• Tuberculosis and Respiratory Diseases
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• 제48권2호
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• pp.260-267
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• 2000

거대세포성 간질성 폐렴은 경금속 도구를 이용한 절삭, 연마공정에서 발생하는 경금속 분진을 흡입하여 발생하는 산업성 폐질환으로 알려져 있다. 저자들은 이러한 특징적인 경금속분진에 대한 노출력이 없이 발생하였던 거대세포성 간질성 폐렴을 수술적 폐생검과 폐조직내 금속 함유량 분석을 통해 진단하였기에 보고 하는 바이다.

• The Korean journal of internal medicine
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• 제33권6호
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• pp.1137-1142
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• 2018

Background/Aims: This study tested the hypothesis that prolonged low-dose cyclophosphamide (CTX) treatment after pulse therapy attenuate paraquat (PQ)-induced lung injury in rats. Methods: PQ (25 mg/kg) was administered intraperitoneally to induce PQ-intoxicated rat model. The rats were randomly divided into four groups: control group (1 mL/day saline solution for 14 days), PQ group (1 mL/day saline solution for 14 days after PQ exposure), pulse group (15 mg/kg/day CTX in 1 mL of saline solution for 2 days and subsequent 1 mL/day saline solution for 12 days), and prolonged low-dose group (15 mg/kg/day CTX in 1 mL of saline solution for 2 days and subsequent 1.5 mg/kg/day CTX in 1 mL of saline solution for 12 days). A 14-day follow-up was conducted to determine the survival rat, and lung hydroxyproline (HYP), wet-to-dry weight ratios (W/Dc) and histopathological changes were evaluated. Results: Results showed similar survival rate (55% vs. 50%, p > 0.05) between prolonged low-dose and pulse groups. Lung W/Dc ($4.94{\pm}0.38$ vs. $5.47{\pm}0.28$, p < 0.01), HYP ($3.34{\pm}0.29{\mu}g/mg$ vs. $3.65{\pm}0.19{\mu}g/mg$, p < 0.001), and fibrosis score ($2.69{\pm}0.84$ vs. $3.13{\pm}0.63$, p < 0.05) were lower in prolonged low-dose group than those in the pulse group. Conclusions: These findings suggested prolonged low-dose CTX treatment after pulse therapy could attenuate PQ-induced lung injury in rats.

• Tuberculosis and Respiratory Diseases
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• 제85권4호
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• pp.313-319
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• 2022

Environmental exposure to air pollution is known to have adverse effects on various organs. Air pollution has greater effects on the pulmonary system as the lungs are directly exposed to contaminants in the air. Here, we review the associations of air pollution with the development, morbidity, and mortality of pulmonary diseases. Short-and long-term exposure to air pollution have been shown to increase mortality risk even at concentrations below the current national guidelines. Ambient air pollution has been shown to be associated with lung cancer. Particularly long-term exposure to particulate matter with a diameter <2.5 ㎛ (PM_2.5) has been reported to be associated with lung cancer even at low concentrations. In addition, exposure to air pollution has been shown to increase the incidence risk of chronic obstructive pulmonary disease (COPD) and has been correlated with exacerbation and mortality of COPD. Air pollution has also been linked to exacerbation, mortality, and development of asthma. Exposure to nitrogen dioxide (NO₂) has been demonstrated to be related to increased mortality in patients with idiopathic pulmonary fibrosis. Additionally, air pollution increases the incidence of infectious diseases, such as pneumonia, bronchitis, and tuberculosis. Furthermore, emerging evidence supports a link between air pollution and coronavirus disease 2019 transmission, susceptibility, severity and mortality. In conclusion, the stringency of air quality guidelines should be increased and further therapeutic trials are required in patients at high risk of adverse health effects of air pollution.

• Clinical and Experimental Pediatrics
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• 제45권4호
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• pp.529-534
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• 2002

저자들은 1개월 전부터 시작된 호흡 곤란과 마른 기침이 주증상인 10세 된 여아에서 조직학적 소견에서 비특이성 간질성 폐렴으로 진단된 1례를 보고하는 바이다.

