Korean Guidelines for Diagnosis and Management of Interstitial Lung Diseases: Part 1. Introduction / 결핵

Idiopathic interstitial pneumonia (IIP) is a histologically identifiable pulmonary disease without a known cause that usually infiltrates the lung interstitium. IIP is largely classified into idiopathic pulmonary fibrosis, idiopathic non-specific interstitial pneumonia, respiratory bronchiolitis-interstitial lung disease (ILD), cryptogenic organizing pneumonia, desquamative interstitial pneumonia, and acute interstitial pneumonia. Each of these diseases has a different prognosis and requires specific treatment, and a multidisciplinary approach that combines chest high-resolution computed tomography (HRCT), histological findings, and clinical findings is necessary for their diagnosis. Diagnosis of IIP is made based on clinical presentation, chest HRCT findings, results of pulmonary function tests, and histological findings. For histological diagnosis, video-assisted thoracoscopic biopsy and transbronchial lung biopsy are used. In order to identify ILD associated with connective tissue disease, autoimmune antibody tests may also be necessary. Many biomarkers associated with disease prognosis have been recently discovered, and future research on their clinical significance is necessary. The diagnosis of ILD is difficult because patterns of ILD are both complicated and variable. Therefore, as with other diseases, accurate history taking and meticulous physical examination are crucial.

Korean Guidelines for Diagnosis and Management of Interstitial Lung Diseases: Part 1. Introduction / 결핵및호흡기질환

Idiopathic interstitial pneumonia (IIP) is a histologically identifiable pulmonary disease without a known cause that usually infiltrates the lung interstitium. IIP is largely classified into idiopathic pulmonary fibrosis, idiopathic non-specific interstitial pneumonia, respiratory bronchiolitis-interstitial lung disease (ILD), cryptogenic organizing pneumonia, desquamative interstitial pneumonia, and acute interstitial pneumonia. Each of these diseases has a different prognosis and requires specific treatment, and a multidisciplinary approach that combines chest high-resolution computed tomography (HRCT), histological findings, and clinical findings is necessary for their diagnosis. Diagnosis of IIP is made based on clinical presentation, chest HRCT findings, results of pulmonary function tests, and histological findings. For histological diagnosis, video-assisted thoracoscopic biopsy and transbronchial lung biopsy are used. In order to identify ILD associated with connective tissue disease, autoimmune antibody tests may also be necessary. Many biomarkers associated with disease prognosis have been recently discovered, and future research on their clinical significance is necessary. The diagnosis of ILD is difficult because patterns of ILD are both complicated and variable. Therefore, as with other diseases, accurate history taking and meticulous physical examination are crucial.

Preoperative Evaluation for the Prediction of Postoperative Mortality and Morbidity in Lung Cancer Candidates with Impaired Lung Function / 결핵

BACKGROUND: The evaluation of candidates for successful lung resection is important. We studied to Our study was conducted to determine the preoperative predictors of postoperative mortality and morbidity in lung cancer patients with impaired lung function. METHOD: Between October 1, 1995 to August 31, 1997, 36 lung resection candidates with FEV1 of less than 2L or 60% predicted due to lung cancer were included prospectively. Age, sex, weight loss, hematocrit, serum albumin, EKG and concomitant illness were considered as systemic potential predictors for a successful lung resection. Smoking history, presence of pneumonia, dyspnea scale(1 to 4), arterial blood gas analysis with room air breathing, routine pulmonary function test were also included for the analysis. In addition, predicted postoperative(ppo)pulmonary factors such as ppo-FEV1, ppo-diffusing capacity(DLco), predicted postoperative product(PPP) of ppo-FEV1% x ppo-DLco% and ppo-maximal O2 uptake(VO2max) were also measured. RESULTS: There were 31 men and 5 women with the median age of 65 years (range 44 to 82) and a mean FEV1 of 1.78 +/-0.06L. Pneumonectomy was performed in 14 patients, bilobectomy in 8, lobectomy in 14. Pulmonary complications developed in 10 patients, cardiac complications in 3, other complications (empyema, air leak, bleeding) in 4. Twelve patients were managed in the intensive care unit for more than 48 hours. Two patients died within 30 days after operation. The ppo-VO2max was less than 10 mg/kg/min in these two patients. MVV was the only predictor for the pulmonary complications. However, there was no predictors for the post operative death in this study.

