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Biomedical subjects

J Bernuau

Publications and source records attributed to J Bernuau.

At least 91 records · Page 5Linked to original sources
PubMed1987

Non-A, non-B fulminant viral hepatitis in France in returnees from Asia and Africa.

Among 61 patients admitted for non-A, non-B fulminant viral hepatitis to Hôpital Beaujon, 10 had returned from Asia or Africa, and 51 had not been outside France, within the month preceding jaundice. This suggests that hepatitis might have been contracted in Asia or Africa in the former, and in France in the latter. The interval between the onset of jaundice and the onset of hepatic encephalopathy was 10 days in the former and 26 days in the latter (P less than 0.03). The serum of the patient returning from Asia contained, and the sera of the nine patients returning from Africa did not contain, antibodies to a virus isolated from the stools of patients suffering from an epidemic fecal-oral non-A, non-B viral hepatitis in Central Asia. It is concluded that infection with Asian-African non-A, non-B viruses can be the cause of fulminant hepatitis in persons returning from these countries, that the course of this type of non-A, non-B fulminant viral hepatitis is shorter than that of non-A, non-B fulminant hepatitis contracted in France, and that different viruses might be responsible for non-A, non-B hepatitis in Asia and Africa.

Adult↗
PubMed1987

Sequences of hepatitis B virus DNA in the serum and liver of patients with acute benign and fulminant hepatitis.

We investigated hepatitis B virus (HBV) DNA in liver samples from 22 patients with acute benign hepatitis (AH) and 26 with acute fulminant hepatitis (FH) and compared the results with those obtained by detection of serum HBV DNA and HBV serological markers. Free HBV DNA forms were detected in 11 patients with AH and one with FH, a reflection of active HBV DNA replication in three patients and the end of viral multiplication in nine. Free monomeric HBV DNA was present in three patients with AH and six with FH, and free oligomers were identified in three patients with AH. Results from two patients with AH and seven with FH suggested the presence of dimeric or multimeric HBV DNA. Thus, the various forms of HBV DNA previously described in chronic HBV carriers may be observed at the acute stage of the viral infection. After comparing serological and hybridization data, we found that nine of 19 patients (one with AH and eight with FH) lacking serum HBV surface antigen might have had acute hepatitis related to infection with HBV or HBV variants.

Acute Disease↗
PubMed1987

Emergency liver transplantation for fulminant hepatitis.

Orthotopic liver transplantation was done in 17 patients with fulminant hepatitis. The cause of the liver disease was infection with hepatitis B virus, or co-infection with hepatitis B virus and hepatitis D virus, or infection with hepatitis A virus in 6 patients; drug hepatotoxicity in 5; and indeterminate in 6. Grafts from incompatible blood groups, steatotic grafts, or reduced-size grafts were used in 5, 4, and 4 patients, respectively. Of the 17 patients, 5 died: 2 of early liver failure due to the poor quality of the graft, 1 presumably of accidentally transmitted acute infection with the human immunodeficiency virus, and 2 of decerebration occurring during or immediately after surgery. The 12 other patients were alive 2 to 15 months after transplantation.

Acute Disease↗
PubMed1986

Inhibitory effect of the acute inflammatory reaction on liver regeneration after partial hepatectomy in the rat.

We evaluated the influence of an acute inflammatory reaction that triggers the synthesis of exportable proteins by hepatocytes on liver regeneration after partial hepatectomy, which induces the synthesis of proteins necessary for liver cell proliferation. In hepatectomized rats with a turpentine-induced acute inflammatory reaction, the first peaks of hepatic DNA synthesis and mitosis were significantly inhibited compared with pair-fed controls subjected to partial hepatectomy only, and the liver DNA concentration at various times after partial hepatectomy was significantly lower in the former than in the latter. Inhibition was not obtained when the acute inflammatory reaction was induced 12 h or more before partial hepatectomy, suggesting that the inhibitory effect of turpentine administration depended on early events in the acute inflammatory reaction. These data suggest that one possible mechanism responsible for inhibition of regeneration might be competition at the transcriptional or the translational level between liver syntheses of various proteins, and that, under certain conditions, liver-specific functions might take precedence over regenerative functions.

Acute Disease↗
PubMed1986

Fulminant and subfulminant liver failure: definitions and causes.

Fulminant or subfulminant liver failure, complicated by encephalopathy and in many cases by death is seen to be a syndrome that may result from numerous causes. Although viral hepatitis, drug-induced hepatitis, and hepatitis due to various types of poisonings, in decreasing frequency, account for 90% of all cases, a variety of miscellaneous conditions account for the remainder. Consideration of the possibility of these less common etiologies by the clinician is of considerable importance, since some, including massive malignant involvement (such as leukemia) or acute fulminant Wilson's disease, may respond to specific treatment measures. Thus, unless hepatic transplantation proves to be applicable in FHF of many etiologic diagnosis may continue to have important therapeutic indications in at least some cases with this syndrome.

Acute Disease↗
PubMed1985

Pirprofen-induced fulminant hepatitis.

We report the cases of 2 female patients aged 69 and 61 yr, suffering from fulminant hepatitis induced by pirprofen, a new nonsteroidal antiinflammatory drug. The duration of pirprofen administration before the onset of hepatitis was long, 7 and 9 mo, respectively. Hepatitis was not preceded or accompanied by hypersensitivity manifestations. The liver lesion consisted of massive, predominantly centrilobular hepatic cell necrosis and microvesicular steatosis. One patient died of liver failure. Although the risk of fulminant hepatitis is very low, we recommend that, in patients taking pirprofen for more than 2 mo and complaining of asthenia, nausea, or vomiting, serum aminotransferase levels should be measured and administration of the drug should be interrupted as soon as an increased level is noted.

Aged↗
PubMed1985

Ketoconazole-induced fulminant hepatitis.

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.

Adult↗
PubMed1984

Multiplication of hepatitis B virus in fulminant hepatitis B.

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.

Adolescent↗