Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have investigated on the clinical features of pleural nodular lesions which have appeared during chemotherapy of tuberculous pleurisy. Such lesions were observed in more than 10% of the cases of tuberculous pleurisy. This type of lesion occurred more frequently in the pleurisy patients whose chest X-ray did not show any tuberculous lesion in lung field and whose sputum was negative of tubercle bacilli. Most of the patients with such lesion were young. From these results, it was suggested that such lesion might develop during the course of primary tuberculosis. Single nodular lesion was more common but multiple nodular lesions were not rare. They had occurred in 2-4 months after the start of anti-tuberculous chemotherapy including RFP, usually accompanied with chest pain. They had disappeared within 6-12 months without any additional therapy. In summary, pleural nodular lesions, which occurred during chemotherapy of tuberculous pleurisy, were not rare, but the clinical course and prognosis of such lesion were favourable and improved without any additional therapy. The etiology of such lesion has remained to be clarified.
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PMID:[The clinical investigation of so-called "pleural tuberculoma" in the last 3 years]. 800 19

A 38-year-old man was admitted to hospital because of chest pain and for the evaluation of a right pleural effusion on his chest X-ray film. Pleural effusion was characterized as exudative lymphocyte-predominant fluid with elevation of adenosine deaminase (ADA). Bacteriologic examination of pleural fluid was negative in both smear and culture of the fluid. PPD was positive and ESR was elevated. Mycobacterial DNA was detected in the pleural effusion using polymerase chain reaction (PCR) with primers which amplified a fragment of Is6110. Following treatment (INH, RFP and EB), the right pleural effusion disappeared. We conclude that PCR technique may be very useful in the rapid diagnosis of tuberculous pleurisy.
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PMID:[A case of tuberculous pleural effusion diagnosed by polymerase chain reaction (PCR)--with reference to tuberculous pleurisy using polymerase chain reaction]. 811 80

A case is 40-year-old man. He presented anterior chest pain. Pericardial effusion was pointed out and a tuberculin skin test was positive. Tuberculous pericarditis was highly suspected, so INH and RFP were medicated. After 6-month medication pericardial effusion decreased, but right pleural effusion appeared on chest X-ray. Chest CT revealed a thickening of pericardium extend to anterior mediastinal mass. Echocardiogram revealed a pressure gradient in right ventricle, which was compressed by the thickened pericardium. We underwent median sternotomy in order to rule out neoplastic diseases. Intraoperative pathologic diagnosis was granulomatous mediastinitis and pericarditis, so we resected granuloma as much as possible to decompress the heart. Although Mycobacterium tuberculosis was not found in the resected granuloma, it was most probable pathogen. He received additional antituberculous chemotherapy for 6 months.
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PMID:[A case of tuberculous granulomatous mediastinitis and constrictive pericarditis simulating malignant mediastinal tumor]. 984 81

A clinical study of 38 patients (28 men and 10 women) with tuberculous pleurisy was conducted. The age of these patients ranged from 19 to 92 years, with an average age of 48.9 years. In 30 patients, the chief complaint was fever, and other common complaints included chest pain, dyspnea, and coughing. Bacillus tuberculosis was found in the pleural fluid of 7.9% of the patients. Tuberculous pleurisy was diagnosed histologically, based on pleural biopsy, in 23.7% of the patients. The diagnosis rate of pleural biopsy was 47.4%. There were no significant differences in results of blood and pleural fluid tests between idiopathic pleurisy and concomitant pleurisy, but the tuberculin skin test was positive in only 50% of the patients with concomitant pleurisy. The tendency was that the longer the time period between symptom onset and first examination, the greater the pleural fluid retention. The diagnosis rate of pleural biopsy was influenced by the severity of pleural fluid retention. A thoracic cavity drain was inserted for continuous drainage in 15 patients, and every patient underwent INH + RFP-based chemotherapy. Tuberculous pleurisy is an important disease among patients with pleural fluid retention, thus clinicians need to know how to treat this disease.
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PMID:[A clinical study of tuberculous pleurisy]. 1185 70

