Isoniazid/pyrazinamide/rifampicin
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Hepatitis: 5 case reports In a study of 22 patients, 5 adult patients (3 men and 2 women) [ages not clearly stated] were described who developed hepatitis after treatment with isoniazid, pyrazinamide or rifampicin for tuberculosis [routes not stated; not all dosages stated]. Patient 4 (group A): The woman received treatment with unspecified anti-tubercular drugs. After 2 weeks, her SGOT level was 44IU and SGPT level was 30IU and was considered to have developed hepatitis. Treatment was discontinued till clinical condition and biochemical tests were normalised. Rifampicin, isoniazid tablet 100mg which was increased to 300mg within 7 days and ethambutol were initiated daily after her abnormal liver functions were normalised. She developed hepatic biochemical abnormalities after 2 weeks of treatment initiation. Her serum bilirubin was 0.9mg%, SGOT level was 41IU and SGPT level was 22IU. She was noted to have developed hepatitis with anorexia, epigastric discomfort, vague ill health and dull pain over the right hypochondrium. Rifampicin and isoniazid were discontinued and hepatitis subsided. Ethambutol was continued and she was initiated on streptomycin. Patient 6 (group A): The man received treatment with unspecified anti-tubercular drugs. After 4 weeks, his SGOT level was 57IU and SGPT level was 77IU and was considered to have developed hepatitis. Treatment was discontinued till his clinical condition and biochemical tests were normalised. Rifampicin, isoniazid tablet 100mg which was increased to 300mg within 7 days and ethambutol were initiated daily after his abnormal liver functions were normalised. He developed hepatic biochemical abnormalities after 4 weeks of treatment initiation. His serum bilirubin was 2.7mg%, SGOT level was 64IU and SGPT level was 85IU. He developed hepatitis with anorexia, epigastric discomfort, vague ill health and dull pain over the right hypochondrium. Rifampicin and isoniazid were discontinued and hepatitis subsided. Ethambutol was continued and he was initiated on streptomycin. Patient 7 (group A): The man received treatment with unspecified anti-tubercular drugs. After 3 months, his SGOT level was 65IU and SGPT level was 28IU and was considered to have developed hepatitis. Treatment was discontinued till his clinical condition and biochemical tests were normalised. Rifampicin, isoniazid tablet 100mg which was increased to 300mg within 7 days and ethambutol were initiated daily after his abnormal liver functions were normalised. He developed hepatic biochemical abnormalities after 2 weeks of treatment initiation. His serum bilirubin was 1.7mg%, SGOT level was 98IU and SGPT level was 99IU. He developed hepatitis with anorexia, epigastric discomfort, vague ill health and dull pain over the right hypochondrium. Rifampicin and isoniazid were discontinued and hepatitis subsided. Ethambutol was continued and he was initiated on streptomycin. Patient 10 (group A): The woman received treatment with unspecified anti-tubercular drugs. After 9 days, her SGOT level was 65IU and SGPT level was
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