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)
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)