RESUMO
S-Adenosyl-L-methionine (SAMe) is a physiologic precursor of thiols and sulfurated compounds, which are known to be decreased in patients with liver disease. The effect of its administration on the hepatic glutathione content of liver patients was investigated. Four groups of subjects were selected: a) 9 patients with alcoholic liver disease treated with SAMe (1.2 g/day orally for 6 months); b) 7 patients with non-alcoholic liver disease treated as above; c) 8 placebo-treated patients with alcoholic liver disease; and d) 15 normal subjects as a control group. Total and oxidized glutathione were assayed by high-performance liquid chromatography of liver biopsy specimens before and after the treatment period. In all patients pre-treatment hepatic glutathione was significantly decreased as compared with controls. SAMe therapy resulted in a significant increase of hepatic glutathione levels both in patients with alcoholic and in those with non-alcoholic liver diseases as compared with placebo-treated patients. SAMe may therefore exert an important role in reversing hepatic glutathione depletion in patients with liver disease.
Assuntos
Glutationa/metabolismo , Hepatopatias/tratamento farmacológico , Fígado/metabolismo , S-Adenosilmetionina/administração & dosagem , Adulto , Feminino , Humanos , Fígado/patologia , Hepatopatias/metabolismo , Hepatopatias Alcoólicas/tratamento farmacológico , Hepatopatias Alcoólicas/metabolismo , Masculino , Pessoa de Meia-Idade , ComprimidosRESUMO
In our study of the effect of acute cimetidine administration on acetaminophen metabolism, 10 healthy subjects were given an oral dose of acetaminophen (1 g) before and after administration of cimetidine (800 mg, po). In another experiment, 10 patients with duodenal ulcer received acetaminophen (1 g, po) before and after 2 months of cimetidine treatment (400 mg twice a day, po). Acetaminophen metabolism in blood and urine was studied for 9 h in each experiment. The half-life of acetaminophen was similar either in the absence or presence of both acute and chronic cimetidine administration. Although acute cimetidine ingestion did not affect acetaminophen urinary excretion, prolonged cimetidine treatment resulted in a slight but significant decrease of acetaminophen mercapturate urinary excretion. These findings suggest that, unlike acute cimetidine, prolonged histamine H2 antagonist therapy inhibits acetaminophen oxidation to its reactive metabolite. The clinical relevance of such an interaction remains to be explored.
