Coeliac disease in chronic hepatitis C: a French multicentre prospective study.

BACKGROUND: A prevalence of 1.2% of coeliac disease (CD) in patients with chronic hepatitis C was recently reported, suggesting a possible epidemiological link between these two diseases. However, other studies have not found this relationship. AIM: To conduct a French multicentre prospective study to assess the prevalence of CD in hepatitis C virus (HCV)-infected patients. METHODS: Between June 2003 and November 2005, 624 consecutive HCV-positive out-patients were tested for antiendomysial IgA antibodies (AEA), antigliadin IgA and IgG antibodies (AGA). Patients with positive AEA or IgA AGA and positive IgG AGA in a context of a high suspicion of CD were asked to undergo gastroscopy with duodenal biopsies. RESULTS: Isolated IgA AEA, IgA AGA and IgG AGA were 0.16%, 5.7% and 4.4%, respectively. Gastroscopy was required for 39 patients, 31 were performed (eight refusals), but only 25 duodenal biopsies were performed as six patients had cirrhosis. CD was never detected. CONCLUSIONS: The prevalence of CD in HCV-positive patients was 0% (95% confidence interval: 0-0.59%), but there is a low prevalence of CD in the whole French population.

Tertiary hepatic syphilis. A treatable cause of multinodular liver.

Although the incidence of syphilis is increasing, liver involvement in tertiary syphilis remains exceptional. We report a case of tertiary syphilis revealed by liver localization. The clinical picture was misleading, mimicking multinodular hepatic metastasis. The final diagnosis was suspected following a fine-needle ultrasound-guided biopsy of a liver nodule showing granulomas as well as acellular necrosis and confirmed by positive serum syphilitic reactions and the presence of spirochetes in the liver. The outcome was uneventful following antibiotic treatment. It is important to be aware of the misleading picture of the disease, which has a favorable prognosis provided that simple treatment is rapidly initiated.

[Aneurysmal malformation of the extrahepatic portal vein]. / Malformation anévrismale de la veine porte extrahépatique.

Malformations of extrahepatic portal vein are rare. We report a case of extrahepatic portal vein aneurysm which was incidentally found in a female patient, aged 67, suffering from alcoholic cirrhosis. This malformation was located at the portal bifurcation and presented ultrasonically as an oval, non-echogenic, parahilar mass, 38 mm in diameter, and in continuity with the portal trunk. On CT-scan and angiography, diagnosis of portal vein aneurysm located at its extrahepatic segment was confirmed. The cause of extrahepatic portal vein aneurysm remains controversial. A congenital and/or acquired origin induced by portal hypertension explains their development.

Does elective sclerotherapy improve the efficacy of long-term propranolol for prevention of recurrent bleeding in patients with severe cirrhosis? A prospective multicenter, randomized trial.

We conducted a prospective, multicenter, randomized trial to compare the efficacy of sclerotherapy plus propranolol with that of propranolol alone in the prevention of recurrent gastroesophageal bleeding in severely cirrhotic patients. For 2 yr (1987 to 1988) 131 patients (96% of whom were alcoholic) with Child-Pugh class B or C cirrhosis (56% were class B and 44% were class C) were randomly assigned to one of our two treatment groups after cessation of variceal bleeding, without hemostatic sclerosis, and were observed for at least 2 yr. Treatment observance was good in 89% of cases; alcohol withdrawal was observed in 62% of cases. Sclerotherapy was performed weekly with 1% polidocanol, and variceal obliteration was obtained in 83% of cases, in a mean number of four sessions. The cumulative percentages (expressed as mean +/- S.D.) of recurrent bleeding at 2 yr were 42% +/- 6% for propranolol plus sclerotherapy and 59% +/- 6% for propranolol alone (a nonsignificant difference). Twenty-eight patients from the propranolol group but only 12 patients from the propranolol-plus-sclerotherapy group had recurrent bleeding from esophageal variceal rupture (p less than 0.01). The total number of blood units per patient with recurrent bleeding was slightly but not significantly more important in the propranolol group (8 +/- 7) than in the propranolol-plus-sclerotherapy group (5 +/- 5; p = 0.09).(ABSTRACT TRUNCATED AT 250 WORDS)

Treatment of severe alcoholic hepatitis by infusion of insulin and glucagon: a multicenter sequential trial.

Severe alcoholic hepatitis is still a therapeutic challenge. It has been recently advocated that a 3-wk infusion with insulin and glucagon reduces its short-term mortality rate. A multicenter, randomized, single-blind, sequential trial was designed to compare this treatment with placebo. The triangular boundary was defined with alpha = 0.05, beta = 0.10 and estimated survival at 4 wk of 50% with placebo, 75% with treatment. Patients with biopsy-proven severe alcoholic hepatitis (presence of one or more of three criteria: encephalopathy, prothrombin activity less than or equal to 50%, bilirubinemia greater than or equal to 100 mumol/L) were randomized into two groups; one treatment group received an infusion (12 hr/day) of an association of insulin (30 IU) and glucagon (3 mg), and a control group received an infusion of glucose. Treatments were administered during a 3-wk period, and the mortality rate was noted at 4 wk. The decision to discontinue the trial was reached on the basis of results from the first 44 patients. Overall results were assessed in the 72 patients included at the time of this decision (treatment group: n = 37; control group: n = 35). Fifty-three patients had cirrhosis. No significant differences were noted between the two groups at inclusion on the basis of clinical, laboratory and histological criteria. The mortality rate was not significantly different in the two groups; 10 patients (27%) in the treatment group and 5 patients (14%) in the control group died. Causes of death were similar in the two groups and consisted primarily of gastrointestinal hemorrhage, hepatic failure and infectious events.(ABSTRACT TRUNCATED AT 250 WORDS)

[Vitamin C. From scurvy to the ideal vitamin balance]. / Vitamine C. Du scorbut à l'équilibre vitaminique idéal.

