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// Sun Min Lim 1, 2 * , Hye Ryun Kim 1 * , Eun Kyung Cho 3 , Young Joo Min 4 , Jin Seok Ahn 5 , Myung-Ju Ahn 5 , Keunchil Park 5 , Byoung Chul Cho 1 , Ji-Hyun Lee 6 , Hye Cheol Jeong 6 , Eun Kyung Kim 6 , Joo-Hang Kim 2 1 Department of Internal Medicine, Division of Medical Oncology, Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, Korea 2 Department of Internal Medicine, Division of Medical Oncology, CHA Bundang Medical Center, CHA University, Seongnam, Korea 3 Department of Internal Medicine, Gachon University Gil Medical Center, Incheon, Korea 4 Department of Oncology, Asan Medical Center, University of Ulsan college of Medicine, Seoul, Korea 5 Division of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea 6 Department of Internal Medicine, CHA Bundang Medical Center, CHA University, Seongnam, Korea * These authors have contributed equally to this work Correspondence to: Joo-Hang Kim, email: kim123@cha.ac.kr Keywords: primary resistance, epidermal growth factor, next-generation sequencing, tyrosine kinase inhibitor Received: March 01, 2016 Accepted: April 05, 2016 Published: April 21, 2016 ABSTRACT Background: Non-small-cell lung cancer (NSCLC) patients with activating epidermal growth factor receptor ( EGFR ) mutations may exhibit primary resistance to EGFR tyrosine kinase inhibitor (TKI). We aimed to examine genomic alterations associated with de novo resistance to gefitinib in a prospective study of NSCLC patients. Methods: One-hundred and fifty two patients with activating EGFR mutations were included in this study and 136 patients’ tumor sample were available for targeted sequencing of genomic alterations in 22 genes using the Colon and Lung Cancer panel (Ampliseq, Life Technologies). Results: All 132 patients with EGFR mutation were treated with gefitinib for their treatment of advanced NSCLC. Twenty patients showed primary resistance to EGFR TKI, and were classified as non-responders. A total of 543 somatic single-nucleotide variants (498 missense, 13 nonsense) and 32 frameshift insertions/deletions, with a median of 3 mutations per sample. TP53 was most commonly mutated (47%) and mutations in SMAD4 was also common (19%), as well as DDR2 (16%), PIK3CA (15%), STK11 (14%), and BRAF (7%). Genomic mutations in the PI3K/Akt/mTOR pathway were commonly found in non-responders (45%) compared to responders (27%), and they had significantly shorter progression-free survival and overall survival compared to patients without mutations (2.1 vs . 12.8 months, P =0.04, 15.7 vs. not reached, P

Objectives Cancer stem cells (CSCs) are considered to play a pivotal role in the process of invasion, metastasis and chemotherapy resistance. Diverse aberrantly expressed microRNAs (miRNAs) have been reported in lung cancer cells. However, there have been few reports about miRNAs that were associated with stemness and invasion of lung cancer. We investigated the role of miRNAs associated with characteristics of CSCs in non-small cell lung cancer (NSCLC). Materials and methods We cultured A549 cells (lung adenocarcinoma) and HCC1588 cells (lung squamous cell carcinoma) in serum free media condition. We isolated sphere-forming NSCLC cells and examined the microRNA expression by microarray and qRT-PCT. By inhibition of CSC-associated microRNAs, we identified the changes of stemness and invasiveness in NSCLC. Results and conclusion We discovered 44 over-expressed, 42 down-regulated miRNAs in the sphere-forming cells compared with the parent cells of NSCLC. By in-silico database search, we selected miR-1246 and miR-1290 that were suspected to be associated with CSCs among aberrantly expressed miRNAs. Inhibition of miR-1246 and miR-1290 showed decreased stemness markers and epithelial-mesenchymal transition (EMT) markers in NSCLC. Anti-miR-1246 and anti-miR-1290 suppressed proliferation, sphere-formation, colony formation and invasion of NSCLC. CSCs-associated miR-1246, or miR-1290 may be important in the invasion or metastasis of NSCLC.

Myocarditis is an inflammatory disease of the myocardium caused by various infectious or noninfectious triggers. Although viral infections are important causes of myocarditis, some drugs or toxins can also cause myocarditis. We report a case of life-threatening fulminant myocarditis which followed an extensive coffee diet program. Despite medical treatment, the patient was not able to maintain hemodynamic stability. She was supported by extracorporeal membrane oxygenation and completely recovered 3 months later.

