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Biomedical subjects

F Degos

Publications and source records attributed to F Degos.

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

Fulminant hepatitis in renal transplant recipients. The role of the delta agent.

In a series of about 300 renal transplant patients followed from 1972 to 1983, 3 cases of fulminant hepatitis were observed in HBs Ag-positive patients. In the liver biopsies of 2/3 of them, the delta antigen was detected by direct immunofluorescence with a specific anti-delta serum. This result demonstrates the responsibility of the delta agent for the development of fulminant hepatitis, and emphasizes the possibility of delta infection in HBs Ag-positive transplant patients with severe hepatitis.

Antigens, Viral↗
PubMed1987

Monoclonal anti-HBs antibodies radioimmunoassay and serum HBV-DNA hybridization as diagnostic tools of HBV infection: relative prevalence among HBsAg-negative alcoholics, patients with chronic hepatitis or hepatocellular carcinomas and blood donors.

Anti-HBs monoclonal antibodies radioimmunoassay (m-RIA) and HBV-DNA hybridization techniques were used to detect HBs antigen (HBsAg)--associated determinants (evidence of HBV on-going infection) and HBV-DNA sequences (evidence of viral multiplication) in the serum samples of 479 patients who were HBsAg negative by standard solid-phase radioimmunoassay. They included 128 alcoholics, 104 patients with chronic hepatitis, fifty-four with an hepatocellular carcinoma, 100 with coagulation disorders and ninety-three blood donors. The aim of this study was the comparison in these populations of the prevalence of the various HBV markers. m-RIA detected HBsAg-associated determinants in 1% of blood donors, 3% of coagulation disorders, 3.1% of the alcoholics, 21.1% of chronic hepatitis and 16.6% of hepatocellular carcinoma; hybridization identified HBV-DNA sequences in 0.9%, 2.2%, 10.9%, 9.6% and 5.5% of these cases, respectively. The combined prevalence of both markers of an on-going HBV infection (with or without viral multiplication) was 14.16%, 26.9% and 22.2% in the latter groups, respectively, as compared with only 3% in patients with coagulation disorders and 2.1% of blood donors. These results confirm the frequency of HBV or HBV-related virus infection in alcoholics, in chronic hepatitis and hepatocellular carcinomas, despite the absence of HBsAg by standard RIA (or even of any other usual marker); this gives further evidence for variations in the expression of HBV infection. A high and quite similar prevalence of usual serum markers and hybridization results was observed in the alcoholics and in the patients with chronic hepatitis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Hepatitis B vaccination in chronic alcoholics.

Given the possible role of hepatitis B virus in the occurrence of hepatocellular carcinoma and the high prevalence of HBV infection in alcoholics, we attempted to prevent HBV infection in alcoholic patients with or without cirrhosis. Among 32 cirrhosis, 20 received three injections of hepatitis B vaccine at monthly intervals and 12 had a 4th injection one month later. Effectiveness was evaluated on the anti-HBs titer at the 6th month; it did not differ between the 3- and 4-injection groups. Two patients were good responders (anti-HBs greater than 300 mU/ml), 14 had a low response (m-30 mU/ml at the peak) and 16 (50%) had no detectable anti-HBs. All alcoholics without cirrhosis were given 4 injections; all had detectable anti-HBs but their mean antibody response was 97.7 +/- 4 SD. No obvious statistical difference in the response to the vaccine was noted on the basis of sex or age, or on the discontinuation or not of alcohol intake. Deficient antibody response to vaccines has not previously been demonstrated in patients with cirrhosis or in alcoholics. It remains to be determined whether this response is specific of HBV and how it could be related to the role of HBV in the occurrence of liver alterations in alcoholics.

Adult↗
PubMed1986

Therapeutic activity of vidarabine in symptomatic chronic active hepatitis related to HBV.

