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Interferon alfa (INF alpha), which is used in chronic active viral hepatitis, presents some safety problems. Side effects observed in 72 treated patients with chronic active hepatitis C are analysed in this retrospective study. Doses used were 3 or 9 M IU, three times a week, for 12 to 24 weeks. There were no contra-indications to the treatment and all patients had the factors predictive of a satisfactory therapeutic response. Apart from general debility, there were side effects in 65 of the 72 patients as follows: flu-like syndrome (n = 39), gastrointestinal (n = 29), dermatological (n = 24), haematological (n = 23), neurological (n = 20), cardiovascular (n = 6) and thyroid (n = 6) disorders. For 30 per cent of the patients, the dose was decreased (n = 6) or the treatment was withdrawn, temporarily (n = 5) or permanently (n = 10). These results are in accordance with those published and emphasize the need for clinico-biological monitoring during and after treatment. Indeed delayed thyroid disorders appear to be relatively common.

To identify prognostic factors taking in account recent advances in diagnosis and treatment, 24 clinical, biological, and morphological factors were evaluated by means of uni- and multivariate analysis in 84 patients with hepatocellular carcinoma diagnosed between 1984 and 1991. Okuda's grading (P < 0.01), creatininemia (P < 0.01), and treatment (P < 0.05) were independent prognostic factors. Des-gamma-carboxyprothrombin reached a significant level (P < 0.05) in a subgroup of 32 recent patients but its prognostic value needs to be confirmed. Further prospective randomized trials comparing surgical and non-surgical treatment should take these factors into account.

No epidemiological data on inflammatory bowel disease (IBD) are available in France. We therefore conducted a prospective epidemiologic study of IBD in the Nord-Pas de Calais region and the Somme department of France (4.5 million inhabitants). Each suspected new case was reported by all (private and public) gastroenterologists (n = 120) and a questionnaire was filled out at the gastroenterologist office by an epidemiologist. The final diagnosis of Crohn's disease (CD), ulcerative colitis (UC), or proctitis (UP) was made in a blind manner by two gastroenterologists. During 1988, 576 IBD patients were identified; 281 (49 percent) had CD, 207 (36 percent) had UC including 75 UP; and 88 (15 percent) had unclassified colitis. The incidence rate per 10(5) was 6.3 for CD and 4.6 for UC. The female/male ratio was 1.4 for CD and 0.9 for UC. The mean age at the time of diagnosis was 31 years for CD and 40.5 years for UC. The mean time between onset of symptoms and diagnosis was longer for CD (15 months) than for UC (6.8 months). These preliminary data suggest that the incidence of IBD is high in Northwestern France and comparable, for CD, to the highest incidence of Northern Europe.

We report the case of a 66-year-old male patient with portal hypertension related to systemic mastocytosis. The liver was enlarged; microscopic examination showed portal mast cell infiltration and fibrosis. Portal hypertension was evidenced by splenomegaly, esophageal varices, and increased wedged-free hepatic venous pressure gradient. Arteriography showed that portal vein was patent. Portal hypertension could be the consequence of intrahepatic block due to mast cell infiltration and/or fibrosis of the liver.

The authors report the case of a non-alcoholic 73-year-old man, treated for arrhythmia with amiodarone for 2 months, and hospitalized because of jaundice and hepatomegaly. There was an important increase in serum alkaline phosphatase activity (4 times the normal value) and a moderate increase in the serum activity of transaminases (3-4 times the normal value). Endoscopic retrograde cholangiography was normal. Serum markers of virus B and tissue antibodies were absent. Histological examination of a liver specimen disclosed portal and periportal fibrosis, mixed inflammatory infiltrate of the portal spaces, and ductular proliferation. Lamellar lysosomal inclusions were demonstrated on electron microscopy. Outcome was favorable after withdrawal of amiodarone. This report, as well as the 7 previously published cases, cannot explain the pathogenesis of amiodarone-induced liver changes.

A cirrhotic patient with massive splenic infarction is described. Celiac angiography showed normally opacified splenic artery and vein and a markedly enlarged spleen with large avascular zones. Splenic infarction was associated with the spontaneous disappearance of a syndrome of hypersplenism. The spleen was surgically removed. Histological examination showed multiple thromboses of the small arterial and venous vessels. The cause of this infarct remained unclear.

