[Cytolytic hepatic lesion associated with the ingestion of piretanide].
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Biomedical subjects
Publications and source records attributed to J L Slama.
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The efficacy of lansoprazole (30 mg/d) and omeprazole (20 mg/d) has been assessed in active duodenal ulcer disease in 144 patients included in a multicentric, randomized, double-blind trial. After two weeks, the healing rates were 74% and 58% in the lansoprazole and omeprazole groups, respectively (P = 0.049). After 4 weeks, the healing rates were 94% in each group (NS). The delay to pain relief was 2 days for lansoprazole and 3 days for omeprazole (NS). Minor side effects occurred in 12% of the lansoprazole treated patients and in 13% of the omeprazole treated patients. No severe adverse events were reported. A slight increase in serum gastrin level was observed, similar in both groups (+35 UI/L and +19 UI/L for lansoprazole and omeprazole respectively). This study confirms previous results concerning the efficacy of both treatments in duodenal ulcer disease. The statistical difference observed for healing rates after 2 weeks could correspond to a faster efficacy for lansoprazole (30 mg) than for omeprazole (20 mg).
To study clinical and biological tolerability, 114 chronically constipated patients of both sexes, aged 18-70, without any organic alteration of the colon, received lactitol over a period of one or two months. Clinical tolerability was found to be good by 80 per cent of patients and biological tolerability excellent. Clinical efficacy was found correct for 80 per cent of patients with a dosage of 20 g (single dose in the evening). All patients, except one, agreed with the packaging and the taste of the product.
The influence of genetically determined oxidation polymorphism on drug hepatotoxicity has been poorly investigated and results are controversial. We studied drug oxidation capacity in 51 patients with hepatitis caused mainly by drugs undergoing oxidative metabolism, using dextromethorphan, a test compound recently proposed as a substitute for debrisoquine. Phenotyping was performed using the metabolic ratio (MR) calculated as MR = 0-10 h urinary output of dextromethorphan/0-10 h urinary output of dextrorphan (the main oxidative metabolite), after oral administration of 40 mg dextromethorphan hydrobromide. Dextromethorphan oxidation capacity was similar in patients and in 103 control subjects as judged by: (a) the prevalence of each phenotype (5.9% versus 3.9% for the poor metabolizer phenotype and 94.1% versus 96.1% for the extensive metabolizer phenotype; (b) the frequency distribution histograms of log metabolic ratio; (c) the mean values of dextromethorphan and dextrorphan urinary outputs and of log metabolic ratio for each phenotype. These results show that hepatotoxicity of several drugs, including amineptine, amodiaquine and Plethoryl, is related neither to an impairment in dextromethorphan oxidation capacity nor to an unusually high capacity to oxidize this drug.
One hundred and ninety duodenal ulcer patients who had relief of pain and endoscopically proven ulcer healing after a short treatment period are allocated at random to double-blind maintenance treatment with a synthetic dehydroprostaglandin-E1, rioprostil, 300 micrograms, or ranitidine, 150 mg, at bedtime for 6 months. Patients are monitored every two months and examined by endoscopy after six months of treatment, or more often if warranted. The cumulative relapse rate in the rioprostil group at six months is 32% (25/78) vs. 28% (20/72) in the ranitidine group. This difference is not significant. The percentage of side effects observed is 17% in the rioprostil group vs. 5% in the ranitidine group, but discontinuation of treatment is observed with the same frequency in the two groups.
A total of 156 patients with endoscopically proven duodenal ulcers are randomized in a double-blind, multicentre trial comparing rioprostil, 300 micrograms b.d., with ranitidine, 150 mg b.d. With rioprostil, the cumulative healing rate by endoscopy is 73% at 4 weeks, and 87% at 6 weeks. With ranitidine it is 79% and 92%, respectively. There is no difference in the occurrence of pain after the two types of treatment, and the side effects are comparable in the two groups. These results show that rioprostil is probably as effective and safe as ranitidine in the treatment of duodenal ulcer.
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A benign villous tumor of the second duodenum was treated by endoscopic excision. Fifty-four previously published cases are reviewed. Villous tumors of the duodenum are very uncommon. Presenting features include intestinal bleeding and/or occlusive symptoms and/or obstructive jaundice. Diagnosis is established by fiberoptic endoscopy and biopsies. Complete removal of the tumor is mandatory because of the high incidence of malignant changes (approximately 33%). Endoscopic excision is only possible in a small number of cases, when the tumor is small, benign, and pedunculated. Complete removal of the tumor ald unequivocal diagnosis of benign tumor on histological examination are required to withstand from further therapy. The best procedure is often surgical excision or segmentary duodenal resection. This is satisfactory for benign lesions or tumors with focal in situ malignant changes. Pancreatoduodenectomy should be considered for invasive malignant tumors.
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Liver specimens obtained by biopsy in 18 patients with asymptomatic HBs Ag were studied with specific immunofluorescent technic for this antigen by light and electron microscopy. Only insignificant changes were disclosed by routine microscopy examination. Under light microscopy "ground glass" hepatocytes were found in eight cases. Specific immunofluorescence was found positive in nine cases and was closely correlated with the "ground glass" hepatocytes in eight of them. In one on the three cases studied by electron microscopy, only spherical and tubular formations, 20 to 30 nm in diameter found in the cisternae of the smooth endoplasma reticulum in a few hepatocytes, seem to be HBs Ag.
Discovered in 1977 by Rizetto and his collaborators, agent delta is today considered as a virus entirely distinct from the H/B virus. This small RNA virus, transmissible to primate and to man, is defective: its replication in the liver is only possible when there is a pre-existing or simultaneous infection by the H/B virus with HBs antigenaemia. Its clinical importance appears very great as agent delta is very pathogenic to the liver: super-infection by this virus of a patient infected by the H/B virus explains a good number of cases of acute fulminant hepatitis and of chronic active hepatitis developing towards cirrhosis, disorders attributed in the past solely to the hepatitis B virus.
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