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M Beauchant

Publications and source records attributed to M Beauchant.

53 records · Page 3Linked to original sources

Oral pharmacokinetics and ascitic fluid penetration of pefloxacin in cirrhosis.

Plasma and ascitic fluid concentrations of pefloxacin in 10 cirrhotic patients and 8 healthy volunteers were determined following administration of a single oral dose of 400 mg. The mean elimination half-life was significantly increased in the patients (29.0 h) compared to in 8 healthy volunteers (12.3 h). In patients, the total plasma clearance (2.71 vs 6.85 l/h) and volume of distribution (1.12 vs 1.67 l/kg) were decreased. Estimated by the ratio of the AUC in peritoneal fluid and plasma, ascitic fluid penetration was 68% after one oral dose, and pronounced accumulation of pefloxacin in ascites was found after repeated doses. Oral pefloxacin would seem to be a convenient and useful treatment of spontaneous, gram-negative, bacterial peritonitis in cirrhosis. However, the decreased hepatic metabolism of the drug leads to a marked accumulation in plasma and ascites after repeated doses, and a reduced dose is required in these patients.

Adult↗

Papaverine-induced chronic liver disease.

The case history of a women with jaundice and laboratory evidence of chronic active hepatitis and cirrhosis is reported. The patient had taken papaverine for 6 yr for cerebral arterial disease. Jaundice improved after the drug was discontinued but reappeared when papaverine therapy was reintroduced. Antinuclear antibody and smooth muscle antibody were present. Clinical manifestations disappeared and laboratory results again returned to normal upon withdrawal of papaverine. This case suggests that papaverine should be added to the list of drugs known to produce chronic active hepatitis and cirrhosis.

Aged↗

[How many cirrhotic patients may receive propranolol after digestive hemorrhage?].

The aim of the present study was to evaluate how many cirrhotics may receive propranolol after upper gastrointestinal bleeding. One hundred and twelve patients were consecutively admitted in a digestive intensive care unit during a two-year study, for bleeding of esophageal (63 p. 100) or gastric (4 p. 100) varices, or acute gastric erosions (33 p. 100). Twenty-one per cent of patients were initially class A (Child's classification). 26 p. 100 were B, and 53 p. 100 were C. Eighteen patients (16 p. 100) died within the first 10 days. Eighty patients (71 p. 100) did not receive propranolol because of: a) contraindication for this drug (asthma, heart failure, diabetes, n = 25); b) carcinoma, mainly of the liver (n = 11); c) foreseeable lack of compliance with the treatment (n = 8); d) criteria for which the efficacy of propranolol has not been demonstrated (small esophageal varices, jaundice, or ascites, n = 36). Only 14 patients (13 p. 100) received propranolol therapy: 5 stopped their treatment, 3 because of gastrointestinal rebleeding. Our experience suggests that propranolol can be used only in a few cirrhotics for prevention of recurrent gastrointestinal bleeding.

Adult↗

[Comparison of the effects of cimetidine and ranitidine in vivo and in vitro on the hepatic microsomal enzyme system in rats].

Cimetidine, administered intraperitoneally to male rats (20 mg/kg and 40 mg/kg) induced a 125 p. 100 and 325 p. 100 increase in the hexobarbital sleeping time, respectively. Ranitidine, at the same dosage, had no effect. Cimetidine (40 mg/kg) decreased the aminopyrine metabolic clearance by 73 p. 100, whereas ranitidine caused no change. In vitro, cimetidine (1 mM) decreased 3 oxiding enzymatic activities, ethylmorphine demethylase, aniline hydroxylase and aminopyrine demethylase, measured in a 9,000 g supernatant fraction of rat liver, by 29 p. 100, 45 p. 100 and 73 p. 100, respectively. Ranitidine (1 mM) did not modify ethylmorphine and aminopyrine demethylase activities and induced a slight decrease of aniline hydroxylase activity (10 p. 100). Bilirubin and p-nitrophenol UDP-glucuronosyltransferase activities, measured on the microsomal fraction, were slightly inhibited (5 p. 100 and 4 p. 100, respectively) by cimetidine (1 mM). Ranitidine (1 mM) did not change these enzymatic activities. The effects of cimetidine and ranitidine on both the oxidizing and conjugating enzymatic activities were not notably affected by pretreatment with phenobarbital (100 mg/kg, intraperitoneally for 3 days). These results point out that: 1) in vivo and in vitro, ranitidine, in contrast with cimetidine, does not inhibit the microsomal drug-oxidizing system; 2) neither ranitidine nor cimetidine decrease the activity of the microsomal drug-conjugating system. They clearly explain why cimetidine interferes with the disposition of drugs oxidized but not of drugs conjugated by the liver.

