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Introduction To date, no prospective phase III trials have directly compared the efficacy of pemetrexed plus cisplatin (Pem-Cis) with docetaxel plus cisplatin (Doc-Cis) in patients with nonsquamous non–small-cell lung cancer. Materials and Methods A total of 148 chemotherapy-naive patients lacking driver mutations were randomized into 21-day regimens of cisplatin 70 mg/m 2 with either docetaxel 60 mg/m 2 (n = 71) or pemetrexed 500 mg/m 2 (n = 77) for ≤ 4 cycles. The primary objective was to assess the noninferiority of progression-free survival (PFS) for patients receiving the Doc-Cis regimen. The secondary endpoints were the response rates, overall survival, and toxicity profiles. Results Partial remission was observed in 24 (31.2%) and 24 (33.8%) patients in the Pem-Cis and Doc-Cis groups, respectively. The median PFS was 4.7 months (95% confidence interval [CI], 4.4-5.0) in the Pem-Cis arm and 4.4 months (95% CI, 3.7-5.1) in the Doc-Cis arm ( P > .05). The median overall survival was longer in the Doc-Cis arm (13.3 months; 95% CI, 8.1-18.5) than in the Pem-Cis arm (11.7 months; 95% CI, 8.6-14.8; P > .05). Between the 2 arms, no significant difference was found in the subsequent treatments after failure of first-line treatment. The rate of grade 3 or 4 neutropenia and febrile neutropenia was greater in the Doc-Cis arm than in the Pem-Cis arm. Conclusion In nonsquamous non–small-cell lung cancer patients lacking driver mutations, the PFS and response rates were similar between the 2 arms, and toxicity was tolerable, although adverse events and more severe toxicities were observed more frequently in the Doc-Cis arm.

Organizing pneumonia (OP) is an inflammatory lung disease characterized pathologically by the presence of buds of granulation tissue in the distal air spaces. There are numerous causes of OP including acute respiratory infections such as viral and bacterial infections. However, Mycobacterium abscessus (M. abscessus) has rarely been reported as a causative pathogen of OP. Here, we report a 67-year-old woman with rapidly progressive pulmonary M. abscessus infection who developed OP and acute respiratory failure (ARF). She was treated successfully with a corticosteroid and anti-mycobacterial therapy. Our observations suggest that pulmonary M. abscessus infection should be added to the list of infectious conditions associated with OP.

Acute respiratory distress syndrome (ARDS) caused by pneumonia in patients with hematologic malignancies can be life-threatening. Extracorporeal membrane oxygenation (ECMO) is the only temporary treatment for patients with ARDS who are refractory to conventional treatment. However, the immunosuppression and coagulopathies in hematological malignancies such as lymphoma and acute leukemia are relative contraindications for ECMO, due to high risks of infection and bleeding. Here, we report a 22-year-old man with acute myeloid leukemia (AML) who developed pneumonia and ARDS during induction chemotherapy; he was treated with ECMO.

Purpose Recently, there has been a rise in the interest to understand the composition of indoor dust due to its association with lung diseases such as asthma, chronic obstructive pulmonary disease (COPD) and lung cancer. Furthermore, it has been found that bacterial extracellular vesicles (EVs) within indoor dust particles can induce pulmonary inflammation, suggesting that these might play a role in lung disease. Methods We performed microbiome analysis of indoor dust EVs isolated from mattresses in apartments and hospitals. We developed diagnostic models based on the bacterial EVs antibodies detected in serum samples via enzyme-linked immunosorbent assay (ELISA) in this analysis. Results Proteobacteria was the most abundant bacterial EV taxa observed at the phylum level while Pseudomonas, Enterobacteriaceae (f) and Acinetobacter were the most prominent organisms at the genus level, followed by Staphylococcus. Based on the microbiome analysis, serum anti-bacterial EV immunoglobulin G (IgG), IgG1 and IgG4 were analyzed using ELISA with EV antibodies that targeted Staphylococcus aureus, Acinetobacter baumannii, Enterobacter cloacae and Pseudomonas aeruginosa. The levels of anti-bacterial EV antibodies were found to be significantly higher in patients with asthma, COPD and lung cancer compared to the healthy control group. We then developed a diagnostic model through logistic regression of antibodies that showed significant differences between groups with smoking history as a covariate. Four different variable selection methods were compared to construct an optimal diagnostic model with area under the curves ranging from 0.72 to 0.81. Conclusions The results of this study suggest that ELISA-based analysis of anti-bacterial EV antibodies titers can be used as a diagnostic tool for lung disease. The present findings provide insights into the pathogenesis of lung disease as well as a foundation for developing a novel diagnostic methodology that synergizes microbial EV metagenomics and immune assays.

