[Giant cell hepatitis in the adult associated with HIV and hepatitis C virus co-infection].
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Biomedical subjects
Publications and source records attributed to B Hanslik.
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BACKGROUND: Ecstasy is a synthetic amphetamine which causes a wide variety of adverse effects. Hepatic toxicity was only recently demonstrated but can be quite severe. CASE REPORT: A 27-year-old male with no past medical or surgical history developed jaundice without fever. He was a regular user of ecstasy and had recently increased the number of doses consumed. No evidence of a viral, alcoholic, metabolic or autoimmune mechanism was found which could explain the hepatitis. Complete cure was obtained by discontinuing ecstasy. DISCUSSION: Few cases of ecstasy hepatic toxicity have been reported. Ecstasy was undoubtedly the causal agent in this case since other known causes of acute hepatitis were excluded, confirming the hepatotoxicity of ecstasy reported in the literature. The liver disease has been reported to range form acute regressive hepatitis to fatal liver failure. Iterative exposure can lead to fibrosis. The pathophysiological mechanism of this toxic effect is not well elucidated. Ischemia alone cannot explain all the clinical forms described, particularly cases without hyperpyrexia. Ecstasy must be added to the list of potential causes of acute hepatitis. Exposure must always be searched for in cases of acute hepatitis in young subjects.
UNLABELLED: The aim of this study was to identify clinical, biological or morphological prognostic factors in 113 patients with HCC in terms of survival. All patients (100 men, aged 65 [28-85], 95% cirrhosis) were diagnosed between 1982-1990. Mean survival time was 21 +/- 3 weeks. Eleven (over 25) variables were isolated by univariate analysis. A multivariate survival analysis (Cox regression model) disclosed that serum creatinine (p = 0.0002), alkaline phosphatase (p = 0.02) and Okuda's stage (p = 0.025) were independent predictors of survival. Comparison of survival curves for different values of these prognostic variables allows division of patients in three groups of prognostic significance in terms of survival (p < 0.05). CONCLUSION: these results facilitate stratification of patients with HCC to design and evaluate future controlled trials.
Several clinical or biological autoimmune disorders, particularly lupoid diseases, are associated with chronic hepatitis C. They may be exacerbated by alpha IFN, but they are not involved in the response to therapy.
Six months alpha IFN therapy was efficient for chronic viral hepatitis C in 31% patients after six months and in 17% after one year. Cirrhosis, low serum albumin or prealbumin levels and elevated IgA seric level were non responsiveness predictive factors.
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