Scurvy is caused by severe deficiency of vitamin C or ascorbic acid, and is usually diagnosed by the overt clinical signs which appear at an advanced stage. Laboratory examinations, and in particular ascorbic acid assays, do not yet enable subclinical vitamin C deficiency to be reliably detected; hence the importance of knowing the situation which expose to this deficiency.

Hepatic venoocclusive disease and perisinusoidal fibrosis secondary to arsenic poisoning.

Hepatic injury secondary to arsenic poisoning has been known long but is poorly documented. A case of a patient with hepatic injury following severe arsenic poisoning is reported. Histological study of the liver demonstrated acute venoocclusive disease and perisinusoidal fibrosis. This case indicates that arsenic poisoning causes veno-occlusive disease in humans. It also suggests that hepatic damage in arsenic poisoning is secondary to vascular endothelial injury and supports the hypothesis that different patterns of hepatic vascular injury might proceed from a common mechanism.

[Serum and tissue concentrations of zinc after oral supplementation in chronic alcoholics with or without cirrhosis]. / Evolution des concentrations sériques et tissulaires de zinc après supplémentation orale chez des alcooliques chroniques avec et sans cirrhose.

Seric and hepatic zinc concentrations are decreased in chronic alcoholics, particularly those with cirrhosis. The purpose of this study was: 1) to assess the duration of zinc intake necessary to normalize seric and hepatic zinc concentrations; 2) to demonstrate that this supplementation did not increase zinc concentrations in other tissues (erythrocytes, leukocytes and hair) and did not induce adverse reactions. Twenty alcoholic patients with (group A: n = 13 or without (group B: n = 7) cirrhosis received zinc sulfate 600 mg daily during 10 days, 10 patients with alcoholic cirrhosis during 30 days (group C) and 7 during 60 days (group D) and were compared with a group of 30 normal subjects. Serum zinc concentrations increased to normal values in all groups of patients. Hepatic zinc increased significantly in groups B (p less than 0.05) and D (p less than 0.01). Zinc concentrations in erythrocytes, leukocytes and hair were unchanged. No adverse reactions were observed. We conclude that seric zinc concentrations reached normal values in alcoholics with or without cirrhosis by daily supplementation of 600 mg zinc sulfate during 10 days to 2 months while hepatic zinc concentrations increased but remained under normal values in some patients, particularly those with cirrhosis.

[Fibronectin in the ascitic fluid: its diagnostic significance]. / La fibronectine dans le liquide d'ascite: sa signification diagnostique.

We studied fibronectin concentration in the ascitic fluid of 102 patients, 71 with cirrhosis, 13 with hepatocellular carcinoma, 12 with malignant peritonitis, and six with miscellaneous disease. Fibronectin concentrations in the first three groups were 45 +/- 45 mg/l, 54 +/- 84 mg/l, and 144 +/- 123 mg/l, respectively. The difference between patients with cirrhosis and malignant peritonitis was significant (p less than 0.01). However, fibronectin concentration greater than 100 mg/l had a sensitivity of 58 per cent and a specificity of 86 per cent for the diagnosis of malignant peritonitis. Ascitic fluid protein content over 30 g/l had the same sensitivity and specificity was 90 per cent. Among cirrhotic patients, high fibronectin concentrations were demonstrated in those with long-standing ascites (m = 134 +/- 58 mg/l) whereas the lowest concentrations were found in patients with severe hepatocellular failure (m = 12 +/- 9 mg/l). Concentrations were significantly different, according to whether or not spontaneous bacterial peritonitis occurred later (20 +/- 13 mg/l versus 52 +/- 49 mg/l); 83 per cent of patients with spontaneous bacterial peritonitis during their clinical course had initial fibronectin concentrations above 30 mg/l in their ascites. We conclude that: 1) measurement of fibronectin concentration in ascitic fluid is of poor diagnostic value for discrimination between malignant and non malignant ascitic, 2) low concentrations of fibronectin are associated with the occurrence of spontaneous bacterial peritonitis in cirrhotic patients. Hypothetically, the quantitative defect of fibronectin could be responsible for bacterial opsonization impairment in these patients.

[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)

CA 125 (ovarian tumour-associated antigen) in ascitic liver diseases.

The presence of Ca 125, an ovarian cancer-associated antigen, was assessed in serum from patients with liver diseases with (n = 26) and without (n = 26) ascites. Abnormal levels of serum CA 125 were observed in all patients with ascites and in 4 patients without ascites (15%). We conclude that CA 125 is a non-specific marker of ascites whatever the origin: ovarian carcinoma, cirrhosis or peritoneal inflammatory process.

[Hepatitis and mononucleosis syndrome related to the ingestion of salazosulfapyridine]. / Hépatite et syndrome mononucléosique liés à la prise de salazosulfapyridine.

The authors report the case of a patient treated by salazosulfapyridine and presenting with hepatitis and mononucleosis. The clinical pattern was similar to infectious mononucleosis including pharyngitis and lymphadenopathy but infection by Epstein Barr virus or cytomegalovirus has been ruled out by serological tests. Responsibility of salazosulfapyridine was highly suggested by the following facts: hepatocellular necrosis was sharply centrolobular, plasmocytosis was the main finding in the white blood cells count and all abnormalities rapidly improved after treatment withdrawal. The authors point out that salazosulfapyridine intolerance could mimic infectious mononucleosis and viral hepatitis. In such cases the drug must be rapidly withdrawn to avoid massive hepatic necrosis.