We experienced 4 cases of agranulocytosis due to anti-tuberculosis drugs (rifampicin [RFP], isoniazid [INH], ethambutol [EB], streptomycin [SM] or pyrazinamide [PZA]) among some 6,400 tuberculosis patients who underwent chemotherapy over the past 20 years from 1981 to 2002 in our hospital, and the incidence rate of agranulocytosis was estimated at 0.06%. The 4 cases of agranulocytosis were as follows. CASE 1: A 51-year-old woman with right chest pain and fever was admitted to our hospital on Jan 4, 2001. The white blood cell (WBC) count was 5,200/microliter. The tubercle bacilli were cultured in her sputum. The treatment with INH 0.3, RFP 0.45, EB 0.75, PZA 1.2 g/day, allopurinol and teprenone was started on Jan 13. Pyrazinamide and allopurinol were stopped because of hyper-uric acidemia on Feb 7. Agranulocytosis and eosinophilia (WBC 1,300 [Neut 1%, Ly 57%, Eos 35%]) developed on Feb 13. All drugs were withdrawn and G-CSF drug nartograstim 100 micrograms was injected subcutaneously for 3 days. The WBC recovered to normal level and she was thereafter treated with INH, EB and Levofloxacin (LVFX) without any further trouble. Agranulocytosis in this case was supposed to be due to RFP. CASE 2: A 66-year-old man who had had nephrotic syndrome and hypothyroidism and has been treated with prednisolone 10 mg/day was admitted to our hospital on Aug 9, 2000 because of miliary tuberculosis. The tubercle bacilli were cultured in his sputum and the treatment with INH 0.3, RFP 0.45, and EB 0.75 g/day were started on Aug 10, but it was withdrawn on Aug 17 because of general skin eruption. After re-starting treatment with EB and INH on Aug 24, RFP was added in small dosage (0.05 g) on Oct 12, but agranulomatosis (WBC 2,300/microliter [Neut 2%]) developed on Nov 21, and all drugs were withdrawn again. The G-CSF drug filgrastim was used once subcutaneously, and WBC recovered immediately. He was thereafter treated with INH, EB, LVFX successfully. Agranulocytosis was supposed to be due to RFP. CASE 3: A 60-year-old woman without symptoms had abnormal chest roentgenograph, and consulted with our hospital on Aug 26, 2002. The broncho-alveolar lavage fluid was smear and culture-negative, but PCR-TB positive, and the case was diagnosed as pulmonary tuberculosis. Treatment with INH 0.3, RFP 0.45, EB 0.75, PZA 1.2 g/day, alloprinol 300 mg and rebamipide 300 mg/day was started on Sept. 5, 2002. Late in September, she complained of appetite loss. The laboratory data on Oct 3 revealed WBC 900/microliter (Neut 1%, Ly 94%), aspartate aminotransferase (AST) 199 IU/l, and alanine aminotransferase (ALT) 253 IU/l, showing agranulocytosis and drug-induced hepatitis. The chemotherapy was immediately withdrawn and she was admitted to our hospital on the next day. Glycyrrhizin derivative (SNMC) 40 ml was injected for 5 days, and WBC recovered, and AST and ALT also became normal. CASE 4: A 60-year-old man was admitted to our hospital on March 11, 1981 because pulmonary tuberculosis had recurred. He had been treated with SM, PAS and INH in 1973 for pulmonary tuberculosis. On admission examination of blood count and blood chemistry were normal. Treatment with RFP, INH and SM was started on March 11. He stopped out from the hospital on April 17, but in a few days he returned back with sore throat, lower lip swelling and gingival bleeding. Blood cell count on April 24 showed pancytopenia with RBC 226, Hb 7.5, WBC 800 (Ly 96%, Eos 4%) and Plt 10,000/microliter. The bone-marrow showed NCC (nuceated cell count) of 5,500, and megakaryocyte 0. Thereafter ground glass appearance shadows were seen on the whole lung field, and he died May 26. Autopsy showed generalized aspergillosis. It was strongly suspected that either of RFP, INH or SM was responsible for his pancytopenia. We collected another 10 cases of agranulocytosis due to anti-tuberculosis drugs in the world wide literature, and found men/women ratio 5/8 (in one case gender was not known), the duration of chemotherapy before appearance of agranulocytosis 1-3 months, no change in the lymphocyte count of the peripheral blood, and the accompanying of another allergic signs such as skin eruption, blood eosinophilia or drug-induced hepatitis in some cases, and these findings suggest that the mechanism of agranulocytosis due to anti-tuberculosis drugs was allergic in nature.
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PMID:[Agranulocytosis due to anti-tuberculosis drugs including isoniazid (INH) and rifampicin (RFP)--a report of four cases and review of the literature]. 1467 45