Background : A pleural effusion is a common medical problem. Despite several diagnostic tests, 15-20% of pleural effusions go undiagnosed. The aim of this study was to evaluate the clinical characteristics and prognosis of a lymphocyte dominant exudative pleural effusion with a low adenosine deaminase (ADA), low carcinoembryonic antigen (CEA), negative cytology and negative acid fast bacilli (AFB) smear.Method : From Jan 2000 to Aug 2001, 43 patients with lymphocyte dominant exudative pleural effusions whose AFB smear and cytologic exam were negative, their pleural fluid ADA level was < 40 IU/L, and their CEA level was < 10 ng/mL were enrolled in this study. A retrospective analysis of the patients' medical records was carried out.Result : Among 31 of the 43 cases (72%), probable underlying diseases causing the pleural effusion were identified: 21cases of malignant diseases, 4 cases of liver cirrhosis, 2 cases of pulmonary tuberculosis, 1 case of end stage renal disease, 1 case of a chylothorax, 1 case of a post CABG (coronary artery bypass graft) state, 1 case of a pulmonary embolism. No clinically suspected etiology was identified in the remaining 12 cases (28%). Of these 12 pleural effusions, 7 cases spontaneously resolved, 2 effusions resolved with antibiotics, and the other 2 cases were persistent. Conclusion : Lymphocyte dominant exudative pleural effusions with a low ADA, low CEA, negative cytological exam, and negative AFB smear, but without a definite cause might have a benign course and clinicians can observe them with attention. (Tuberc Respir Dis 2005; 58:5-10)
Background : Interferon-gamma (IFN- ) is essential in the immune response to mycobacterial infections, and a complete or partial deficiency in the IFN- receptor 1 (IFN R1) or the IFN- receptor 2 (IFN R2) have been reported to confer susceptibility to a disseminated infection with nontuberculous mycobacteria. However, similar mutations in the IFN- receptor have not been specifically examined in the patients with clinical tuberculosis. Methods : This study searched for mutations in the IFN- receptor gene that resulted in a partial IFN- receptor deficiency in six patients with disseminated tuberculosis. The previously identified IFN R1 and IFN R2 coding regions were sequenced after amplification.Results : There was no partial IFN R1 deficiency including a homozygous recessive missense mutation causing an amino-acid substitution in the extracellular domain of the receptor (I87T) and a hotspot for small deletions (818delT, 818del4, 818insA) found in any of the patients. In addition, a partial IFN R2 deficiency of the homozygous missense mutation (R114C) was not found in any of the patients.Conclusion : Genetic defects causing a partial IFN- receptor deficiency were not identified in our patients with disseminated tuberculosis. (Tuberc Respir Dis 2005; 58:11-17)
Background : Endobronchial tuberculosis often complicates bronchostenosis, which can cause dyspnea due to an airway obstruction, and can be misdiagnosed as bronchial asthma or lung cancer. This study investigated the possible correlation between the interferon- (IFN- ) and transforming growth factor- (TGF- ) levels in the serum and bronchial washing fluid and the treatment results in endobronchial tuberculosis patients. Methods : Sixteen patients, who were diagnosed as endobronchial tuberculosis using bronchoscopy, and 10 healthy control subjects were enrolled in this study. The IFN- and TGF- levels were measured in the serum and bronchial washing fluid of 16 endobronchial tuberculosis patients before and after treatment using the ELISA method. The endobronchial tuberculosis patients were divided into those who showed bronchial fibrostenosis