It is well known that oral corticosteroid and anti-tumor necrosis factor-α agents increase the risk of TB. However, little is known about whether inhaled corticosteroid (ICS) increases the risk of TB. We performed this study to assess the risk of pulmonary TB among ICS users, based on the presence of the radiologic sequelae of pulmonary TB.A retrospective cohort study was performed. Between January 1, 2000, and December 31, 2005, a total of 778 patients who had COPD were recruited. Among them, 162 patients were excluded according to the exclusion criteria. In total, 616 patients were followed until December 31, 2010. They were divided into four groups according to whether they used ICS and whether they had radiologic sequelae of prior pulmonary TB.A total of 20 patients developed pulmonary TB. Kaplan-Meier estimates showed an increased risk of pulmonary TB among the ICS users who had radiologic sequelae of prior pulmonary TB ( P , .001). Multivariate Cox regression showed that ICS use was an independent risk factor for the occurrence of pulmonary TB in patients who had a normal chest radiograph (hazard ratio, 9.079; 95% CI, 1.012-81.431; P 5 .049) and in patients who had radiologic sequelae of prior pulmonary TB (hazard ratio, 24.946; 95% CI, 3.090-201.365; P 5 .003).ICS use increases the risk of pulmonary TB in patients with COPD and the risk is greater in patients who have radiologic sequelae of prior pulmonary TB.

Large cell neuroendocrine carcinoma (LCNEC) of the lung is a rare and aggressive tumour with a poor prognosis. Lung cancer metastases to the prostate are also uncommon, and are usually found incidentally during autopsy. Most reported primary lung cancers with prostatic metastases are small cell carcinomas, and prostatic metastases from LCNEC of the lung have not been reported previously. This case report describes a 70-year-old man with LCNEC of the lung and metastases in the prostate, brain, bone, liver and lymph nodes.

Summary Background A recently conducted randomized, phase III study that compared irinotecan plus cisplatin (IP) with etoposide plus cisplatin for the patients with extensive disease SCLC revealed a superior median survival rate and a superior 2-year survival rate for the IP combination therapy. Yet there have been few such reports on the patients suffering with limited disease SCLC (LD-SCLC). We conducted a phase II trial to evaluate the efficacy and toxicity of administering IP with concurrent radiotherapy for the patients with LD-SCLC. Patients and Methods Twenty chemotherapy-naive patients with LD-SCLC were enrolled in our study. The patients were treated with 40 mg/m2 irinotecan on days 1, 8 and 15 and with 60 mg/m2 cisplatin on day 1 every 4 weeks until a maximum of six cycles was delivered. Once-daily radiotherapy included the administration of 50.4 Gy in 28 fractions. After completion of the radiation therapy, the dose of irinotecan was increased to 60 mg/m2. Results The response rate was 85% (CR: 6; partial response, PR: 11). The median survival was 20.0 months (95% CI: 15.6–24.4 months) with 1-year and 2-year overall survival rates of 85 and 35%, respectively. The median progression free survival (PFS) was 12 months (95% CI: 6.2–18.1 months) with a 1-year PFS of 36%. The major hematologic toxicities of this regimen were neutropenia (60%), leukopenia (55%), anemia (20%) and thrombocytopenia (10%). The non-hematologic toxicities were nausea/vomiting (55%), diarrhea (35%) and dysphagia (15%). Conclusions Our data show that IP with concurrent radiotherapy is an effective and tolerable regimen for the treatment of LD-SCLC and these findings warrant further investigation.

Background Acute pulmonary thromboembolism (APTE) remains an important cause of morbidity and mortality in Western countries. In Korea, both the incidence and the mortality rate of APTE were thought to be low compared to Western countries. We performed the present study to investigate the current status of APTE in Korea. Methods Eight hundred and eight registry patients with APTE were analyzed with respect to clinical symptoms and signs, the presence of underlying diseases or predisposing factors, diagnostic methods, treatment and clinical course. Results The most common risk factors were prolonged immobilization (22.9%), deep venous thrombosis (22.0%), a recent operation (19.2%), and cancer (15.8%). The most common symptoms were dyspnea (78.6%), and chest pain (26.9%). The most common abnormality on chest radiography was effusion. The overall mortality rate at 3 months was 11.0%. Multivariate logistic regression analysis demonstrated that increased mortality risk was independently associated with the following baseline factors: onset in hospital (OR 1.88; 95% CI 1.03–3.42; p =0.03), lung cancer (OR 9.20; 95% CI 1.96–43.27; p =0.005), tachycardia (OR 3.50; 95% CI 1.86–6.60; p =0.0001), cardiogenic shock (OR 6.74; 95% CI 2.73–16.64; p =0.0001), and cyanosis (OR 3.45; 95% CI 1.27–9.44; p =0.01). Conclusions Some differences did exist for the risk factors, symptoms, chest X-ray findings, mortality rate and prognostic factors as compared with those for Western patients. These results can prove especially helpful in the diagnosis as well as for the treatment of patients with APTE.