Purpose Recent experimental evidence shows that extracellular vesicles (EVs) in indoor dust induce neurtrophilic pulmonary inflammation, which is a characteristic pathology in patients with severe asthma and chronic obstructive pulmonary disease (COPD). In addition, COPD is known to be an important risk factor for lung cancer, irrespective of cigarette smoking. Here, we evaluated whether sensitization to indoor dust EVs is a risk for the development of asthma, COPD, or lung cancer. Methods Serum IgG antibodies against dust EVs were measured in 90 healthy control subjects, 294 asthmatics, 242 COPD patients, and 325 lung cancer patients. Serum anti-dust EV IgG titers were considered high if they exceeded a 95 percentile value of the control subjects. Age-, gender-, and cigarette smoke-adjusted multiple logistic regression analyses were performed to determine odds ratios (ORs) for asthma, COPD, and lung cancer patients vs the control subjects. Results In total, 4.4%, 13.6%, 29.3%, and 54.9% of the control, asthma, COPD, and lung cancer groups, respectively, had high serum anti-dust EV IgG titers. Adjusted multiple logistic regression revealed that sensitization to dust EVs (high serum anti-dust EV IgG titer) was an independent risk factor for asthma (adjusted OR, 3.3; 95% confidence interval [CI], 1.1-10.0), COPD (adjusted OR, 8.0; 95% CI, 2.0-32.5) and lung cancer (adjusted OR, 38.7; 95% CI, 10.4-144.3). Conclusions IgG sensitization to indoor dust EVs appears to be a major risk for the development of asthma, COPD, and lung cancer.

Background Antituberculosis drugs (ATD) is the most common cause of drug-induce liver injury in many countries. While the mechanism of ATD-induced hepatitis is poorly understood, oxidative stress is suggested to be involved in the development of liver injury to drug metabolites. In this regards, we explored the possible associations between glutathione related enzymes (GCLM, GCLC and GSTP1) gene polymorphisms and ATD-induced hepatitis.

Malignant pleural mesothelioma (MPM) is an aggressive, treatment-resistant, and generally fatal disease. A 68-year-old male who was diagnosed with MPM at another hospital came to our hospital with dyspnea. We advised him to take combination chemotherapy but he refused to take the treatment. That was because he had already received chemotherapy with supportive care at another hospital but his condition worsened. Thus, we recommended photodynamic therapy (PDT) to deal with the dyspnea and MPM. After PDT, the dyspnea improved and the patient then decided to take the combination chemotherapy. Our patient received chemotherapy using pemetrexed/cisplatin. Afterwards, he received a single PDT treatment and then later took chemotherapy using gemcitabine/cisplatin. The patient showed a survival time of 27 months, which is longer than median survival time in advanced MPM patients. Further research and clinical trials are needed to demonstrate any synergistic effect between the combination chemotherapy and PDT.

Genetic variants in ATP-binding cassette (ABC) transporter genes are associated with increased susceptibility to adverse drug reactions. We hypothesized that genetic variant ABC transporters (ABCB1 and ABCC2) may be candidate markers for predicting maculopapular eruption (MPE) induced by antituberculosis therapy. We compared the genotype distributions of single nucleotide polymorphisms and haplotypes in the ABCB1 and ABCC2 genes between 62 antituberculosis drug (ATD)-induced MPE cases and 159 ATD-tolerant controls using multivariate logistic regression analysis. There was no significant association between genetic polymorphisms in ABCB1 and ATD-induced MPE (P>0.05). Among seven selected SNPs of ABCC2, IVS3-49C>T in intron and I1324I were associated with ATD-induced MPE (P=0.029 and 0.036, respectively). In an analysis of the ABCC2 haplotypes (ht; -1549G>A_-24C>T_IVS3-49C>T_V417I), ht1[G-C-C-G] was significantly associated with ATD-induced MPE (P=0.032, OR=0.35, 95% CI: 0.16-0.95). No significant association between the other haplotypes and ATD-induced MPE was observed. An ABCC2 haplotype is associated with the presence of ATD-induced MPE in patients with tuberculosis and may be a genetic risk factor for the development of MPE induced by ATD.

