[How many cirrhotic patients may receive propranolol after digestive hemorrhage?]. / Combien de cirrhotiques sont-ils susceptibles d'être traités par le propranolol au décours d'une hémorragie digestive?

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.

[Does oral zinc improve the cellular immunity of patients with alcoholic cirrhosis?]. / L'apport oral de zinc améliore-t-il l'immunité cellulaire des malades atteints de cirrhose alcoolique?

A depressed response to delayed hypersensitivity skin tests is frequent in patients with alcoholic cirrhosis. Immune dysfunction in these patients is presumably dependent on nutritional factors. Zinc deficiency, a common finding in alcoholic cirrhosis, inhibits cellular immunity and might be one of these factors. The aim of our study was to show that zinc supplementation may improve cellular immunity in patients with alcoholic cirrhosis. We therefore compared 2 groups of patients: patients in the treated group (n = 18) had a daily oral intake of zinc-sulfate, 200 mg, during 2 months, patients in the non treated group (n = 20) received no supplementation. Both groups had a free diet. Delayed hypersensitivity skin tests to 7 antigens were performed with the Multitest IMC System at the beginning and at the end of the study. The immunity score was determined by the number of tests producing a skin induration greater than 2 mm. The evolutive index, calculated in each patient, was the difference between the final and initial immunity scores. The 2 groups were similar for all studied parameters. Cumulated immunity scores improved from 35 to 53 in treated patients (p less than 0.02), and from 42 to 44 (NS) in non treated patients. The evolutive index was 1 +/- 1.4 in treated patients and 0.1 +/- 1 in non treated patients (p less than 0.05). We conclude that in patients with alcoholic cirrhosis, daily intake of zinc sulfate, 200 mg, improves responsiveness to delayed hypersensitivity skin tests.(ABSTRACT TRUNCATED AT 250 WORDS)

[Severe jaundice in Legionnaires' disease: a case with early hepatic biopsy]. / Ictère intense au cours de la maladie des Légionnaires: un cas avec biopsie hépatique précoce.

Although liver tests are frequently disturbed in Legionnaires' disease, jaundice occurs rarely except as a terminal event. The authors report the case of a 68 year-old man with jaundice as a presenting feature of the disease. Jaundice deepened rapidly until death a few days later. Drugs and other causes of cholestasis could be ruled out. An early liver biopsy was performed. The liver was histologically normal except for mitochondrial margination in the hepatocytes. No Legionella could be demonstrated by direct fluorescent assay. These findings suggest that: jaundice in Legionnaires' disease is not related to direct bacterial insult, cholestasis is probably consecutive to endotoxinemia, the mitochondrial margination, a rare histologic finding, could result from Legionnaires' disease. This last point needs confirmation by further studies.

[Hepatic fibrosis and portal hypertension in chronic vitamin A poisoning]. / Fibrose hépatique et hypertension portale au cours d'une intoxication chronique par la vitamine A.

The authors report the case of a 36-year-old man who was hospitalized for portal hypertension. The patient had been receiving 200 millions units of vitamin A for ten years duration as treatment of psoriasis. There were no extrahepatic signs of hypervitaminosis A and the serum concentration of vitamin A was low. Microscopic examination of a liver specimen showed: a) spontaneous fluorescence due to vitamin A accumulation in sinusoidal cells; b) portal, periportal and perisinusoidal fibrosis; c) hyperplasia and hypertrophy of Ito cells. Hepatic vitamin A concentration was markedly increased. Hemodynamic study showed increased wedged hepatic venous pressure. Low serum concentration of retinol binding protein, which could be due to severe denutrition, explained the low serum vitamin A. This case report emphasizes that severe hepatic injury due to chronic hypervitaminosis A may be observed in the absence of extrahepatic signs of vitamin A intoxication and increase in serum vitamin A concentration. In such cases, histologic examination of a liver specimen and determination of hepatic vitamin A concentration are the only means of diagnosis.

[Treatment of hepatitis C virus infection in the Poitou- Charentes region]. / Prise en charge de l'infection par le virus de l'hépatite C dans la région Poitou-Charentes.

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.