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J Bernuau

Publications and source records attributed to J Bernuau.

At least 55 records · Page 3Linked to original sources
PubMed1994

[Hyperthyroidism: a possible factor of cholestasis associated with hyperemesis gravidarum of prolonged evolution].

We report two cases of hyperemesis gravidarum with hyperthyroidism and jaundice. The cessation of vomiting associated with supportive care was followed by complete recovery in 5 weeks. Hyperthyroidism occurs in 60% of hyperemesis gravidarum, but jaundice is uncommon. The association of jaundice and hyperthyroidism suggests that hyperthyroidism is a possible factor of cholestasis in patients with hyperemesis gravidarum.

Adult↗
PubMed1994

[Recurrent acute hepatic steatosis in pregnancy].

Acute fatty infiltration of the liver in pregnancy (AFILP) is a rare disorder with a severe prognosis, improved by diagnosis of the minimally symptomatic form. AFILP is classically considered to be non-recurrent. We nevertheless report the fourth case of the recurrent form.

Acute Disease↗
PubMed1993

Prevalence of hepatitis C virus infection in asymptomatic anti-HIV1 negative pregnant women and their children.

The prevalence of hepatitis C virus (HCV) infection was studied prospectively in pregnant women in France and their children by detection of anti-HCV with second-generation ELISA (ELISA2). In ELISA2-positive women, anti-HCV was detected with second- and third-generation RIBA (RIBA2 and RIBA3) and serum HCV RNA was detected with PCR. Among 670 women, anti-HIV1-negative, 26 (3.9%) were positive with ELISA2. RIBA2 was positive in 13 and HCV RNA was found in 10. Ten ELISA2-positive women had a further evaluation with assessment of HCV infection in their children. Among the 10 children born to the index pregnancy, only one was positive with ELISA2 and RIBA2 but negative with RIBA3 and PCR; the nine other children were ELISA2, RIBA2, RIBA3, and PCR negative. All 26 siblings (2-16 years old), of whom 14 were born to PCR-positive mothers, were ELISA2 and RIBA2 negative. We conclude that among anti-HIV1-negative pregnant women with normal serum ALT levels, the prevalence of HCV infection is relatively high but the risk for mother-to-infant transmission of HCV seems to be low.

Adult↗
PubMed1993

Hepatitis C virus RNA and hepatitis B virus DNA in serum and liver of patients with fulminant hepatitis.

BACKGROUND: The role of hepatitis C virus (HCV) in the development of fulminant hepatitis is poorly understood. METHODS: The polymerase chain reaction was used to detect HCV RNA and hepatitis B virus (HBV) DNA in serum and liver of 40 patients with fulminant or subfulminant hepatitis. RESULTS: HCV RNA was detected in none of the 23 subjects with hepatitis B surface antigen (HBsAg)-negative hepatitis of unknown etiology. HBV DNA was found in 1 of these 23 subjects. In contrast, 8 of the 17 patients with HBsAg-positive hepatitis were HCV RNA positive. Among the latter, 5 had immunoglobulin (Ig) M antibody to hepatitis B core antigen (anti-HBc) and thus were acutely coinfected by HBV and HCV, whereas 3 others without IgM anti-HBc had superinfection by HCV. The active replication of HCV in the liver was shown by detection of high titers of HCV RNA and of negative-stranded HCV RNA. CONCLUSION: This investigation therefore shows no evidence of a role for HCV infection in sporadic cases of fulminant hepatitis without defined etiology. However, it suggests that HCV might be implicated in a significant number of patients with HBV-related fulminant hepatitis.

Adolescent↗
PubMed1993

Low prevalence of precore mutations in hepatitis B virus DNA in fulminant hepatitis type B in France.

The presence of mutants of the precore region of the hepatitis B virus genome was investigated in French patients with fulminant hepatitis. Only one of the 10 subjects had a detectable mutation by direct sequencing. On the other hand, 2/10 and 3/10 had evidence of coinfection by hepatitis D virus and hepatitis C virus. These results indicate that the precore stop mutation at codon 28 is not a general condition in fulminant hepatitis B and might reflect epidemiological factors.

Adult↗
PubMed1993

[Fatal fulminant hepatitis induced by nilutamide (Anandron)].

The first case of fatal fulminant hepatitis probably caused by nilutamide, a non steroidal antiandrogen derivative, is reported. Nilutamide administration had been continued for 6 days after the occurrence of jaundice, 52 days after beginning of treatment. The rapidly fatal outcome might have been promoted by coadministration of phenobarbital.

Adenocarcinoma↗
PubMed1993

Persistence of systemic and splanchnic hyperkinetic circulation in liver transplant patients.