Background : Airborne particles during Yellow Sand phenomena are known to be associated with the respiratory disease. The purpose of this study was to evaluate the concentration and metal component properties of Yellow Sand particles and compare with airborne microbial concentration and species in non Yellow Sand and Yellow Sand phenomena. Methods : Samplings were carried out in 2002 in Seosan, during non Yellow Sand and Yellow Sand phenomena. Samples were taken using the 8-stage Cascade impactor and metallic elements were analyzed by XRF. Those were culture on the media for bacterial and fungal culture and celline for virus. Results : The concentration of total suspended particulate matter were respectively , in non Yellow Sand and Yellow Sand phenomena. The concentration of metallic elements such as Ca, Fe, Cu and Zn in Yellow Sand phenomena were higher than its in non Yellow Sand. Two bacteria, Bacillus species and Staphylococcus were grown in two periods. In both periods, several fungal spores(Mucor species, Cladosporum, Alternaria, Aspergillus, Penicillium, and Alternaria species) were identified. The differences of bacteria and fungus species not observed in Yellow Sand and non Yellow Sand. Any viruses were not isolated in between both periods. Conclusions : The concentration of total suspended particulate matter and some metallic elements in Yellow Sand phenomena were higher than its in non Yellow Sand. The difference of bacteria and fungus species was not observed in non Yellow Sand and Yellow Sand phenomena.

Sarcoidosis is a rare systemic disorder with unknown cause that is characterized pathologically by non-caseating granuloma. The lung and mediastinal lymph nodes are almost always involved, and most patients experience acute or insidious respiratory symptom. Because sarcoidosis is an interstitial lung disorder involving the alveoli and bronchioles, the most common radiological finding is a reticularnodular lesion with lymphatic distribution. However, cavitation is quite rare. Sarcoidosis is also a major cause of hepatic granuloma in Western countries, accounting for 12% to 30% of cases. In most patients, the course of hepatic sarcoidosis is benign. However, chronic intrahepatic cholestasis or portal hypertension may develop in some patients. We report a case of sarcoidosis with cavitation and hepatic involvement.

Background :N itric Oxide (NO) is a multi-faceted molecule with dichotomous regulatory roles in many areas of biology. NO can promote apoptosis in some cells, whereas it inhibits apoptosis in other cell types. This study was performed to characterize NO-induced cell death in lung epithelial cells and to investigate the roles of cell death regulators including iron, bcl-2 and p53. Methods :A 549 cells were used for lung epithelial cells. SNP (sodium nitroprusside) and SNAP (S-nitroso-N-acetyl- penicillamine) were used for NO donor. Cytoxicity assay was done by MTT assay and crystal violet assay. Apoptotic assay was done by fluorescent microscopy after double staining with propidium iodide and hoecst 33342. Iron inhibition study was done with RBCs and FeSO4. For bcl-2 study, bcl-2 overexpressing cells (A549-bcl-2) were used and for p53 study, Western blot analysis and p53 functionally knock-out cells (A549-E6) were used. Results :S NP and SNAP induced dose-dependent cell death in A549 cells and fluorescent microscopy revealed that SNAP induced apoptosis in low doses but necrosis in high doses while SNP induced exclusively necrotic cell death. Iron inhibition study using RBCs and FeSO4 significantly blocked SNAP-induced cell death. And also SNAP-induced cell death was blocked by bcl-2 overexpression.

Background : IFN-γ is the main effector mediator of the host immune response against Mycobacterium tuberculosis. Evaluating the IFN-γ gene expression in response to M. tuberculosis antigens may help in elucidating the host defense mechanism against M. tuberculosis and in the development of a vaccine. Methods : The IFN-γ mRNA expression in the lymphocytes obtained from pleural effusions from tuberculous pleurisy patients (TB-PLC) after in vitro stimulation with whole cell M. tuberculosis(H37Rv), purified protein derivatives(PPD), man-lipoarabinamman (man-LAM), ara-LAM and Antigen 85B(Ag85B) were evaluated. The degree of IFN-γ mRNA expression was determined by a semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) method. Results : M. tuberculosis induced the expression of IFN-γ mRNA in the TB-PLC in time and dose dependent manners. The PPD and Ag85B induced high levels of IFN-γ mRNA expression in the TB-PLC. However, man-LAM inhibited IFN-γ mRNA expression in the TB-PLC, while ara-LAM did not. Conclusion : IFN-γ mRNA expression in TB-PLC is stimulated by PPD and Ag85B, but inhibited by man-LAM. (Tuberc Respir Dis 2004; 57:25-31)

