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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.

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.

Background: Few reports have documented the clinical characteristics and treatment outcomes of adult patients with Elizabethkingia meningoseptica infection. Methods: Medical records of patients over 18 years of age and suspected of having an E. meningoseptica infection from March 1, 2006 to February 28, 2013 were reviewed retrospectively. Their clinical characteristics, antimicrobial susceptibility results, and treatment outcomes were analyzed. Results: E. meningoseptica was isolated from 30 patients. Median age was 68.5 years, and infections were more frequent in males (17, 56.7%). The most common isolation source was sputum (23, 76.7%), and pneumonia was the most common condition (21, 70%) after excluding two cases of colonization. This bacterium was most susceptible to minocycline (27, 90%) and fluoroquinolones, including levofloxacin (20, 66.7%) and ciprofloxacin (18, 60%). The mortality rate due directly to E. meningoseptica infection was 20% (6/30), and uncontrolled pneumonia was the only cause of death. After isolating E. meningoseptica, the numbers of patients with pneumonia (9/9, 100% vs. 12/21, 57.1%), history of hemodialysis (5/9, 55.6% vs. 3/21, 14.3%), tracheostomy (8/9, 88.9 vs. 10/21, 47.6%), and median Charlson comorbidity index score (6 [range, 3–9] vs. 4 [range, 0–9]) were significantly higher in non-survivors than those in survivors (p < 0.05, for each). However, only 12 (40%) patients received appropriate antibiotics. Conclusions: E. meningoseptica infection most commonly presented as pneumonia in adults with severe underlying diseases. Despite the high mortality rate, the rate of appropriate antibiotic use was notably low.

Background While the mechanisms underlying the development of drug-induced liver injury are not clear, there is evidence to suggest that tumor necrosis factor-α (TNF-α) plays an important role in drug- or drug metabolite-induced immune responses. We hypothesized that polymorphisms in the TNF-α gene are associated with anti-tuberculosis drug (ATD)-induced hepatitis. Methods Patients who suffered from ATD-induced hepatitis were enrolled in the study. ATD-induced hepatitis was defined as an increase in liver transaminase levels that were more than three times the upper limit of normal. ATD-tolerant patients were used as a control. Patients were treated with first line ATD therapies including isoniazid, rifampicin, ethambutol, and pyrazinamide. We compared the genotype frequencies of the TNF-α polymorphism -308G/A in 77 patients with ATD-induced hepatitis and 229 ATD-tolerant patients. Results The frequency of carrying the variant allele (AG or AA) was significantly higher in patients with ATD-induced hepatitis compared with ATD-tolerant patients [26.0% vs. 15.3%, P = 0.034, OR (95% CI) = 1.94 (1.04–3.64)] and the frequency of the A allele was significantly different between the two groups [0.143 vs. 0.079, P = 0.018, OR (95% CI) = 1.95 (1.11–3.44)]. Conclusion These results reveal that the TNF-α genetic polymorphism -308G/A is significantly associated with ATD-induced hepatitis. This genetic variant may be a risk factor for ATD-induced hepatitis in individuals from Korea.

It has been suggested that drug-metabolizing enzymes might play important roles in the development of anti-tuberculosis drug (ATD)-induced maculopapular eruption (MPE), as in ATD-induced hepatitis. We investigated the associations between the genetic polymorphisms of drug-metabolizing enzymes and ATD-induced MPE.We enrolled 62 patients with ATD-induced MPE (mean age 47.2 ± 19.0, male 59.7%) and 159 patients without any adverse reactions to ATD (mean age 42.8 ± 17.6, male 65.4%), among patients with pulmonary tuberculosis (TB) and/or TB pleuritis and treated with first-line anti-TB medications, including isoniazid, rifampin, ethambutol, and pyrazinamide. We compared the genotype distributions of single nucleotide polymorphisms and haplotypes in four drug-metabolizing enzymes (N-acetyltransferase 2 (NAT2), cytochrome P450 (CYP) 2 C9, CYP2C19, and CYP2E1) among patients with ATD-induced MPE and patients tolerant to ATD using a multivariate logistic regression analysis. These analyses were made without identification of the responsible ATD.-1565 C T of CYP2C9 showed a significant association with ATD-induced MPE (P = 0.022, OR = 0.23, 95% CI 0.07-0.78), with a lower frequency of genotypes carrying minor alleles (CT or TT) in the case group than in the controls. Additionally, W212X of CYP2C19 was significantly associated with the risk of ATD-induced MPE (P = 0.042, OR = 0.27, 95% CI 0.09-0.82). In an analysis of the CYP2C19-CYP2C9 haplotypes (-1418 C T_W212X_-1565 C T_-1188 C T), ht3[T-A-T-C] showed a significant association with the development of ATD-induced MPE (P = 0.012, OR = 0.13, 95% CI 0.03-0.57). No significant associations between the other genetic polymorphisms and ATD-induced MPE were observed.CYP2C19 and CYP2C9 genetic polymorphisms are significantly associated with the risk of developing ATD-induced MPE, and the genetic variants in NAT2 and CYP2E1 are not closely related to the development of this adverse reaction.

