Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The urinary excretion of D-glucaric acid and the plasma clearance of antipyrine were estimated during the acute phase of viral hepatitis and again during recovery. The plasma clearance of antipyrine was impaired during the acute stage of hepatitis, while the urinary excretion of D-glucaric acid was paradoxically high. Both parameters returned to normal during recovery. These findings suggest that the use of urinary D-glucaric acid excretion as an index of microsomal enzyme induction is unreliable when there is liver injury.
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PMID:Paradoxical urinary excretion of D-glucaric acid in acute viral hepatitis. 95 55

Three cases with drug-induced liver diseases (hepatitis caused by hydralasine, steatosis caused by methimazole, choletasis caused by birth control pill) were investigated with respect to their drug metabolising ability. Clinical diagnoses were based on the exclusion of other pathogenetic factors, on histological findings of liver biopsy specimens and on the clinical chemical tests. Investigation of biotransforming ability was carried out using test materials (menthol loading, antipyrine, sulfadimidine, caffeine, indocyanine green kinetics) and measurement of D-glucaric acid excretion. In all cases the results show a defective capacity in some respect of drug metabolism. Possible pathogenetic role of reactive metabolites is discussed in the pathomechanism of genesis of drug-induced liver diseases.
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PMID:Drug metabolism in drug-induced liver diseases: pathogenetic role of active metabolites. 259 19

Enzyme induction during an antituberculous treatment with Rifampin, Isoniazid and Ethambutol was studied in 21 patients with tuberculosis. Two tests were used: increase in urinary excretion of D-saccharic acid and decrease of the half-life of antipyrineee. Induction is constant with D-saccharic acid. On the other hand there is a significant decrease in the half-life of antipyrin in only 10 patients. There is an increase in the 11 other patients: all of them are slow acetylators for isoniazid. We suggest that INH has an inhibitor effect on the hydroxylation of antipyrin. This study allows us to discuss the interactions of drugs with INH and Rifampin, as well the predominance of rapid acetylators among subjects suffering of isoniazid hepatitis, recently questioned.
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PMID:[Simultaneous study of the induction effect of rifampicin and the phenotype for acetylation of isoniazid in 21 patients with tuberculosis undergoing a combination treatment]. 718 65