Background : Gemcitabine is a new anti-cancer agent for treating non-small cell lung cancer. Functioning as an antimetabolite, it induces anti-cancer effects by suppressing DNA synthesis after being incorporated into the DNA as a cytosine arabinoside analogue. When Gemcitabine is incorporated into the DNA, the p53 gene may be activated by induction of the DNA defect. However, there are a few studies on the molecular mechanisms of Gemcitabine-induced cell death. This study examined the role of p53 in Gemcitabine-induced cell death. Methods : A549 and NCl-H358 lung cancer cells were used in this study. The cell viability test was done using a MTT assay at Gemcitabine concentrations of 10nM, 100nM, 1uM, 10uM and 100uM. A FACScan analysis with propium iodide staining was used for the cell cycle analysis. Western blot analysis was done to investigate the extent of p53 activation. For the functional knock-out of p53, stable A549-E6 cells and H358-E6 cells were transfected pLXSN-16E6SD which is over expresses the human papilloma virus E6 protein that constantly degrades p53 protein. The functional knock out of p53 was confirmed by Western blot analysis after treatment with a DNA damaging agent, doxorubicine. Results : Gemcitabine exhibited cell toxicity in dose-dependent fashion. The cell cycle analysis resulted in an S phase arrest. Western blot analysis significant p53 activation in time-dependent manner. Gemcitabine-induced cytotoxicity was reduced by 20-30% in the A549-E6 cells and the 30-40% in H358-E6 cells when compared with the A549-neo and H358-neo control cells. Conclusion : Gemcitabine induces an S phase arrest, as expected for the anti-metabolite, and activates the p53 gene, Furthermore, p53 might play an important role in Gemcitabine-induced cell death. Further investigation into the molecular mechanisms on how Gemcitabine activates the p53 gene and its signaling pathway are recommended.

Background : Interstitial lung disease has various manifestations that are differentiated by their pathology, progress and treatment. However, all manifestations eventually progresses to pulmonary fibrosis. Recent studies have shown that apoptosis of pulmonary epithelial cells might be related to pulmonary fibrosis. The correlation of the apoptotic index with the clinical manifestations, pathological findings, HRCT findings and the response to treatment were examined. Materials and Methods : Twenty subjects (14 men, 16 women), who had been diagnosed with interstitial lung disease through an open lung biopsy, were enrolled in this study. The subtypes were one AIP, two NIP, eight BOOP, and seven UIP cases. The apoptotic index was scaled from 0-2 depending on the fraction of positive staining cells by TUNEL method. The clinical severity was assessed by a modification of a previously developed CRP scoring system. The pathologic scores were based on 4 components: fibrosis, cellularity, desquamation, and granulation. In the HRCT study, each lobe was scored by the radiologists on a scale for both fibrosis and ground-glass attenuation. The treatment response was assessed by an increase in more than 10% of the CRP score, and comparing the results 3 months before and after treatment. Results : The apoptotic index showed no correlation with the CRP and HRCT scoring system. The apoptotic index correlated with the pathologic elements including fibrosis, cellularity and the desquamation score (p

Background : Steroid therapy has been shown to improve the clinical outcome in acute respiratory distress syndrome (ARDS) patients with histological evidence of fibroproliferation in the lung tissue and no identifiable source of infection. Because the histopathological features of acute interstitial pneumonia(AIP) are identical with that of ARDS, early steroid therapy was used in AIP patients who had histological evidence of fibroproliferation in the lung tissue and no identifiable source of infection. We analyzed seven years of our experience to evaluate the efficacy of early steroid therapy in AIP. Materials and Methods : A retrospective review was performed on AIP patients who received steroid therapy within 7 days of mechanical ventilatory support in Dankook university Hospital between May 1995 and May 2002. AIP was diagnosed clinically by ARDS without a known cause of the etiology and pathologically by a lung biopsy showing a fibroproliferative stage of diffuse alveolar damage. The clinical response and physiologic parameters were evaluated during steroid therapy. Results : Five AIP patients received intravenous methylprednisolone (1-2 mg/kg every 6 hours) after days of mechanical ventilatory support. Lung biopsies were performed after days of mechanical ventilatory support. Four patients(80%) survived and were extubated after days of steroid therapy with improvement in the ratio ( at day 0 to at day 7) by steroid therapy. However, one patient(20%) died of respiratory failure after 15 days of steroid therapy. Conclusion : Early steroid therapy sppears to be beneficial in AIP patients without evidence of infection. However, as our study group was too small, further large scale studies to define the effectiveness of steroids are required.