We encountered a case of primary biliary cirrhosis in a nonalcoholic man who had been operated on for idiopathic retroperitoneal fibrosis 20 years previously. Chronic pancreatitis was also detected on endoscopic retrograde examination. After several episodes of digestive bleeding due to ruptured esophageal varixes, the patient died of massive hemorrhage. Postmortem examination showed stage 3 primary biliary cirrhosis and a thick retroperitoneal fibrous plaque, consisting of densely fibrotic areas of collagen with rare vessels and mononuclear cells. We suggest that idiopathic retroperitoneal fibrosis may be a new autoimmune disorder associated with primary biliary cirrhosis and that primary biliary cirrhosis is a potential cause of portal hypertension, cholestasis, or both in the course of idiopathic retroperitoneal fibrosis.

In a prospective study of liver function in 19 patients with Crohn's disease, examination of liver biopsies showed a sinusoidal dilatation in 16 patients. This dilatation was moderate in 5 cases and pronounced in 6 cases and was associated with a closely parallel dilatation of the centrilobular vein. There was no correlation between these diffuse vascular changes and the site of the bowel disease, the clinical presentation, and the course of the disease. The pathogenesis of this sinusoidal dilatation is unknown.

We report on the observation of a 26-year-old woman with portal vein obstruction, diagnosed at the age of 3, and liver iron overload. Celiac and superior mesenteric angiography showed large and multiple venous collaterals between the portal and caval systems. Liver biopsy demonstrated, on Perl's staining, an important hemosiderin deposition, confirmed by an increased hepatic iron concentration (15.6 mumol/100 mg dry weight). No other histologic abnormality was found. This report suggests that large spontaneous portosystemic shunting may stimulate hepatic iron deposition in an otherwise normal liver. This mechanism could, at least in part, explain the significant hepatic siderosis observed in some cirrhotic patients.

The authors report the case of a 32-year old woman admitted for hepatomegaly, weight loss, and moderate diarrhea. Liver function tests showed anicteric cholestasis with slight increase in serum level of transaminases. Liver biopsy demonstrated massive steatosis. Biological and radiological investigations of the small intestine showed a malabsorption pattern. Stool fat excretion was 54 g per day. Duodenal biopsies disclosed total villous atrophy. A ten-day treatment with metronidazole (1,5 g per day), followed by a gluten-free diet, resulted in rapid improvement of hepatic and intestinal symptoms. This case report shows that: 1) adult celiac disease may be the cause of severe steatosis; 2) anicteric cholestasis with or without hepatomegaly during the course of adult celiac disease may be secondary to steatosis, as well as primary biliary cirrhosis or malignant infiltration of the liver; 3) bacterial overgrowth should be searched and eventually treated in the case of massive fatty liver occurring in adult celiac disease.

The case of a 28-year-old epileptic woman, treated for 3 months with carbamazepine and who developed jaundice, fever and exfoliative dermatitis is reported. Biological investigations showed an increase in the activity of serum transaminases and alkaline phosphatases as well as in the blood eosinophilic count. Liver biopsy revealed centrolobular necrosis and cholestasis with portal inflammatory infiltrate. Drug challenge was followed by the rapid recurrence of clinical and biological signs. The definitive outcome was favorable. The analysis of the 12 previously published cases, and particularly the frequency of granulomatous hepatitis, suggests an immunoallergic mechanism for the development of carbamazepine hepatitis.

The authors have observed 5 cases of cholestatic jaundice with cytolysis during treatment with amineptine, a new tricyclic compound recently made available. The responsibility of the drug was virtually certain for the following reasons: (a) there was no other cause of jaundice, such as viral infection, gallstones, toxic agents or association with other hepatotoxic drugs; (b) clinical and biochemical findings were similar in all patients; (c) in 2 patients, reintroduction of the drug after temporary withdrawal resulted in rapid recurrence of the condition, with the same symptoms and course. The shorter delay (2 and 8 days instead of 11 and 18 days) between absorption of amineptine and reappearance of the symptoms in these two patients is suggestive of an immunoallergic mechanism.