Biomedical subjects
Publications and source records attributed to B Rueff.
We report the cases of two adult patients in whom fulminant hepatitis developed after 17 and 103 days of ketoconazole administration. Histologic administration showed massive, predominantly centrilobular necrosis. Clinical manifestations of hypersensitivity and eosinophilia were absent in both patients, which suggests that ketoconazole hepatotoxicity is not mediated through an immunoallergic mechanism.
We assessed the prevalence of overt and latent primary myeloproliferative disorders in hepatic vein thrombosis. Cultures of bone marrow or peripheral blood mononuclear cells were done in 20 patients with Budd-Chiari syndrome. Erythroid colony formation in the absence of erythropoietin, which is a reliable indicator for a primary myeloproliferative disorder, was seen in 16 patients in whom Budd-Chiari syndrome was due to hepatic vein thrombosis, including 13 women aged 18 to 45 years. Among these 16 patients, the conventional criteria for the diagnosis of a primary myeloproliferative disorder were met in only 2. Primary myeloproliferative disorder, often without peripheral blood changes, is a major cause of hepatic vein thrombosis in young women.
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The presence in serum of hepatitis B e antigen (HBeAg) and hepatitis B virus DNA, which are each regarded as reflecting multiplication of hepatitis B virus, were looked for one to five days after the onset of hepatic encephalopathy in 64 patients with fulminant hepatitis B. HBeAg and hepatitis B virus DNA were found in the serum of only 24 (37%) and six (9%) patients, respectively. Hepatitis B virus DNA was absent from the serum in all 13 patients positive for anti-HBs. These findings indicate that replication of hepatitis B virus stopped after the onset of hepatic encephalopathy in most of the patients and support the view that an enhanced immune response stops the replication. Agents that inhibit viral multiplication would probably not have any effect at this stage of the disease.
We describe a 28-yr-old woman who presented with severe, recurrent cholangitis due to Caroli's disease in association with congenital hepatic fibrosis. Cystic dilatation of the segmental bile ducts was diffuse, but predominated in the right lobe and left medial segment of the liver. Extended right lobectomy was followed by cessation of cholangitis. Partial hepatectomy should be considered for the treatment of Caroli's disease in the patients with severe, recurrent cholangitis in whom cystic dilatation of the intrahepatic bile ducts predominates in a part of the liver.
The existence of jaundice induced by hyperemesis gravidarum is controversial. We report the case of a woman who suffered from three episodes of jaundice during the first trimester of three consecutive pregnancies, a few days after the onset of hyperemesis gravidarum. Jaundice was caused by conjugated hyperbilirubinaemia. Serum alanine aminotransferase activity was increased and scarce necrotic hepatocytes were shown on light and electron microscopic examinations. Cessation of vomiting was rapidly followed by complete recovery. This observation supports the view that severe vomiting can cause jaundice in pregnant women.
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Six episodes of acute rhabdomyolysis were observed within a two-year period in 5 male adult alcoholic patients hospitalised in a hepatology intensive care unit. Painful muscle swelling was discrete of absent in 4 of the 5 patients. Acute rhabdomyolysis was preceded by grand mal seizures in 4 patients, delirium tremens in 1 and high fever with shivers in 3. All cases were rapidly diagnosed on the finding of very high serum creatinine phosphokinase levels. One patient developed acute respiratory failure and recovered after prolonged mechanical ventilation. Three patients had acute renal failure with severe hyperkalemia in one but none required dialysis. Three patients died within 2 to 6 days of the diagnosis, but the deaths were not directly related to rhabdomyolysis. It would appear that in alcoholic patients: the prevalence of rhabdomyolysis is probably underestimated; any muscular hyperactivity as seen in seizures, delirium tremens and prolonged shivers may be a precipitating factor; the condition is easily diagnosed by measuring serum creatinine kinase activity; some cases of acute renal failure in patients with alcoholic cirrhosis might be explained by acute rhabdomyolysis with minimal symptoms.
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In a 25-month period, 100 cirrhotic patients, in our intensive care unit (ICU) needed endotracheal intubation and mechanical ventilation. The overall mortality rate was 89%; the mortality rate was 100% among patients with septic shock and/or superimposed acute hepatitis and/or severe cirrhosis defined with clinical signs: jaundice and/or ascites and/or spontaneous hepatic encephalopathy and/or severe malnutrition. With these prognostic indices, using Bayes theorem, the probability of fatal evolution ranges from 95%-100% (alpha = 5%). These results allow a group of patients with high cost and poor prognosis to be defined.
Four patients are described, admitted during a three-year period, who recovered from acute fatty liver of pregnancy; vomiting and jaundice were the main manifestations of the disease; coma and anuria were absent. During the same period, we observed one patient who died of acute fatty liver of pregnancy. This experience suggests that the non-fatal form of the disorder may be much commoner than the fatal form.
We report the cases of four adult patients suffering from acute hepatitis due to isaxonine phosphate (Nerfactor), a drug recently proposed for the treatment of the lesions of peripheral nerves. Hepatitis developed 14 to 166 days after the beginning of the administration of the drug. In all the patients, predominantly centrilobular hepatocytic necrosis was present. In two of our patients, the course of hepatitis was fatal. Hepatitis induced by isaxonine phosphate is likely to be due to an immuno-allergic mechanism.