연구배경: 운동이 폐기능에 미치는 영향에 대해서는 그동안 많은 연구가 진행되었으나 운동이 폐활량에 미치는 영향에 대해서는 이견이 많다. Impulse oscillometry(IOS)는 최근 관심의 대상이 되고 있는 새로운 방법의 폐기능 측정법이나 이 방법으로 운동의 효과를 연구한 보고는 아직 없는 실정이다. 본 연구에서는 일반 성인을 대상으로 운동의 정도에 따른 노력성 호기성 폐활량 측정법과 IOS를 이용하여 폐기능 검사를 시행하여 운동이 폐기능에 미치는 영향에 대해서 알아보고자 하였다. 방 법: 호흡기 증상이 없는 59명의 젊은 성인을 대상으로 최근 땀이 날 정도의 운동을 하는 시간에 따라 1주에 30분 이내인 제 1군 (23명), 30분에서 3 시간사이인 제 2군 (18명), 그리고 3시간 이상인 제 3군(18명)으로 나누고 이들에 대해 노력성 호기성 폐활량 측정법과 IOS를 이용한 폐기능 검사를 시행하였다. 결 과: 운동이 폐활량 측정법에 미치는 영향으로 호기성 폐활량(FVC)의 예측치에 대한 백분율은 운동시간이 1주에 3시간 이상인 군에서 1주에 30분 이내인 군에 비해 유의하게 높았으나(1군: $93.8{\pm}9.9%$ , 3군: $102.4{\pm}14.8%$ , p-value=0.017), 1초간의 노력성호기성 폐활량(FEV1)과 노력성 호기중간 기류량(FEF50%)의 예측치의 백분율은 각 군 사이에 유의한 차이가 없었다. 운동이 IOS 지표에 미치는 영향으로 5Hz에서의 유도저항에서 예측치를 뺀 값은 운동시간이 1주에 3 시간 이상인 군에서 30분 이내인 군에 비해 유의하게 낮았으나 (1 군 : $-0.093{\pm}0.036hPa/1/s$ , 3군: $-0.166{\pm}0.123hPa/1/s$ , p-value= 0.006), 공명주파수(Resonance frequency), 5Hz, 20Hz, 35Hz에서의 기도저항은 각 군 사이에 유의한 차이가 없었다. 결 론: 운동은 노력성 폐활량을 증가시키고 5Hz에서의 유도저항(X5)을 감소시킨다. 【Background: The effects of exercise on pulmonary function are complex and have been the subject of many investigations. But, there has been disputes about the effect of exercise on spirometric parameters and there is no study about the effect of exercise on IOS(Impulse Oscillometry)parameters. IOS, a new method of pulmonary function test, is based on the relationship between the pressure and flow oscillation which is produced by applying sinusoidal pressure oscillation to the respiratory system via the mouth. Method: Fifty-nine young adults without respiratory symptoms were divided into three groups according to degree of exercise(hard exercise group: mean exercise time is over three hours per week at least for the last one month, light exercise group : between thirty minutes to three hours, nonexercise group : less than thirty minutes) and undertaken pulmonary function test(simple spirometry and IOS). Results: The effects of exercise on spirometric parameters; percentage of predictive value of forced vital capacity(FVC % pred) was higher in hard exercise group than nonexercise group(hard exercise group: $102.4{\pm}14.8$ , nonexercise group: $93.7{\pm}9.9$ , p=0.017), but there was no significant difference in percentage of predicted value of forced expiratory volume in one second(FEV 1 % pred) and percentage of predicted value of forced expiratory flow 50% (FEF 50% pred) between groups. The effects of exercise on IOS parameters: Reactance at 5Hz(X5) was significantly lower in hard exercise group than nonexercise group(hard exercise group: $-0.166{\pm}0.123hPa/1/s$ , nonexercise group: $-0.093{\pm}0.036hPa/1/s$ , p=0.006) but there was no significant difference in central resistance(Rc), peripheral resistance(Rp), resonance frequency(RF) and resistance at 5Hz, 20Hz between groups. Conclusion: Hard exercise increased FVC % pred on spirometric parameters and decreased reactance at 5Hz(X5) on IOS parameters.】