The potential inhibitory effects of nucleoside analogues such as ARA-A and acyclovir on HBV-DNA-polymerase were first demonstrated in vitro and then confirmed in vivo in open dose finding studies. The therapeutic efficacy of both ARA-A and ARA-AMP which appeared the most potent drugs was then confirmed by various studies in symptomatic HBeAg-positive patients. These studies demonstrated a similar benefit of therapy with 38 and 40% of treated patients given ARA-A and ARA-AMP, respectively, who permanently cleared HBV replication after a single course, and 67-80% who did so after two courses. Significant improvement in transaminases and histologic activity was also documented (P less than 0.001). Myalgias were observed in 10 and 30% of the patients, respectively. Patients who failed to respond to nucleosides, and those coinfected with HDV, were treated with interferons. Out of 8 cases of HDV/CAH given 5 MU thrice weekly of fibroblast beta-interferon (UPSA) for 3 months, DNA-p activity fell transiently in all 6 initially elevated cases. A parallel decrease in anti-HD titers (P less than or equal to 0.05), inflammation (P less than or equal to 0.001) and necrosis (P less than or equal to 0.05) were observed. alpha-Recombinant interferon was given i.m. for 4 months (2-7 MU/m2 X 2/7 days) to 10 CAH with high DNA-p values. HBV replication was permanently inhibited in 4 cases and dramatically reduced in 3 additional patients. Three failed to respond. Careful monitoring of DNA-p values appeared to be the single most important factor in assessing activity.

Clinical Trials as Topic↗
PubMed1986

Hepatitis B virus DNA in mononuclear blood cells. A frequent event in hepatitis B surface antigen-positive and -negative patients with acute and chronic liver disease.

We have investigated 38 hepatitis B surface antigen (HBsAg)-positive and 34-negative patients with acute and chronic liver disease for the presence of hepatitis B virus (HBV) DNA in peripheral mononuclear blood cells. Among the HBsAg-positive subjects HBV DNA was detected in the mononuclear cells of asymptomatic HBV carriers (2/6), patients with acute hepatitis (8/8), chronic active hepatitis (18/21), and with hepatocellular carcinoma (2/3); the viral DNA sequences were also identified in the mononuclear cells of patients with HBsAg-negative acute hepatitis (2/3), chronic active hepatitis (5/15) and hepatocellular carcinoma (5/16), some of these showing no evidence of HBV by conventional serological markers. By contrast HBV DNA was not detected after resolution of the acute viral infection. For 7 patients different mononuclear cell-enriched subpopulations were assayed and the viral DNA was observed in T lymphocytes (both OKT4+ and OKT8+ enriched subsets) and/or in B enriched lymphocytes; the restriction DNA patterns showed in some patients a genetic organisation of the viral DNA similar to those observed in the liver (including free monomeric and oligomeric HBV DNA and results consistent with integrated viral sequences); however, no HBV DNA replicative forms were detected. These results show that the hepatitis B virus infection of mononuclear blood cells (including lymphoid cells) is a frequent event at all stages of the viral infection which might be related to immunological abnormalities observed in HBV carriers; in addition the mononuclear blood cells analysis may provide an insight to the liver cells status.

B-Lymphocytes↗
PubMed1986

Serial transmission of a human non A-non B hepatitis viral strain to HBV-protected chimpanzees: successive histological and ultrastructural studies.

A NANB agent of human origin was inoculated in HBV-immunized chimpanzees. Infection was proven in two animals and serially passed to two others. The absence of anti-HBc in serum and the absence of HBsAg and HbcAg in liver are arguments against the HBV nature of the transmitted infection. Moreover, the reproducible appearance of the NANBcAg/Ab system at each passage from man to chimpanzee and from chimpanzee to chimpanzee, a response not elicited in control animals, suggests that this reaction may be a specific immunologic marker for the strain. NANB infection was transmitted in all chimpanzees. Distinctive hepatic morphologic features were obtained in the liver biopsies of the human donor and the inoculated chimpanzees: eosinophilic alterations of hepatocytes and numerous inflammatory cells. Inflammation was more prominent than necrosis, appearing earlier and lasting longer, but was not topographically close to the eosinophilic changes. On electron microscopy, particles characteristic of NANB agent were observed in the cytoplasm of the hepatocytes. No particles were demonstrated in the nucleus of these cells.

Animals↗
PubMed1986

[HBe antigen and B virus DNA in patients with chronic active hepatitis].

