BACKGROUND: In Korea, the prevalence of tuberculosis and hepatitis is high, and combined therapy with rifampicin and pyrazinamide is used in tuberculosis, so drug induced hepatitis is not only problem of tuberculosis therapy but also cause of treatment failure. However most of recent reports on drug induced hepatitis during antituberculosis medication have dealt with its pathogenesis and have stressed the biochemical, and histopathological aspects of the disorder, whereas this study was designed primarily to provide information on the clinical features. METHOD: The subjects of study were 1414 patients treated with antituberculosis drugs on the department of chest medicine at National Medical Center during the 5-year 6-month period from January 1, 1988, to June 30, 1993. Retrospective analysis of clinical features for the 29 patients who developed drug induced hepatitis was done. RESULTS: 1) The incidence of antituberculosis drug induced hepatitis was 2.1%. 2) Male to female ratio of antituberculosis drug induced hepatitis was 2:1, but case rates among males and females were not significantly different. 3) Rates of drug induced hepatitis according to age distribution shows the most common incidence between 35 to 49 year old age group, but rates among groups of age were not significantly different. 4) Drug induced hepatitis was most common in the case of moderate advanced Pulmonary tuberculosis(rate is 2.78%), but rates among types of tuberculosis were not significantly different. 5) 18 cases(62%) of antituberculosis drug induced hepatitis patients had no signs or symptoms. In remaining cases, they were nausea, vomiting, jaundice, hepatomegaly, icteric sclera, right upper quadrant -tenderness in order 6) 22 cases(76%) of antituberculosis drug induced hepatitis cases had occurred within the first month. 7) The duration of abnormal liver function was 28±5(Mean±SD), ranged from 5 days to 180 days. 8) One case of antituberculosis drug induced hepatitis died. 9) The levels of abnormal GOT ranged from 64 to 1055U/L and GPT from 68 to 931U/L. CONCLUSION: There are no decided predisposing factors of antituberculosis drug induced hepatitis, so it should be done biochemical monitoring as week as close monitoring for overt signs or symptoms of hepatitis to avoid the development of irreversible hepatic reaction, especially at the treatment of the first month.
Age Distribution ; Causality ; Female ; Hepatitis* ; Hepatomegaly ; Humans ; Incidence ; Jaundice ; Korea ; Liver ; Male ; Nausea ; Prevalence ; Pyrazinamide ; Retrospective Studies ; Rifampin ; Sclera ; Thorax ; Treatment Failure ; Tuberculosis ; Vomiting

BACKGROUND: Evaluation of coronary artery disease(CAD) by radionuclide myocardial perfusion scintigraphy is safe, convenient and informative for diagnosis of CAD & assessment of functional significance of stenotic lesions. We tried to evaluate the characteristics of CAD in dibetics by intravenous dipyridamloe (99m)Tc-MIBI(methoxy isobutyl isonitrile) SPECT(Single Photon Emission Computed Tomography). METHOD: (99m)Tc-MIBI SPECT and coronary arteriography(CAG) were performed simultaneously in less than 2 week interval in 41 diabetics(diabetic group) and 103 non-diabetics(non-diabetic group) with clinical suspicion of CAD. The sensitivity and specificity of (99m)Tc-MIBI SPECT for detection of CAD were compared between two groups. The site and number of involved vessels, the extent of perfusion defect and redistribution pattern were compared between two groups. RESULT: 1) The sensitivity and specificity of (99m)Tc-MIBI SPECT for detection of CAD were 97% and 80% in diabetics, these were comparable to those in non-diabetics(97% and 78%). 2) Three vessel disease were common(p<0.01)in diabetics(SPECT 28.1%, CAG 32.3%) than in non-diabetics(SPECT 11.4%, CAG 7.5%). Distal lesions were also more common(p<0.005) in diabetics(CAG 40.3%) than in non-diabetics(CAG 15.7%). 3) On stress SPECT, the extent of perfusion defect was not different in individual vessel areas between diabetics and non-diabetics. However the perfusion defect of left ventricle as a whole was significantly higher(p<0.05) in diabetics(35.2+/-16.2%) than in non-diabetics(26.4+/-15.5%). 4) On rest SPECT, the percent redistribution was significantly lower in diabetics than in non-diabetics(left anterior descending artery area ; diabetic group 31.1+/-22.5% vs non-diabetic group ; 49+/-28.5%, p<0.05, left ventricle as a whole ; diabetic group 30.6+/-21.2% vs non-diabetic group 48.2+/-27.6%, p<0.02). CONCLUSION: Quantitative (99m)Tc-MIBI SPECT provided high sensitivity and specificity for detection of CAD in diabetics. Multiple vessel disease, distal lesion and fixed lesions were more common in diabetics than in non-diabetics, (99m)Tc-MIBI SPECT is useful noninvasive test for diagnosis of CAD & important prognostic implications.
Arteries ; Coronary Artery Disease* ; Coronary Vessels* ; Diagnosis ; Heart Ventricles ; Perfusion ; Perfusion Imaging ; Sensitivity and Specificity ; Tomography, Emission-Computed, Single-Photon*

Dense deposit disease (DDD) is a rare disorder characterized by the deposition of abnormal electron-dense material within the glomerular basement membrane of the kidneys. The diagnosis is made in most patients between 5 and 15 years of age, and within 10 years, approximately half of the affected patients progress to end-stage renal disease. We report a rare case of regressive DDD without C3 deposition after steroid therapy in an 11-year-old boy. The patient presented with edema, gross hematuria, and nephrotic-range proteinuria. Laboratory testing revealed a serum creatinine level of 1.17 mg/dL, albumin level of 2.3 g/dL, and serum C3 level of 125 mg/dL (range 90-180 mg/dL). The results of the renal biopsy were consistent with DDD without C3 deposition. After 6 weeks of steroid therapy, the nephrotic syndrome completely resolved. The follow-up renal biopsy showed a significant reduction in mesangial proliferation and disappearance of electron-dense deposits in the GBM.
Biopsy ; Child ; Creatinine ; Dichlorodiphenyldichloroethane ; Edema ; Follow-Up Studies ; Glomerular Basement Membrane ; Glomerulonephritis ; Glomerulonephritis, Membranoproliferative ; Hematuria ; Humans ; Kidney ; Kidney Failure, Chronic ; Nephrotic Syndrome ; Proteinuria ; Remission Induction