• Journal of Chest Surgery
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• 제54권3호
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• pp.191-199
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• 2021

Background: Tracheal replacement is a challenge for thoracic surgeons due to stenosis in the trachea-prosthesis anastomosis. We propose that stenosis occurs due to fibrosis as a result of an abnormal healing process, characterized by an increased expression of wound healing growth factors (vascular endothelial growth factor [VEGF], survivin, and CD31), which promote angiogenesis and decrease apoptosis. We analyzed the immunoreactivity of VEGF, survivin, CD31, and caspase-3 in the development of fibrotic stenosis in prosthetic tracheal replacement. Methods: Fourteen dogs were operated on: group I (n=7) received a 6-ring cervical tracheal segment autograft, while in group II (n=7), a 6-ring segment of the cervical trachea was resected and tracheal continuity was restored with a Dacron prosthesis. The follow-up was 3 months. Immunoreactivity studies for VEGF, survivin, CD31, and caspase-3 were performed. A statistical analysis was done using the Wilcoxon signed rank test. Results: Four animals in group I were euthanized on the 10th postoperative day due to autograft necrosis. Three animals completed the study without anastomotic stenosis. Moderate expression of VEGF (p=0.038), survivin (p=0.038), and CD31 (p=0.038) was found. All group II animals developed stenosis in the trachea-prosthesis anastomotic sites. Microscopy showed abundant collagen and neovascularization vessels. Statistically significant immunoreactive expression of VEGF (p=0.015), survivin (p=0.017), and CD31 (p=0.011) was observed. No expression of caspase-3 was found. Conclusion: We found a strong correlation between fibrosis in trachea-prosthesis anastomoses and excessive angiogenesis, moderate to intense VEGF, CD31, and survivin expression, and null apoptotic activity. These factors led to uncontrolled collagen production.

• Tuberculosis and Respiratory Diseases
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• 제51권5호
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• pp.437-447
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• 2001

배 경 : TNF-$\alpha$는 UIP 환자의 폐 섬유화에 관계하는 cytokine으로 잘 알려져 있지만, 폐 섬유화를 일으키는 기전에 대해서는 알려져 있지 않다. TNF-$\alpha$에 의해 AP-1(c-jun N-terminal kinase, JNK의 하부 신호 전달체계) 같은 전사 인자가 활성화되고 이들에 의해서 PDGF 나 IGF-I fibrogenic cytokines의 전사가 관계있을 것으로 추측된다. 더구나 방사선에 의한 폐 섬유화 과정에서 JNK가 활성화되어 있는 것이 확인되었다. 본 연구의 목적은 UIP 환자에서 JNK의 활성도를 확인하고자 하였다. 방 법 : UIP 환자의 폐 조직과 대조군으로 이용된 폐암 환자의 정상 폐조직에서 phosphorous JNK (p-JNK), 대식세포의 표현자인 CD68, 그리고 cytokeratin을 이용하여 면역화학검사를 시행하였다. JNK의 in vitro kinase assay는 UIP 환자와 호흡기 증상이 없는 정상인에서 기관지 폐포세척술로 획득한 대식세포를 이용하였다. 결 과 : 면역조직화학검사에서 UIP 환자의 대부분의 폐포 대식세포는 p-JNK를 발현하였지만, 폐암 환자의 정상조직에서는 UIP 환자보다는 p-JNK 발현이 거의 없었다. 그러나 폐포 대식세포를 이용한 in vitro JNK kinase assay에서는 UIP 환자와 정상인 모두에서 JNK 활성도를 관찰할 수 없었다. 더구나 10 ng/mL의 TNF-$\alpha$로 자극하여도 JNK 활성도는 관찰할 수 없었다. 결 론 : UIP 환자의 폐 조직에서 JNK가 활성화되어 있음을 간접적으로 확인하였고, 추후 이들 활성화된 JNK와 fibrogenic cytokines과의 관계는 더 연구되어져야 할 과제로 생각된다.

