• Tuberculosis and Respiratory Diseases
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• 제80권4호
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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.

• Biomolecules & Therapeutics
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• 제8권2호
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• pp.107-112
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• 2000

To investigate the alteration of airway mucin in airway disease patients, immunoassay procedures were employed using monoclonal antibodies HM02 and HM03 (Hybridoma, 18,457-463, 1999). Alteration of mucin release was determined by ELISA and the integrity of mucin was determined by Western blot. In ELISA, it was found that mucin release increased from pneumonia, chronic cough, bronchiectasis, eosinophilic pneumonia, lung cancer and bronchial asthma patients. In Western blot, the increase in immunoreactivity was observed in case of pneumonia, chronic cough, bronchiectasis and bronchial asthma. In bronchial asthma, there was no obvious degradation of mucin while in other diseases, varying degree of mucin degradation was observed. The data from the present study implicate that HMO2 and HM03 are suitable for the immunological analysis of mucin in airway disease patients. The role of increased mucin release and varying degree of mucin degradation on airway diseases should be further investigated in the future.

• Tuberculosis and Respiratory Diseases
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• 제60권5호
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• pp.510-515
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• 2006

연구 배경 : 만성폐쇄성폐질환(COPD)은 45세 이상의 성인에서 국내 유병률 17.2%로 주요 질환이다. 하지만, 국내 COPD 환자의 사망원인에 대한 연구는 불충분한 상황이다. 이에 국내 COPD 환자 사망원인에 대해서 알아보고자 서울아산병원 의무기록을 후향적으로 조사하였다. 방 법 : 2003년 1년간 서울아산병원에서 COPD로 진료한 1,078명의 사망여부를 통계청에 의뢰하여 총 사망자 88명을 얻었고 이중 폐결핵 후유증, 기관지확장증, 폐암 등 암 환자를 제외한 후 남은 28명의 COPD 환자 대상으로 사망원인을 분석하였다. 결 과 : COPD 환자의 사망원인은 폐렴 등 호흡기 원인이 16명 (57%), 심장 원인 5명 (18%), 급사 3명 (11%), 기타 4명 (14%) 등이었다. 서울아산병원 내에서 사망한 환자와 외에서 사망한 환자의 호흡기 관련 사망이 각각 83%(10명/12명)과 38%(6명/16명)이었다 (P=0.05) $FEV_1$이 50%예측치보다 큰 환자와 작은 환자의 호흡기 관련 사망은 각각 43%과 55%이었다 (P=0.89). 결 론 : 국내 3차 병원에서 진료하는 COPD 환자의 사망 원인은 폐렴 등 호흡기 원인 다수를 차지한다.

• IMMUNE NETWORK
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• 제19권1호
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• pp.5.1-5.12
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• 2019

Autophagy is a homeostatic mechanism that discards not only invading pathogens but also damaged organelles and denatured proteins via lysosomal degradation. Increasing evidence suggests a role for autophagy in inflammatory diseases, including infectious diseases, Crohn's disease, cystic fibrosis, and pulmonary hypertension. These studies suggest that modulating autophagy could be a novel therapeutic option for inflammatory diseases. Eosinophils are a major type of inflammatory cell that aggravates airway inflammatory diseases, particularly corticosteroid-resistant inflammation. The eosinophil count is a useful tool for assessing which patients may benefit from inhaled corticosteroid therapy. Recent studies demonstrate that autophagy plays a role in eosinophilic airway inflammatory diseases by promoting airway remodeling and loss of function. Genetic variant in the autophagy gene ATG5 is associated with asthma pathogenesis, and autophagy regulates apoptotic pathways in epithelial cells in individuals with chronic obstructive pulmonary disease. Moreover, autophagy dysfunction leads to severe inflammation, especially eosinophilic inflammation, in chronic rhinosinusitis. However, the mechanism underlying autophagy-mediated regulation of eosinophilic airway inflammation remains unclear. The aim of this review is to provide a general overview of the role of autophagy in eosinophilic airway inflammation. We also suggest that autophagy may be a new therapeutic target for airway inflammation, including that mediated by eosinophils.

• Tuberculosis and Respiratory Diseases
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• 제60권2호
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• pp.215-220
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• 2006

연구 배경: 폐활량측정법 정상예측식이 한국인을 대상으로 개발되었다. 한국인 정상예측식을 실제 진료에 사용하기 위해서 그 동안 많이 사용하던 정상 예측식 중 하나인 Morris 예측식을 적용하였을 때와 한국인 예측식을 적용하였을 때 장애 양상 해석 및 질병 중증도 평가가 어떻게 달라지나 비교하고자 하였다. 방 법: 서울아산병원의 호흡기검사실에서 2004년도 11월 한 달간 폐활량측정법을 시행한 남자 926명과 여자 694명을 대상으로 하였다. 나이, 성, 키, 몸무게, 그리고 폐활량측정법으로 $FEV_1$ [forced expiratory volume in one second], FVC [forced vital capacity], $FEV_1/FVC$ 등을 구하였다. 한국인 예측식과 Morris 예측식을 사용하여 장애 양상 해석과 질병 중증도 평가를 하였고 그 차이를 비교하였다. 폐활량측정법 장애 양상은 $FEV_1/FVC$과 FVC 값에 따라서 정상, 제한성, 폐쇄성, 양상 미정 등으로 정의하였고 질병 중증도는 기류제한이 있는 환자는 $FEV_1$ 값에 따라서 기류제한이 없는 환자는 FVC값에 따라서 정의하였다. 결 과: Morris 예측식에서 한국인 예측식으로 바꾸어 적용하면 장애 양상 해석이 남자 환자의 경우 22.5% (208/926) 달라졌고 여자의 경우 24.8% (172/694) 달라졌다. 한국인 예측식을 적용하였을 때, 기류제한이 있는 환자의 경우 질병의 중증도가 남자에서 30.2% (114/378) 바뀌었고 여자에서 39.4% (37/94) 바뀌었다. 기류제한이 없는 환자의 경우는 질병의 중증도가 남자에서 27.9% (153/548) 바뀌었고 여자에서 30.2% (181/600) 바뀌었다. 결 론: 폐활량측정법 정상예측식이 바뀌면 장애 양상 해석과 질병 중증도 평가에 유의한 영향을 미칠 수 있다.