Adverse reactions induced by antituberculosis drugs (ATD) often result in serious morbidities, impeding scheduled treatment and cure. In the development of ATD-induced adverse reactions, glutathione S-transferase has been suggested to play a protective role as an intracellular scavenger by conjugating toxic reactive metabolites of ATD. This study examined the association of null mutations in GST enzyme genes (GSTT1 and GSTM1) with the development of ATD-induced hepatitis and cutaneous reactions. We compared the frequencies of GSTT1 and GSTM1 null mutations in 57 patients with hepatitis, 94 patients with cutaneous adverse reactions, and 190 ATD-tolerant controls. The frequency of null mutations in GSTT1 and GSTM1 in patients with ATD-induced hepatitis was not significantly different from that of controls (59.6% vs. 54.2% and 45.6% vs. 54.7%, respectively). Additionally, no significant difference was observed in the frequency of either null mutation in patients with ATD-induced cutaneous reactions, including maculopapular eruption, compared with controls (58.5% vs. 54.1% for GSTT1 and 59.6% vs. 54.6% for GSTM1). These findings indicate that GSTT1 and GSTM1 null mutations are not associated with the development of ATD-induced hepatitis or cutaneous reactions in this Korean population, and suggest that glutathione S-transferase enzymes do not play important roles in the pathogenesis of these conditions.

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.

Unusual drug accumulation is a common mechanism underlying serious drug-induced liver injury. Polymorphisms in three drug transporter genes (ABCB1, SLCO1B1 and ABCC2) may be risk markers for hepatitis induced by the unusual accumulation of anti-tuberculosis drugs (ATDs). We therefore investigated whether polymorphisms and haplotypes of these genes are associated with ATD-induced hepatitis by comparing the frequencies and distributions of single nucleotide polymorphisms and haplotypes of these three drug transporter genes among 67 patients with ATD-induced hepatitis and 159 patients tolerant to ATDs using a multivariate logistic regression analysis. We found that the frequencies of polymorphisms and haplotypes of ABCB1, SLCO1B1 and ABCC2 were similar in patients with ATD-induced hepatitis and ATD-tolerant controls. The present results suggest that these drug transporters do not play important roles in the pathogenesis of ATD-induced hepatitis in Korean patients.

Aims: Although some genetic risk factors have been reported for the development of hepatitis due to anti-TB drugs, an extensive candidate gene approach evaluating drug-metabolizing enzymes has not been attempted. This study aimed to investigate the association of genetic polymorphisms in drug-metabolizing enzymes with anti-TB drug-induced hepatitis. Materials & methods: We compared genotype distributions of tagging SNPs in promoter, exons and haplotypes in seven drug-metabolizing enzyme genes (CYP2C9, CYP2C19, CYP2D6, CYP2E1, NAT2, UGT1A1 and UGT1A3) between 67 cases and 159 controls. Results: Among four tagging SNPs of N-acetyltransferase 2 (NAT2), -9796T>A in promoter and R197Q were significantly associated (p = 0.0016 and p = 0.0007, respectively). NAT2 haplotype 2 [A-A-A-G] carrying A allele of -9796T>A and A allele of R197Q showed significant association (p = 0.0004). However, there was no significant association between genotypes of other enzyme-metabolizing genes and anti-TB drug-induced hepatitis. The constructs containing -9796A of NAT2 showed significantly lower luciferase activity (p < 0.01), suggesting decreased expression of NAT2. The variant alleles and haplotype 2 showed significantly higher peak serum levels of isoniazid, lower acetyl isoniazid:isoniazid ratio and lower isoniazid clearance compared with wild-types. Conclusion: These findings suggest that genetic variants in the promoter and exons of NAT2 increase the risk of anti-TB drug-induced hepatitis by modifying acetylation phenotypes and/or gene expression of NAT2, and there is no essential role for genetic mutation of the other metabolizing enzymes in the development of this adverse reaction.

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.

기관지 동맥류는 세계적으로 드문 질환으로 파열될 경우 치명적인 출혈을 발생할 수 있다. 저자들은 공동성 결핵 병변에서 발생한 기관지 동맥류의 파열로 대량 객혈이 발생하여 기관지 동맥 색전술과 외과적 절제술로 치료한 환자를 경험하였기에 문헌고찰과 함께 보고하는 바이다.