after treatment and those who did not. Results : The IFN- and TGF- levels in the bronchial washing fluid in endobronchial tuberculosis patients were elevated comparing to the control (p<0.05). After treatment, 7 of the 16 endobronchial tuberculosis patients showed bronchial fibrostenosis and the other 9 cases healed without this sequela. In the patients with fibrostenosis after treatment, the initial serum TGF- level was lower than the patients without fibrostenosis after treatment (p<0.05). Moreover, the serum TGF- level after treatment further decreased comparing to the patients without fibrostenosis after treatment(p<0.05).Conclusion : Elevated IFN- and TGF- levels in the bronchial washing fluid in endobronchial tuberculosis patients are believed to be related to the pathogenesis of endobronchial tuberculosis. The decreased initial serum TGF- level and the change in the serum TGF- level after treatment are believed to be involved in bronchial fibrostenosis during the course of the disease. (Tuberc Respir Dis 2005; 58:18-24)
Background : An insertion-deletion polymorphism of angiotensin converting enzyme (ACE) gene has been shown to be associated with enzyme activity levels of ACE. Reported results that have been mutually contradictory about asthmatic hypersensitiveness and occurrence according to ACE gene insertion (I)/deletion (D) polymorphism. Also, the involvement of the ACE genes as the genetic basis of bronchial asthma is currently controversy. We investigated whether there was any association between polymorphisms of the ACE genes and airway hyper-responsiveness in chronic obstructive pulmonary disease (COPD).Methods : A total of 100 patients with COPD were enrolled in this study. The ACE genotypes were determined in all subjects by polymerase chain reaction. Pulmonary function test including bronchodilator response (BDR), methacholine bronchial provocation test (MBPT) were done in those patients. Airway hyper-responsiveness include any findings of positive BDR or MBPT.Results : In COPD patients, the ACE genotype distribution did not differ significantly among groups of patients with severities of COPD, and with or without airway hyper-responsiveness.Conclusions : These results suggest that polymorphisms of the ACE gene may not be associated with airway hyper-responsiveness, development and severity of COPD. (Tuberc Respir Dis 2005; 58:25-30)
배 경 : 폐기종에서 발생하는 폐포 파괴의 원인으로서 전통적으로 protease/anti-protease 불균형과 산화성 스트레스가 주요 가설로 여겨져 왔으나 최근 폐포세포의 아포프토시스가 폐포파괴 및 폐기종의 원인이 된다는 이론이 제기되고 있어서 A549 폐상피세포에서 흡연추출물에 의한 세포사의 특성을 규명하고자 본 연구를 시행하였다.방 법 : A549 폐상피세포주에서 여러 농도의 흡연추출물 및 억제제를 첨가한 후 MTT assay를 잉용하여 세포생존율을 측정하였다. 세포사 분석은 FACScan을 이용한 DNA 분절확인, 전자현미경 검사, Hoecst/PI 이중염색을 이용한 현광현미경 검사를 이용하였고 cyt ochrome c 유리는 면역형광법을 이용하였다. Bcl-2 과발현세포주를 이용하여 bcl-2의 역할을 확인하였고 p53 Western blot 및 HPV-E6 과발현 세포주를 이용하여 p53의 역할을 확인하였다. 결 과 : A549 세포주에서 흡연추출물에 의한 세포사는 FACScan에서 DNA 분절에 의한 subG1 분획의 확인 및 Hoecst/PI 이중염색 및 현광현미경 소견 상 아포프토시스임이 확인되었고 전자현미경 소견상 저농도에서는 아포프토시스가 발생하지만 고농도에서는 괴사가 발생함을 확인하였다. Cytochrome c가 세포질로 유리됨을 확인하였으나 caspase 억제제에 의해서 세포사가 차단되지 않았다. 흡연추출물에 의한 세포사는 Bcl-2과발현에 의해 억제되었고 p53활성화를 유도하고 p53이 기능적으로 knock-out 된 세포주에서 억제되었다.
연구 배경 : 비소세포 폐암의 암화 과정에서 에스트로겐과 프로제스테론 단백의 역할에 대한 면역조직화학 염색을 이용한 연구들이 진행 중이다. 그러나 이 연구들은 아직 일치된 결과를 보이고 있지 않으며 이는 상용하는 면역조직화학 염색법이 한 문제로 제시되고 있다. 저자 들은 최근 새로 개발된 조직미세배열법을 이용하여 비소세포 폐암 환자의 조직에서 이들 호르몬 수용체 발현을 연구하였다. 대상 및 방법 : 대상은 70예의 비소세포 폐암 환자로 남성이 74%, 여성이 26%이었다. 이들의 포르말린 고정, 파라핀 포매 조직을 이용하여 조직미세배열을 구축하였다. 가열을 통한 항체 재생 후에 폐암 조직에서 일차 단일클론 항체 (ER1D5와 PR1A6)를 이용한 면역조직화학 염색을 시행하였다. 결 과 : 흡연력은 현재 흡연자가 49%이었고, 비흡연자와 금연자는 각각 27%와 24%이었다. 폐암의 조직학적 분류는 편평상피세포암이 34예이었고, 선암, 편평상피선암, 기타 세포형은 각각 24예, 9예와 3예이었다. 단일클론 항체를 이용한 염색에서 양성 결과를 보이는 비소세포 폐암 세포는 관찰되지 않았다.