• Korean Journal of Radiology
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• 제21권9호
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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.

• Tuberculosis and Respiratory Diseases
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• 제78권1호
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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.

• Clinical and Experimental Pediatrics
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• 제49권6호
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• pp.581-588
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• 2006

Asthma is a chronic inflammation of the airway associated with increased bronchial hyperresponsiveness that leads to recurrent episodes of cough, wheezing, breathless, chest tightness. According the recent studies, repeated airway inflammation leads to structural changes so called 'airway remodeling' and associated with decreased pulmonary function. Airway remodeling begins form the early stage of asthma and the early diagnosis and management is very important to prevent airway remodeling. Medication for asthma can be classified into acute symptom reliever and chronic controller. Short acting beta2 agonist is a well-known reliever that reduced asthma symptoms within minutes. Controllers should be taken daily as a long-term basis to control airway inflammation. Inhaled corticosteroid(ICS) is the most effective controller in current use. However, in some patients ICS monotherapy is not sufficient to control asthma. In those cases, other medications such as long acting beta2 agonist, leukotriene modifier or sustained-release theophylline should be added to ICS, which called Add-on-Therapy. Combination inhaler devices are easy to use. Oral leukotriene modifier has a good compliance especially in children. Finally, as asthma is a chronic disease, the development of on-going partnership among health care professionals, the patients, and the patients' family is necessary for the effective management of asthma.

• Tuberculosis and Respiratory Diseases
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• 제87권2호
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• pp.165-175
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• 2024

Background: The prevalence of small airway dysfunction (SAD) in patients with chronic obstructive pulmonary disease (COPD) across different ethnicities is poorly understood. This study aimed to estimate the prevalence of SAD in stable COPD patients. Methods: We conducted a cross-sectional study of 196 consecutive stable COPD patients. We measured pre- and post-bronchodilator (BD) lung function and respiratory impedance. The severity of COPD and lung function abnormalities was graded in accordance with the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines. SAD was defined as either difference in whole-breath resistance at 5 and 19 Hz > upper limit of normal or respiratory system reactance at 5 Hz < lower limit of normal. Results: The cohort consisted of 95.9% men, with an average age of 66.3 years. The mean forced expiratory volume 1 second (FEV₁) % predicted was 56.4%. The median COPD assessment test (CAT) scores were 14. The prevalence of post-BD SAD across the GOLD grades 1 to 4 was 14.3%, 51.1%, 91%, and 100%, respectively. The post-BD SAD and expiratory flow limitation at tidal breath (EFL_T) were present in 62.8% (95% confidence interval [CI], 56.1 to 69.9) and 28.1% (95% CI, 21.9 to 34.2), respectively. COPD patients with SAD had higher CAT scores (15.5 vs. 12.8, p<0.01); poor lung function (FEV₁% predicted 46.6% vs. 72.8%, p<0.01); lower diffusion capacity for CO (4.8 mmol/min/kPa vs. 5.6 mmol/min/kPa, p<0.01); hyperinflation (ratio of residual volume to total lung capacity % predicted: 159.7% vs. 129%, p<0.01), and shorter 6-minute walk distance (367.5 m vs. 390 m, p=0.02). Conclusion: SAD is present across all severities of COPD. The prevalence of SAD increases with disease severity. SAD is associated with poor lung function and higher symptom burden. Severe SAD is indicated by the presence of EFL_T.

• Journal of Yeungnam Medical Science
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• 제36권1호
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• pp.8-15
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• 2019

Connective tissue diseases (CTDs) can affect all compartments of the lungs, including airways, alveoli, interstitium, vessels, and pleura. CTD-associated lung diseases (CTD-LDs) may present as diffuse lung disease or as focal lesions, and there is significant heterogeneity between the individual CTDs in their clinical and pathological manifestations. CTD-LDs may presage the clinical diagnosis a primary CTD, or it may develop in the context of an established CTD diagnosis. CTD-LDs reveal acute, chronic or mixed pattern of lung and pleural manifestations. Histopathological findings of diverse morphological changes can be present in CTD-LDs airway lesions (chronic bronchitis/bronchiolitis, follicular bronchiolitis, etc.), interstitial lung diseases (nonspecific interstitial pneumonia/fibrosis, usual interstitial pneumonia, lymphocytic interstitial pneumonia, diffuse alveolar damage, and organizing pneumonia), pleural changes (acute fibrinous or chronic fibrous pleuritis), and vascular changes (vasculitis, capillaritis, pulmonary hemorrhage, etc.). CTD patients can be exposed to various infectious diseases when taking immunosuppressive drugs. Histopathological patterns of CTD-LDs are generally nonspecific, and other diseases that can cause similar lesions in the lungs must be considered before the diagnosis of CTD-LDs. A multidisciplinary team involving pathologists, clinicians, and radiologists can adequately make a proper diagnosis of CTD-LDs.