Portal pressure and portal-systemic collateral circulation after orthotopic liver transplantation have not been investigated. We studied systemic and splanchnic hemodynamics in 17 patients with cirrhosis before and 205 +/- 146 days after orthotopic liver transplantation. Among the 17 orthotopic liver transplantation patients, 12 had undergone hemodynamic study in the 6 mo before orthotopic liver transplantation. Controls were 50 patients with normal liver architecture. Cardiac index remained elevated in orthotopic liver transplantation patients compared with controls (3.6 +/- 0.9 vs 3.1 +/- 0.4 L/min.m2; p < 0.05). Azygos blood flow, which was elevated before orthotopic liver transplantation (585 +/- 402 ml/min), remained elevated after orthotopic liver transplantation (553 +/- 343 ml/min). In transplant patients, hepatic blood flow was higher than it was in controls (2.26 +/- 0.86 vs. 1.38 +/- 0.57 L/min; p < 0.05). Elevated hepatic blood flow correlated with cardiac index (r = 0.647, p < 0.025). In patients with normal graft function, hepatic venous pressure gradient was normal (2 +/- 1 mm Hg). In a patient with acute rejection, a sharp elevation in the hepatic venous pressure gradient was observed; it returned to normal 45 days after treatment. We conclude that despite normal portal pressure, portal-systemic collateral blood flow remains elevated after orthotopic liver transplantation. Possibly because of persistent collateral circulation, which may keep portal tributary blood flow elevated, hepatic blood flow is increased after orthotopic liver transplantation. Elevated splanchnic blood flow, in turn, contributes to the high cardiac index in liver recipients. Finally, a sharp elevation in portal pressure, which may be observed during acute rejection and subsides after treatment, merits further study.

Adult↗
PubMed1992

Persistent delta antigenaemia in chronic delta hepatitis and its relation with human immunodeficiency virus infection.

The prevalence of persistent hepatitis delta (HD) antigenaemia and associated factors in patients with chronic infection with the hepatitis delta virus (HDV) were investigated. Among 157 consecutive patients known to be carriers of hepatitis B surface antigen (HBsAg), 36 (23%) had one serum marker of HDV infection (anti-HD and/or HDAg). Nine of the patients with an HDV marker were HDAg positive, including three who were anti-HD negative. A follow-up over a mean period of 13 months showed that five of five patients had a persistent HD antigenaemia. This serological profile was associated with the presence of antibody to the human immunodeficiency virus (anti-HIV) (P < 0.01), serum HIV antigen (HIVAg) (P < 0.2), and the female sex (P < 0.05). Persistent HD antigenaemia could be the consequence of the suppression of T cell cytotoxic activity against hepatocytes expressing HDAg, a lower humoral response, and/or hormonal factors.

Adult↗
PubMed1992

Fipexide-induced fulminant hepatitis. Report of three cases with emergency liver transplantation.

Fipexide belongs to a new class of cognition activators and is noted for its lack of amphetamin-like side effects. We describe three patients who developed fulminant hepatic failure less than 2 months after beginning fipexide administration. The mean interval from the onset of jaundice to the onset of encephalopathy was 8 days. Emergency liver transplantation was undertaken when factor V was 20% of normal or less and coma developed. All patients were transplanted less than 1 week after the onset of encephalopathy. Two survived and one died immediately after transplantation. Histologic examination of the livers revealed massive liver cell necrosis, predominantly centrilobular, and a moderate inflammatory infiltrate within the portal spaces. We conclude that fipexide can induce massive liver cell necrosis and fulminant liver failure. As a result of this life-threatening complication, reconsideration of the indications for this drug is warranted.

Adolescent↗
PubMed1992

Herpesvirus infection of the respiratory tract in patients with alcoholic hepatitis.

Respiratory herpesvirus infections have rarely been described in alcoholics. We report four cases of severe respiratory herpesvirus infections in patients with alcoholic liver disease. Two were related to Herpes Simplex Virus and two to Cytomegalovirus. Both chronic alcoholism and severe liver disease induce immunosuppression, which might account for these unusual herpesvirus infections of the respiratory tract. These cases suggest that infections with herpesviruses should be considered in patients with alcoholic liver disease and pulmonary or tracheobronchial disease unresponsive to standard antibiotic therapy. Bronchoscopy, viral culture, and serological tests appear warranted, particularly given the existence of specific therapy.

Adult↗
PubMed1991

Severe monochlorobenzene-induced liver cell necrosis.

Benzene derivatives can induce severe liver cell necrosis in animals. A case of a 40-year-old man whose daily consumption of alcohol was 200 g and who had a severe monochlorobenzene-induced liver necrosis is described. Liver biopsy specimen showed centrilobular and mediolobular necrosis, similar to that in mice after experimental bromobenzene administration. Monochlorobenzene serum concentration, assayed from day 3 to day 15 after poisoning, decreased monoexponentially with a half-life of 40.3 hours. Prostaglandin E1 was administered from day 3 to day 8. The patient ultimately recovered. The mechanism of monochlorobenzene-induced liver injury and the possible aggravating role of chronic alcohol consumption are discussed.

Adult↗