Background: Etiologic diagnosis of pleural effusion is usually made by clinical characteristics, pleural fluid analysis and pleural biopsy. But, despite careful diagnostic study, the cause of pleural effusion cannot be found in about 20 percent of patients, especially in loculated pleural effusions. Tuberculous pleurisy is one of the most common cause of pleural effusion in Korea. But, pleural fluid culture for Mycobacterium tuberculosis are positive in only 20 to 30 percent of patients and typical pleural biopsy finding in less than 50 percent of patients with this disease. In recent studies, adenosine deaminse(ADA) and its isoenzymes were proposed to be a useful diagnostic tool for differential diagnosis of pleural effusion. We investigated the pattern of ADA and its iscenzyme activities in various cause of pleural effusions to evaluate the diagnostic value of measuring ADA and its isoenzymes. Method: We measured total ADA and its isoenzyme activities in pleural fluid and serum from 54 patients with pleural effusion(25 tuberculous pleural effusion, 10 parapneumonic effusion, 14 malignant pleural effusion, 5 transudative pleural effusion), including 5 loculated tuberculous pleural effusions and 6 loculated parapneumonic effusions. Total ADA activity was measured by the spectrophotometric method and ADA2 isoenzyme activity was measured with same method using EHNA, potent inhibitor of ADA1 isoenzyme activity. Result: Total ADA activity of tuberculous pleural effusion was higher than malignant pleural effusion(p, parapneumonic effusion: , malignant pleural effusion: ). Percentage of ADA2 activity to total ADA activity(ADA2%) of pleural effusion of tuberculous pleurisy was higher than parapneumonic effusion(p, parapneumonic effusion: , malignant pleural effusion: ). In loculated pleural effusion, ADA2% of tuberculous pleural effusion was higher than parapneumonic effusion(tuberculous pleural effusion: , parapneumonic effusion: ). Conclusion: Measurement of ADA isoenzyme activity is useful for differentiating tuberculous pleural effusion from parapneumonic effusion, especially in loculated pleural effusion.

Background : Impulse Oscillometry is a noninvasive and effort-independent test used to characterize the mechanical impedance of the respiratory system. The clinical potential of the IOS is rapid and demands only passive cooperation which makes it especially appealing for children, for epidemiologic surveys and for conditions in which quiet breathig instead of forced expiratory maneuvers are preferred. However, several studies have shown conflicting results that the role of IOS about detection of smoking induced small airway diseases or early airway obstruction Methods : Study was to evaluate the clinical ability of the IOS to detect about smoking induced early airway obstruction in persons with normal spirometry test. Respiratory asymptomatic study groups were formed that one is non-smoking group, another is smoking group. Results : The parameters of spirometry were not significantly differences between non-smoking group and smoking group. Among the parameters of IOS, total resistance(non-smoking group : smoking group= : ), peripheral resistance( : ), bronchial compliance( : ) were not statistically significant different (p : , p : , p). Conclusion : Impulse oocillometer(IOS) is clinically available method to detect about smoking induced early airway obstruction. And clinically potential parameters of IOS were considers that total resistance, peripheral resistance, bronchial resistance, and reactance of low frequency at 5Hz, 10Hz.

Background : Diagnosis of tuberculous pleurisy is sometimes difficult using conventional diagnostic methods. We have investigated the utility of pleural fluid cell production assay in the diagnosis of tuberculous pleurisy. Methods : We prospectively performed pleural fluid cell production assay in 39 patients with tuberculous pleural effusions (TPE) and in 26 patients with nontuberculous pleural effusions (NTPE) (13 malignant pleural effusions and 13 parapneumonic effusions). Pleural fluid cells were cultured in DMEM media and stimulated with purified protein derivatives (PPD), and phytohemagglutinin (PHA) for 24 hr. The amount of released in the culture supernatant was quantitated by ELISA assay. We have also measured adenosine deaminase (ADA) activities and concentrations in the pleural fluid. Results : 1) The pleural fluid levels of ADA activity and concentrations were significantly higher in TPE than NTPE (p production in TPE cells stimulated by PPD () was significantly higher than NTPE cells () (p concentrations over 10,000 pg/ml is a criteria for the diagnosis of TBE, sensitivity and specificity of the test were 97.4 and 92.3%, respectively. 3) The ratios of production by the stimulation with PPD and PHA (PPD/PHA) were significantly higher in TPE cells () than NTPE cells ()(p production assay may be useful for the diagnosis of tuberculous pleurisy.