Animals↗

[The digestive system and pancreas in 1982].

The present review is concerned with the main pathophysiological, clinical and therapeutic progresses in the following fields: gastro-esophageal reflux, gastric antisecretory drugs, chronic inflammatory bowel diseases, cancer of colon and esophagus, pancreatic diseases (chronic pancreatitis, pancreatic carcinoma), acute bacterial diseases of the digestive tract, acquired immunodeficiency syndrome of the adult, diffuse nodular lymphoid hyperplasia of the adult small bowel.

Bacterial Infections↗

[Treatment of hepatitis C virus infection in the Poitou- Charentes region].

OBJECTIVES: The prognosis of hepatitis C virus infection could be improved by early treatment. However, this is only possible if most patients with hepatitis C consult a specialized institution. The aim of this study was to evaluate the modalities of care of hepatitis C virus infection in one French district. METHODS: Between November and December 1997, 89 biological laboratories from the "Poitou-Charentes" district were asked to provide results of hepatitis C virus serology tests performed during this period. A questionnaire concerning epidemiological and follow-up data was sent to the medical practitioner who prescribed the test, for all positive tests. RESULTS: Seventy eight out of 89 (88%) laboratoires agreed to participate in the study. During the study period, 6,168 subjects were tested and 196 (3.2%) were positive. This test was a diagnostic test in 69 cases (53%) and a confirmation test in 61 cases (47%). The epidemiological questionnaire was filled out in 130 cases. The main putative factors of viral contamination were: intravenous or nasal drug addiction in 69 cases (53%), blood transfusion in 39 cases (30%), and a nosocomial risk factor in 16 cases (12%). Treatment and care of virus infection was evaluated in 113 cases from the follow-up questionnaire: a liver biopsy was performed in 30 cases (27%) and interferon therapy was administered in 13 cases (12%). Liver biopsy was not performed in 83 cases (73%) due to normal transaminase levels or a contraindication to interferon therapy. The main causes of an absence of care or follow-up were: fear of complications of liver biopsy and/or side effects to interferon therapy (19%), chronic alcoholism (18%) and active drug addiction (8%). CONCLUSION: The main causes of failure to administer adequate care in hepatitis C patients were chronic alcoholism, drug addiction and fear of liver biopsy or side effects of interferon therapy. These data should be taken into account for future screening or information compaigns for the general population.

Adult↗

[Acute intermittent porphyria associated with hyperaldosteronism and inappropriate antidiuretic hormone secretion syndrome].

Acute intermittent porphyria, the most commun acute porphyria in France, is an autosomal dominant disorder of heme biosynthesis. The basic biochemical defect is reduced activity of the enzyme porphobilinogen deaminase. Clinical evolution is characterized by acute attacks, with a severe prognosis due to acute abdominal pain and risk of neurological complications, induced by drug intake, infection, alcohol intake or unknown factors. We report the case of a patient with an inappropriate antidiuretic secretion syndrome and secondary hyperaldosteronism associated with acute intermittent porphyria and polyradiculoneuritis syndrome. This syndrome was found to be induced a delayed reaction to thiopental. A favorable response was achieved with heme-arginate treatment.

Adult↗