Abnormal expression of let-7a microRNA (miRNA) in non-small cell lung cancer (NSCLC) cells and tissue has been previously reported. Our objective was to investigate whether let-7a miRNA is aberrantly expressed in the blood of NSCLC patients. Using real-time PCR (RT-PCR), we analyzed let-7a miRNA in archived whole blood from 65 participants, 35 of whom had NSCLC and 30 of whom did not. Using RT-PCR, we also investigated the expression of let-7a miRNA in NSCLC cell lines (A549 and HCC 1588), a normal human lung fibroblast cell line (WI-38) and in 40 human NSCLC tissues. The 2(-ddCt) of let-7a miRNA in the blood of normal subjects and those with NSCLC was 3242.49±355.28 and 747.85±177.74, respectively. The relative expression of let-7a miRNA in the A549 and HCC 1588 cancer cell lines was approximately 0.3 and 0.35, respectively, compared to WI-38 cells. The 2(-ddCt) of let-7a miRNA in the normal human lung tissues and human NSCLC tissues was 42.30±3.98 and 27.73±3.86, respectively. Let-7a miRNAs were under-expressed in the blood of NSCLC patients, as well as NSCLC cells and NSCLC tissues, compared to normal controls. The possibility of using let-7a miRNA as a serologic marker for lung cancer warrants further study.

A 59-year-old man was rushed to the emergency room. The patient complained of headache with impaired memory function. Brain MRI showed a necrotic tumor in Lt cerebral hemisphere, with severe peritumoral edema (Fig. 1). Pathologic examination of the brain lesion confirmed that the tumor was a small cell lung cancer (SCLC). Chest computed tomography revealed a large soft tissue mass with central necrosis at subcarinal area in spite of an initial normal chest X-ray (Fig. 2). Bronchoscopic biopsy of the polypoid mass at subcarina revealed that the mass was a SCLC (Fig. 3). This is the case of SCLC only with an extrapulmonary symptoms despite of a normal chest X-ray. When metastatic brain tumor was found, appropriate chest evaluation should be performed even though chest X-ray was normal because brain is a common site of invasion of lung cancer. (J Lung Cancer 2010;9(1):24 󰠏 25)

Pulmonary arterial thrombosis develops during hypercoagulable states, intra-arterial tumorous conditions, and congenital heart disease accompanied by pulmonary hypertension. Thrombosis in the main pulmonary arterial stump after pneumonectomy can also occur. Herein, we report a very rare case of pulmonary arterial thrombosis in a patient with pulmonary hypertension and a lung destroyed by tuberculosis. He presented with aggravated dyspnea without fever or purulent sputum. His chest computerized tomography scan showed left main pulmonary arterial thrombosis as a convex shape, with the ipsilateral distal arteries and arterioles showing parenchymal destruction. After excluding pulmonary thromboembolism and hypercoagulable disorders, we diagnosed pulmonary arterial thrombosis and treated him with an anticoagulant.

