ECSC's equation -4.49) in women. The equations with the lowest sum of residuals in the Diffusing capacity were Roca's equation in males (sum of residual: -13.66 ml/min/mmHg) and Park's in women (25.08) in Hanyang University Guri hospital and Park's equation in all cases in the Asan Medical Center (male: -1.65, female: -6.46). Conclusions: Until a reference equstion can be made for healthy Koreans by sampling, ECSC's equation can be used for estimating the lung volume and Park's can be used for estimating the diffusing capacity.

• 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.