• Tuberculosis and Respiratory Diseases
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• 제53권2호
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• pp.136-147
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• 2002

연구배경 : 간질성 폐질환은 병리소견, 임상경과 및 치료에 대한 반응에 있어서 다양한 양상을 보이지만 궁극적으로는 폐섬유화로 진행한다. 최근 간질성 폐질환의 병태생리에 있어서 폐상피세포의 아포프토시스가 폐섬유화로의 진행에 관여한다는 것이 보고되고 있다. 이에 저자들은 간질성 폐질환 환자에서 아포프토시스가 갖는 임상 및 병리학적 의미를 확인하기 위하여 TUNEL을 이용한 아포프토시스의 지수와 임상양상, 병리소견, HRCT소견, 그리고 치료반응 등과의 상관관계를 분석하였다. 방 법 : 개흉폐생검을 통해서 확진된 간질성 폐질환 환자 20명을 대상으로 하였다. 아포프토시스의 지수는 TUNEL 양성세포의 분율에 따라서 0-2로 구분하였다. 임상양상은 CRP 점수체계를 응용하여 이용하였다. 병리소견은 섬유화, 세포충실도, 탈락화, 육아조직성 정도에 따라 점수화하였다. HRCT소견은 간유리음영과 봉와양음영을 각 엽별로 침범한 정도에 따라서 점수화하였다. 치료의 반응은 치료전과 치료후 3개월째에 시행한 CRP 점수체계의 변화율이 10%이상 증가하였을 때 치료효과가 있는 것으로 판정하였다. 결 과 : 대상 환자는 20명(남 14명, 여 6명)으로 조직학적 아형으로는 AIP 3명, NIP 2 명, BOOP 8명, UIP 7 명이었다. 아포프토시스 지수와 CRP 점수체계의 요소들과는 유의한 상관관계가 없었으며 또한 HRCT소견인 간유리음영점수와 섬유화점수는 역시 유의한 상관관계가 없었다. 조직학적소견에서는 섬유화 점수, 세포충실도 점수, 그리고 탈락화 점수에서 아포프토시스 지수와 유의한 상관관계를 보였다. 부신피질호르몬 치료를 받은 16명의 환자중에서 9명 (56.3%)에서 치료효과가 있었는데 부신 피질호르몬 치료효과 유무와 아포프토시스 지수사이에는 상관관계는 없었다. 급, 아급성 간질성폐렴에서는 세포충실도 점수와 탈락화 점수가 아포프토시스 지수와 유의한 상관관계를 보였으며 만성 간질성 폐렴에서는 섬유화 점수와 세포충실도 유의한 상관관계를 보였다. 결 론 : 간질성 폐질환에서 아포프토시스 지수와 병리학적 지표들과의 유의한 상관관계를 관찰한 본 연구를 통하여 간질성 폐질환의 병태생리에 아포프토시스가 관여한다는 사실을 확인할 수 있었다.

• Tuberculosis and Respiratory Diseases
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• 제50권4호
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• pp.493-498
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• 2001

저자들은 4개월간의 호흡곤란을 주소로 내원하여 피부병변은 없었지만 흉강경하 폐생검과 식도내압검사, 핵항체검사 등으로 경피증을 확진한 Systemic sclerosis sine scleroderma 1례를 경험하였기에 문헌 고찰과 함께 보고하는 바이다.

• Biomolecules & Therapeutics
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• 제31권5호
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• pp.484-495
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• 2023

Idiopathic pulmonary fibrosis (IPF) can be defined as a progressive chronic pulmonary disease showing scarring in the lung parenchyma, thereby resulting in increase in mortality and decrease in the quality of life. The pathophysiologic mechanism of fibrosis in IPF is still unclear. Repetitive microinjuries to alveolar epithelium with genetical predisposition and an abnormal restorative reaction accompanied by excessive deposition of collagens are involved in the pathogenesis. Although the two FDA-approved drugs, pirfenidone and nintedanib, are under use for retarding the decline in lung function of patients suffered from IPF, they are not able to improve the survival rate or quality of life. Therefore, a novel therapeutic agent acting on the major steps of the pathogenesis of disease and/or, at least, managing the clinical symptoms of IPF should be developed for the effective regulation of this incurable disease. In the present review, we tried to find a potential of managing the clinical symptoms of IPF by natural products derived from medicinal plants used for controlling the pulmonary inflammatory diseases in traditional Asian medicine. A multitude of natural products have been reported to exert an antifibrotic effect in vitro and in vivo through acting on the epithelial-mesenchymal transition pathway, transforming growth factor (TGF)- β-induced intracellular signaling, and the deposition of extracellular matrix. However, clinical antifibrotic efficacy of these natural products on IPF have not been elucidated yet. Thus, those effects should be proven by further examinations including the randomized clinical trials, in order to develop the ideal and optimal candidate for the therapeutics of IPF.

• 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.