Background : Recently, there have been several studies showing that irinotecan hydrochloride, a topoisomerase I inhibitor, is effective against extensive disease(ED) small cell lung cancer (SCLC). We conducted a phase II trial to evaluate the efficacy and toxicity of irinotecan plus cisplatin as a 1st line therapy for both limited and extensive disease SCLC. Methods : The study was conducted between January 2002 and June 2004. Patients were treated with irinotecan on day 1, 8, 15 and cisplatin on day 1, every 4 weeks. During concurrent thoracic irradiation for limited disease (LD)-SCLC patients, dose of irinotecan was reduced to . Prophylactic cranial irradiation was given to patients with complete remission (CR) after chemotherapy. Results : Median ages of LD- and ED- SCLC were 64 years and performance status (PS) was 0-2. In patients with LD-SCLC, the response rate after concurrent chemoradiotherapy was 85% (CR, 6; Partial response [PR], 11). The median survival was 20 months (95% CIs, 15.6 to 24.4) with 1-and 2-year survival rates of 85% and 35%, respectively. Median progression free survival (PFS) was 12 months (95% CIs, 6.2 to 18.1) with 1- year PFS of 36%. In ED-SCLC, the response rate was 83.4% (CR, 1; PR, 14). The median survival was 14.5 months (95% CIs, 8.8 to 20.1) with 1-year survival rates of 75%. Median PFS was 6.3 months (95% CIs, 5.6 to 7.1) with 1- year PFS of 20%. The major toxicities (grade 3 or 4) of this regimen included leukopenia, anemia, thrombocytopenia, nausea/vomiting, and diarrhea without life threatening complication. Conclusion : Our data shows that the combination of irinotecan plus cisplatin as a first line therapy is effective and tolerable in the treatment of both LD- and ED- SCLC.

Backgroud : Lung cancer is the leading cause of cancer deaths in Korea and the number of lung cancer deaths is increasing. The higher response rates, decreased toxicity and improved performance status of the first-line treatments have resulted in an increased number of patients becoming candidates for second-line therapy. Several new antineoplastic agents, including gemcitabine, docetaxel and paclitaxel, have recently demonstrated second-line activity. This phase II study evaluated the efficacy and toxicity of gemcitabine and vinorelbine as combination chemotherapy for Korean patients with NSCLC as a second-line treatment. Methods : Sixty response-evaluable patients were enrolled from December 2000 to July 2003. We conducted a phase II study of a combination gemcitabine and vinorelbine chemotherapy for patients with histologically confirmed NSCLC that was stage IIIB and IV disease at the time of diagnosis, and the disease had progressed onward or the patients had relapsed after first-line platinum-based chemotherapy. They were treated with intravenous gemcitabine and intravenous vinorelbine on days 1 and 8. This chemotherapy regimen was repeated every 3 weeks. Results : A total of 215 cycles of treatment were given and the mean number of cycles was 3.6 cycles. All the patients were evaluable for the toxicity profile. The response rate was 10% according to the WHO criteria. The median progression free survival was 3.8 months and the median survival time was 10.1 months. The 1-year survival rate was 32.9%. Grade III and IV neutropenia were seen in 20 (33.3%) and 7 (11.7%) patients, respectively. Conclusion : The combination of gemcitabine and vinorelbine is active and well tolerated as a second-line therapy for patients with advanced nonsmall cell lung carcinoma.

Background: Persistent nonproductive cough is a major adverse effect encountered with ACE inhibitor treatment and the most frequent reason for withdrawal of the drug. The mechanism of cough was postulated to be associated with accumulation of bronchial irritants which are substrates of ACE. It has been speculated that occurrence of this adverse effect is genetically predetermined ; in particular, variants of the genes encoding ACE. To investigate this relationship, we determined ACE gene Insertion/Deletion polymorphism in subjects with and without a history of ACE inhibitor-induced cough. Methods: Among the 339 patients with ACE inhibitor treatment, subjects who developed cough that resolved when not taking medication were designated to cough group and other subjects who did not complain cough were designated to non-cough group. Clinical characteristics of the patients were collected by review of medical records. ACE genotypes were determined by PCR amplification of DNA from peripheral blood and agarose gel electrophoresis. Results: 37 patients complained of dry cough(cough group) and 302 patients did not complained of cough(non-cough group). The incidence of ACE inhibitor induced dry cough was 10.9%. There was a preponderance of females in the cough group (M : F=24.3% : 75.7%) compared to the non-cough group (M : F=49.7% : 50.3%, p=0.004). There was no significant difference in mean age, underlying diseases, and kinds and frequencies of ACE inhibitors and their mean dosage between the both groups. ACE genotypic frequencies were I/I : I/D : D/D=16.2% : 18.9% : 64.9% in the cough group and 18.9% : 18.2% : 62.9% in the non-cough group which showed no significant difference between the both groups(p=0.926). Allelic frequencies were I : D = 25.7% : 74.3% and 28.0% : 72.0% in the cough and non-cough group respectively and the difference was not significant(p = 0.676). Conclusion: The incidence of ACE inhibitor-induced cough are 10.9%, and women are more susceptible to ACE inhibitor-induced cough. ACE inhibitor-induced dry cough is not associated with ACE gene Insertion/Deletion polymorphism.