Inflammatory cells and T lymphocytes in bronchoalveolar lavage fluid from asthmatic patients: Relationship with development of asthmatic symptoms and therapeutic responese / 알레르기

OBJECTIVES: Chronic asthma has a number of characteristic feature; the increased airway responsiveness and bronchial inflammation. Although these mechanisms are not clear, activated T-cell has had an important role in migration and activation of inflammatory cells. In order to evaluate the role of T-lymphocyte and T-cell subsets in the development of asthmatic symptoms and the posibility for predicting the therapeutic response, we performed bronchoalveolar lavage from asymptomatic and symptomatic asthmatic subjects and inflammatory cell count, T-cell subset, activated T-lymphocyte were analysed and they were compared with healthy controls. METHOD: 76 bronchial asthmatics and 54 healthy controls were enrolled in this study. Asthmatic patients were classified into symptomatic and asymptomatic group according to symptom severity. Symptomatic group was divided into two groups according to therapeutic response ; early responder(ER) and late responder(LR). Lymphocytes(T-lymphocytes subsets and activation marker) in bronchoalveolar lavage(BAL) cells were analyzed using a flow-cytometry. RESULTS: The counts of eosinophil and neutrophil in BAL fluid were significantly higher in both asymptomatic and symptomatic asthmatic patient than those of healthy controls (p0.05), the numbers of T3 and T4 lymphocyte subsets were significantly higher in LR than in healthy controls, and the number of T3-IL2R+, T4-IL2R+ lymphocytes were significantly higher in ER than in healthy controls(p<0.05). CONCLUSION: We could conclude that the infiltration and activation of T-lymphocytes might be associated with the development of asthmatic symptoms and responsiveness to therapy.

A Study of EFFECT and MECHANISM of IL-2on SURVIVAL of EOSINOPHILS / 결핵

BACKGROUND: Interleukin-5 (IL-5) is responsible for eosinophilia in allergic diseases. In allergic bronchial asthma, there is a correlation between the extent of eosinophil infiltration in bronchial mucosa and IL-5 concentrations. In addition, IL-2 concentration is elevated in the airways and associated with eosinophilia in symptomatic patients with bronchial asthma. In animal studies, IL-2 can induce eosinophilia by increasing the synthesis of IL-5, however, it is still unknown how IL-2 can induce eosinophila in human being. The aim of this study is to evaluation the effect and mechanism of IL-2 on prolongation of eosinophil survival. METHODS: After purifiing the eosinophils from the venous blood of allergic patients with eosinophilia, we measured the survival rates of eosinophils using trypan blue dye exclusion test, and the number of eosinophils with Randolp's solution. We compared the survival rates of eosinophils in the presence of IL-2 or IL-5. Neutralizing antibody for IL-5 was added in IL-2 treated eosinophils to reveal whether IL-2 induced prolongation of eosinophil survival was mediated by IL-5. We checked IL-5 m-RNA expression of lymphocytes in the presence of IL-2 by using Reverse transcription-Polymerase chain reaction (RT-PCR) method to revealed the effect of IL-2 on IL-5 m-RNA expression on lymphocyte. alpha and beta IL-2 receptors were measured on eosinophils and lymphocytes with flow-cytometer after stimulated with IL-2. RESULTS: 1) Eosinophil survival rates increased dose dependently on IL-5 and IL-2. 2) The eosinophil survival rates increased by IL-2 were not inhibited by the pretreatment with neutralizing antibody for IL-5. 3) IL-5 m-RNA was not expressed on lymphocytes by the treatment with IL-2 up to 96 hours. 4) IL-2 upregulate the expression of IL-2Ralpha on eosinophils, instead of no effect on the expression of IL-2Rbeta. CONCLUSION: Interleukin-2 had the enhancing effect on the survival rates of eosinophils. The mechanism behind IL-2 induced eosinophilia might be the increment of IL-2 receptors on eosinophils rather than IL-5 synthesis by lymphocytes.