Purpose: Fibroblast growth factor 2 (FGF2) has been shown to inhibit airway inflammation, mucus production, and airway hyperresponsiveness in mouse model of asthma. The aim of this study was to evaluate the safety and efficacy of inhaled recombinant FGF2 in asthmatic patients. Methods: Eight asthmatics were eligible for the study. All patients were admitted to a hospital, and recombinant FGF2 was administered using a nebulizer at a concentration of 4.5 ng/mL three times a day for one week. Pulmonary function test, methacholine bronchial provocation test, induced sputum analysis, asthma control test (ACT), and asthma quality of life questionnaire (AQLQ) were performed at the beginning of wash-out period, before and after the treatment, and at the end of study. And all these parameters were compared before and after FGF2 treatment. Results: There were no serious adverse events associated with recombinant FGF2 during five-week study period. Daytime and nocturnal symptoms improved after the treatment (P=0.028 and P=0.012, respectively). AQLQ and ACT also improved after the treatment (P=0.017 and P=0.011, respectively). However, lung function, airway hyperresponsiveness, and airway inflammation showed no significant difference before and after the treatment. Conclusion: Inhaled recombinant FGF2 was safely used to eight asthmatics without any serious adverse events, and improved daytime and nocturnal symptoms, and quality of life in adult asthmatics. FGF2 may be a potential drug in the treatment of asthma.

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.

Human placenta contains various kinds of nutritional elements essential for embryonic development. Currently, human placenta extracts are widely overused in Korea to improve certain health conditions (postmenopausal syndrome, liver function, and cosmetic purposes) without scientific evidence that they actually work. The use of placenta extracts should be restricted, due to a lack of systematic research on the therapeutic effectiveness and adverse results from these treatments. While the common adverse effects that have been reported are fever, rash, itching, nausea, vomiting, breast pain, and rare cases of anaphylactic shock, there have been no reports of pulmonary complications such as hypersensitivity pneumonitis. Recently, we experienced a patient with hypersensitivity pneumonitis following a placenta extract injection. To our knowledge, this is the first case of hypersensitivity pneumonitis associated with placenta extract use.Key Words: Placenta, Placenta extract, Hypersensitivity pneumonitis

Most studies on the effects of ambient ozone on asthmatics have been based on ozone concentration measurements taken by air monitors in downtown areas. Using a passive ozone sampler, we investigated the effects of on-site ozone concentra- tions on the pulmonary function and symptoms of asthmatics. Twenty moderate to severe asthmatics who had been managed for at least 2 months without changes of their medication were enrolled from 3 June to 18 July 2005. Respiratory, nasal and ocular symptoms, peak expiratory flow (PEF), which was measured twice a day, and medication use were recorded on a daily basis during the study period. Data for 17 subjects were analyzed. The average ozone exposure level was 28.2 ±23.6 ppb (3.4-315.3 ppb). There was no significant correlation between PEF and ozone concentration (p>0.05) on the same day or 1-, 2-, or 3-day lags. Interestingly, the degree of asthma symptoms was influenced by the ozone concentration ( = 0.303, p

Primary pulmonary artery sarcoma is a rare malignant tumor arising from the pulmonary artery. Diagnosis of primary pulmonary artery sarcoma is quite difficult and the conditon is often misdiagnosed as a more common disease, such as a pulmonary embolism. PET can help in diagnosing a pulmonary artery sarcoma due to the increased uptake of in the area of the tumor. However, the poor anatomic resolution of PET has limited its clinical applications in pulmonary vascular disease. The recently developed PET/CT is the fusion of PET and CT that improves the anatomical resolution of PET. We report a case of a primary pulmonary artery sarcoma mimicking a pulmonary embolism that was diagnosed with PET/CT and confirmed with a surgical resection.

Background: Recent studies have suggested an association between chronic cough and gastroesophageal reflux. Our study aimed to assess the utility of a proton-pump inhibitor in unexplained chronic cough patients. Methods: Patients with chronic cough of unknown etiology were evaluated using a chest x-ray, methacholine challenge test, and an empirical trial of postnasal drip therapy. After excluding other potential causes of the cough, forty patients were included in the study and treated for 8 weeks with a proton-pump inhibitor. Results: Eleven and three patients in the first and second 4 weeks were lost to follow-up, leaving twenty-six patients finally included in the study. Of these patients, two were unimproved, eight partially responded to the proton-pump inhibitor and sixteen responded completely after the 8 week treatment. Conclusion: We suggest that empirical treatment with a proton pump inhibitor in all patients with persistent cough, which is not secondary to asthma or postnasal drip syndrome, represents a practical and simple approach to this ailment.

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 : 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 : 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.

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.