연구배경: 만성기침이란 기침이 적어도 3주 이상 지속되는 경우로, 원인으로는 후비루 증후군, 기관지천식, 위식도역류, 기관지 확장증, 만성기관지염, 안지오텐신 전환 효소 길항제 사용 등이 있다. 하지만 특별한 원인을 발견할 수 없고, 다른 증상 없이 단지 만성기침만 있는 경우에 대해서는 그 임상상과 조직병리소견이 아직도명확하게 규명되어 있지 않다. 이에 저자 들은 특별한 원인을 밝힐 수 없고, 다른 호흡기 증상이 없이 만성기침만을 호소하는 환자를 대상으로 임상상과 조직소견을 조사하여, 그 병인기전과 원인을 규명하고자 본 연구를 시행하였다. 방 법: 대상환자는 3주 이상 만성기침 외에 다른 호흡기 증상이 없는 25명의 환자들이었고, 후비루증후군, 위식도 역류, 약물 복용력 및 흉부질환, 심혈관 질환, 전신질환이 없었으며, 과거에 기관지 천식을 진단 받은 병력이 없었고, 폐기능 검사, 흉부 X-선 검사상 특이 소견이 없었다. 남자 10명 여자 15명으로 평균연령은 39.8세였고, 흡연가가 5명, 비흡연가가 20명이었다. 폐기능 검사, 메타콜린 유발검사, 알레르기 피부 단자 검사, 기관지 내시경하 점막 조직 생검을 시행하였고, 조직 비교를 위하여 정상 대조군 5명에 대해서도 기관지 내시경하 점막 조직 생검을 시행하였다. 모든 검사가 끝난 후, prednisolone 20~30 mg/일을 1~2주간 투여하였고, cough score로 치료반응 여부를 확인하였다. 결 과: 정상 대조군의 조직소견과 비교해 볼 때, 염증세포의 분포에 따라 대상군은 호산구 침윤이 저명한 경우(호산구 침윤군), 림프구 침윤이 저명한 경우(림프구 침윤군)의 두 군으로 구분이 되었다. 호산구 침윤군이 21예로, 호산구 수는 펑균 89.8 $cells/mm^2$ 였고, 정상 대조군은 평균 0.4 $cells/mm^2$ 였다 (P=0.005). 림프구 침윤군은 4예였으며, 림프구 수는 평균 84.3 $cells/mm^2$ 였고, 정상 대조군은 평균 28.4 $cells/mm^2$ 였다(P=0.026). 정상 대조군의 기저막 두께가 평균 $3.50\pm1.37\;{\mu}m$ 였던데 비하여, 대상군에서는 평균 $14.20\pm5.20{\mu}m$ 로 의미있게 두꺼운 소견을 보였다(p=0.001). 메타콜린 유발검사와 병리소견으로 대상군의 만성기침의 원인을 유추해보면, 호산구 침윤군 21예 중 메타콜린 유발검사 양성인 경우는 7예로, 기침형 천식으로 진단할 수 있었고, 14예는 메타콜린 유발검사가 음성으로, 호산구성 기관지염으로 진단할 수 있었다. 림프구 침윤균 4예는 모두 메타콜린 유발검사가 음성으로, 림프구 침윤에 의한 기관지염이었다. 호산구성 기관지염 14예 중 3예(21.4%)에서 아토피 양성이었다. 대상환자 25예중 22예(88.0%)에서 스테로이드 투여 후 증상지수가 호전되었다. 호산구성 기관지염 14예 중 12예(85.7%), 기침형 천식 7예 중 7예(100%), 림프구 침윤에 의한 기관지염 4예 중 3예(75.0%)에서 증상지수가 호전되었다. 병리소견으로 호산구 침윤군과 림프구 침윤군으로 구분했을 때, 증상지수가 호전된 경우가 각각 90.5%, 75.0%로 염증세포의 종류에 따른 차이는 없었다. 결 론: 흉부 X-선 및 폐기능 검사가 정상이며, 다른 증상이 없는 만성기침은 호산구 또는 림프구 침윤에 의한 기도염증과 연관이 있었다. 메타콜린 유발검사와 기관지 조직검사로 유추해 볼 때, 그 원인으로는 호산구성 기관지염, 기침형 천식, 림프구 침윤에 의한 기판지염이었다(이상 빈도순). 스테로이드 치료에 88%에서 증상지수가 호전되었다. 【Background: The purpose of this study was to examine the causes and pathologic process of chronic non-productive cough as an isolated symptom with a normal spirometry and chest radiograph by investigating clinicopathologic findings. Method: We studied 25 adults with chronic non-productive cough over a 3-week period with a normal chest radiograph and pulmonary function tests without any other symptoms. Clinical assessment, cough score, chest and sinus radiograph, pulmonary function tests, methacholine challenge, allergic skin prick test, and bronchoscopy for bronchial biopsies were performed. Subjects were then treated with prednesolone 20 to 30 mg/day for 1 to 2 weeks. Results: The experimental group was divided into two subgroups-those infiltrated with eosinophils, and those infiltrated with lymphocytes depending on eosinophil and lymphocyte counts, both of which were respectively higher than those of the control group. Eosinophils infiltrated group had mean numbers of eosinophil of 89.8 $cells/mm^3$ while control group's mean was 0.4 $cells/mm^2$ (p=0.005). Lymphocyte infiltrated group was 4 patients whose mean was 84.3 $cells/mm^2$ with 28.4 $cells/mm^2$ of control group(P=0.026). In addition, the mean thickness of the basement membrane of experimental group was $14.20{\pm}5.20{\mu}m$ in contrast of control group whose mean was $3.50{\pm}1.37{\mu}m$ (P=0.001). With the methacholine challenge test, 7 of the 21 eosinophil infiltrated subjects were diagnosed with cough variant asthma ; the other 14 with eosinophilic bronchitis. Three subjects with eosinophilic bronchitis were atopic positive (21.4%) with the skin prick test In the lymphocyte dominant group, all four subjects were diagnosed with lymphocytic bronchitis. Cough score was improved after steroid treatment in 22 of 25 subjects in the experimental group (88.0%). Conclusion: These results suggest chronic non-productive cough as an isolated symptom with a normal spirometry and chest radiograph was associated with airway inflammation by eosinophil and lymphocyte infiltration. The causes for chronic non-productive cough were eosinophilic bronchitis, cough variant asthma, and lymphocytic bronchitis(written in frequency). They further suggest that therapeutic treatment with steroids can provide effective symptomatic relief.】