The detection of HBe antigen (HBeAg) in the sera of chronic HBV carriers is classically used as a marker of viral replication and therefore of development and infectivity of the disease. On this basis, it was used for the selection of patients for antiviral treatment. However, discrepancies between the presence of HBeAg and signs attesting to viral replication, namely HBV DNA and DNA polymerase, have been reported. We attempted to determine the prevalence of markers of viral replication in a group of patients with chronic active hepatitis associated or not with cirrhosis. All 41 patients were HBs Ag carriers; HBe Ag was present in 36 (88 p. 100), and HBV DNA in 28 (68 p. 100). A statistically positive correlation was found between the presence of cirrhosis and the absence of viral replication. In spite of the detection of HBe Ag, no direct signs of viral replication were observed in 30 p. 100 of patients, mainly those with cirrhosis. Therefore it is clear that the detection of HBe Ag alone cannot be considered as a sign of viral replication. Direct signs of viral replication should help to select patients for antiviral therapy, which should be started before the occurrence of cirrhosis.

Adult↗
PubMed1985

Hepatitis B virus DNA in patients with chronic liver disease and negative tests for hepatitis B surface antigen.

We assessed the presence of hepatitis B virus (HBV) DNA in liver or serum samples from 134 patients with hepatitis B surface antigen (HBsAg)-negative chronic liver disease, including 20 with hepatocellular carcinoma. HBV DNA sequences were detected in 52 of the 88 liver samples (59 per cent), including 17 of the 20 samples from patients with hepatocellular carcinoma. Presumably "replicative forms" of HBV DNA were detected in only 5 of the 88 liver samples, 3 of which were from patients with no serologic marker for HBV. In most of the liver samples the DNA patterns were consistent with the presence of HBV or a closely related virus. Of the 105 serum samples tested, HBV DNA sequences were identified in 10 (9.5 per cent), 6 of which had no HBV serologic marker. Moreover, HBsAg-associated determinants were detected in 5 of 17 patients who were positive for HBV DNA and in none of 14 patients who were negative. This study demonstrates the high frequency of HBsAg-negative HBV DNA-positive viral infection of the liver and suggests that multiplication of HBV may occur in the absence of any conventional serologic marker for HBV.

Antibodies, Monoclonal↗
PubMed1985

Presence of HBV DNA in spermatozoa: a possible vertical transmission of HBV via the germ line.

Using molecular hybridization we studied the presence and state of HBV DNA in sperm samples obtained from 17 patients with HBV infection (eight HBsAg chronic carrier, nine acute hepatitis B). Presence of HBV DNA was detected in three samples of seminal fluid from three patients with acute hepatitis. Restriction enzyme patterns of cellular DNA were consistent with presence of integrated HBV DNA sequences in spermatozoa from two of these three patients. The results indicate that HBV DNA may be present in the semen, at least during the acute phase of HBV infection. The presence of HBV DNA in seminal fluid confirms the possibility of venereal transmission. The presence of integrated sequences in spermatozoa suggests the possibility of true vertical transmission of HBV via the germ line.

DNA, Viral↗
PubMed1985

[Encephalopathy following portal shunting in nodular regenerative hyperplasia of the liver].

Two patients with nodular hyperplasia of the liver developed a chronic disabling encephalopathy after an interposition mesocaval shunt. Both had a low total hepatic blood flow-rate postoperatively. Encephalopathy disappeared following surgical occlusion of the shunt. These observations emphasize the risk of postshunt encephalopathy in patients with non-cirrhotic intrahepatic portal hypertension.

Adult↗
PubMed1984

Liver involvement in nonamyloid light chain deposits disease.

Liver examination performed in seven patients who had renal failure related to light chain deposits demonstrated in all cases the presence of liver light chain deposits. In all of our patients clinical renal involvement antedated the liver disease. The portal areas and the Disse spaces contained a granular material which strongly reacted with antilight chain antiserum (kappa or gamma). In one patient in whom lesions were severe, the sinusoid edge was ruptured and a pelliosis -like lesion was observed. In the five patients who were hemodialyzed for more than several months at the time of discovery of liver deposits, increased amounts of collagen were present in the Disse spaces, and one patient had extensive liver fibrosis by light microscopy. Clinical liver involvement was defined by moderate hepatomegaly in five patients, with ascites in two. A slight increase in phosphatase alkaline activity was frequently observed and bromsulphalein retention was present in two. In one patient liver tests remained entirely normal despite the presence of diffuse kappa light chain deposits.

Aged↗