A-67-year old man was hospitalized due to fever, cough and dyspnea upon exertion, and was treated with intravenous antibiotics. During the hospital course he presented with weakness in his low extremities. The laboratory tests showed an elevated CK level and myoglobinuria. He was diagnosed with rhabdomyolysis with community-acquired pneumonia and treated accordingly. Subsequently, his symptoms and signs of rhabdomyolysis improved. (Tuberc Respir Dis 2005; 58:59-63)
We report here on an uncommon case of mediastinitis that occurred after central venous catheterization. A patient with colon and jejunal cancer complained high fever, right shoulder pain, chest pain, and limited motion of the affected shoulder just 6 days after central venous catheterization. Bacterial culture of the blood, shoulder abscess, and catheter puncture site revealed methicillin-resistent staphylococcus aureus. Right upper mediastinal widening on chest film also suggested mediatinitis. Mediastiotomy and pus drainage was performed along with adequate antibiotics therapy. In this case, it seems that initially formed bacteria from the puncture site migrated to the mediastinum through the tissue plane to start the mediastinitis. Careful dressing of puncture site and correct handling of catheter is important to prevent this serious complication. (Tuberc Respir Dis 2005; 58:64-67)
Pulmonary sequestration is a very rare congenital malformation in which a mass of pulmonary tissue is detached from the normal lung and receives its blood supply from a systemic artery. It may be clinically asymptomatic or it has a wide spectrum of various clinical manifestations. The clinical therapeutic approach is to resect the sequestered lobe to prevent frequent complication such as infection. The arterial embolization of feeding artery is a new technique and a less invasive treatment than conventional surgical removal. We have experienced a 17- year-old male with pulmonary sequestration whose complaints were pain in left lower chest. He was diagnosed by computed tomography and aortography and successfully treated with embolization of feeding artery. We report a case of pulmonary sequestration treated with arterial embolization instead of surgery. (Tuberc Respir Dis 2005; 58:68-72)
Lemierre syndrome is characterized by an acute oropharyngeal infection with secondary septic thrombophlebitis of the internal jugular vein and frequent metastatic infections such as septic pulmonary emboli and suppurative arthritis. In the preantibiotic era, this condition generally had a fatal outcome. The presentation is so distinctive that a clinical diagnosis is possible in most cases, and a cure is expected with the appropriate therapy in the majority of patients. We present a case report of Lemierre syndrome with a review of the relevant literature.(Tuberc Respir Dis 2005; 58:73-77)
Propylthiouracil(PUT) is a drug which used at Grave's disease. But PTU has recently been observed to associated with antineutrophil cytoplasmic antibody(ANCA)-positive vasculitis resulting in, infrequently, diffuse alveolar he morrhage. We report the case of a patient who developed diffuse pulmonary hemorrhage after she had been taking PTU for two years. She had received a diagnosis of Grave's disease at two years ago. The serologic study was positive for ANCA with myeloperoxidase(MPO) specificity. Bronchoalveloar lavage(BAL) fluid analysis revealed hemosiderin- laden macrophages. Such findings suggested propylthiouracil induced dffuse pulmonary hemorrhage associated with antineutrophil cytoplasmic antibody. To our knowledge, this represents the first documentation in a case of PTU-induced diffuse pulmonary hemorrhage in Korea. (Tuberc Respir Dis 2005; 58:78-82)
Leflunomide is a new disease modifying anti rheumatic drug (DMARD) for the treatment of active rheumatoid arthritis. Its mechanism of action differs from other DMARDs in that it inhibits the de novo pyrimidine synthesis by inhibiting dihydroorotate dehydrogenase and therefore prevents the proliferation of activated lymphocytes. As it has been prescribed worldwide, there is a great deal of much concerns regarding its potential adverse effects. Because leflunomide has an active metabolite with a long elimination half life of approximately 2 weeks, serious adverse reactions may occur even after the leflunomide treatment has been stopped. The profile of serious reactions includes liver dysfunction, hematological disorders, severe skin reactions and respiratory dysfunction. Respiratory dysfunctions with leflunomide therapy are very rare and its incidence is lower than that of methotrexate therapy. However, there are reports in Japan showing that 5 patients died of interstitial pneumonitis and another 11 patients developed serious lung complications associated with leflunomide. This suggests the possibility of fatal respiratory toxicity of leflunomide. There are no reports of interstitial pneumonitis associated with leflunomide in Korea. We report a case of a 62 year old woman who developed interstitial pneumonitis, which might have been induced by leflunomide during the treatment of rheumatoid arthritis. (Tuberc Respir Dis 2005; 58:83-88)