Background : Leukotriene (LT) , , and , the main components of slow-reacting substance of anaphylaxis (SRS-A), have been suggested to play an important role in bronchial asthma such as antigen-induced bronchoconstriction, airway hyperreactivity, and pulmonary eosinophil accumulation. The purpose of this study was to evaluate the effects of treatment with the cysteinyl-LTs (cys-LTs) antagonist, pranlukast on allergen-induced guinea pig asthma model. Methods : Guinea pigs of treatment and placebo groups were sensitized by subcutaneous injection of ovalbumin(OVA) and challenged by inhalation of aerosolized OVA (1% weight/volume OVA). Normal control group did not sensitize with OVA. Oral ingestion of pranlukast and normal saline to the treatment and placebo groups was performed. In the treatment and placebo groups, airway resistance was measured before and after oral ingestion. Serum and eosinophilic infiltration of the bronchiolar and peribronchiolar tissues were measured after ingestion in the treatment and placebo groups. Results : Allergen-induced airway constriction developed in 20 (8 in treatment group, 12 in placebo group) among 35 guinea pigs. Airway resistance was significantly decreased at 3 and 6 minutes after OVA challenge in the pranlukast treatment group. In the placebo group, there was no difference of airway resistance between before and after saline ingestion. Serum levels showed 348.4 pg/ml in the treatment group, 373.9 pg/ml in the placebo group, and 364.4 pg/ml in the control group. There were no statistically significant difference between treatment and placebo group (p=0.232), and treatment and control group (p=0.501). Eosinophilic infiltrations in the peribronchiolar region per one-microscopic field (400 high power fields) demonstrated 7.06 in the treatment group, 19.2 in the placebo group, and 4.50 in the control group. There was significant decrement of eosinophilic infiltration in the treatment group which was compared with placebo group (p=0.001). Conclusion : These results demonstrate that pranlukast, a cys-LTs receptor antagonist, can attenuate allergen induced early-phase bronchoconstriction and eosinophilic infiltration in the bronchiolar tissues.