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C Brechot

Publications and source records attributed to C Brechot.

152 records · Page 9Linked to original sources
PubMed1979

[Thrombocytopenic purpura during heparinotherapy. Two cases (author's transl)].

In two patients treated by heparin for thrombosis, thrombocytopenia under 10 000/cumm occured accompanied with bleeding cud recurrent thrombosis. The demonstration in the patients' serum of a factor inducing platelet aggregation and serotonin release in the presence of heparin suggests that the thrombocytopenia could be of immuno-allergic origin. In both cases, the discontinuation of heparin resulted in clinical and biological improvement. The rare cases of heparin-induced thrombocytopenia reported in the literature are discussed.

Aged↗
PubMedDate not supplied

Detection of hepatitis B virus DNA in serum by a simple spot hybridization technique: comparison with results for other viral markers.

A simplified spot method for determination in serum of hepatitis B virus DNA (HBV DNA) by molecular hybridization is proposed. For simultaneous testing of 30 serum samples, it reduced to about 1 hr the duration of the steps preceding hybridization proper. The method also greatly reduced the loss of DNA during these steps and allowed more sensitive detection in samples of only 25 or 50 microliters. HBV DNA was determined in 181 serum samples by this method, and the results were pooled with 67 previous determinations by the Southern blot technique. Results for the pool were then compared to those obtained with radioimmunoassay for serological HBV markers. Ninety-six of the 248 samples were HBV DNA positive. Eleven others gave variable or inconclusive results, probably due to low viral particle titers. Seventy-two HBsAg- and HBeAg-positive sera contained HBV DNA, confirming that HBeAg is a marker of active viral replication. Fourteen other HBsAg- and HBeAg-positive sera, obtained from eight patients, were either HBV DNA negative or oscillated between negative and positive, or, again, were weakly positive; serological follow-up in 7 patients showed seroconversion to anti-HBe in 5, 3 of which became HBsAg negative. Eight of the HBsAg-positive sera were negative or borderline for HBeAg but contained HBV DNA and may, therefore, have been infective; seven of these sera had anti-HBe. Six HBsAg-negative sera contained HBV DNA and may also have been infective; five of these exhibited HBV antibodies. These results indicate that molecular hybridization not only provides a more sensitive and direct method for detecting hepatitis B virus in serum but also defines additional serological patterns with predictive or epidemiological value.

DNA, Viral↗
PubMedDate not supplied

Hepatitis B virus DNA in serum from patients with acute hepatitis B.

Sera from 77 consecutive patients with acute type B hepatitis were examined for hepatitis B virus DNA (HBV DNA) by a spot hybridization method. The median follow-up time was 8 months (range, 1 week to 3 years). HBV DNA was detected in 26 (34%) patients on admission to the hospital. A significant positive correlation was found between short duration of symptoms and the presence of HBV DNA (p less than 0.025). Twenty-four (46%) of 52 HBeAg-positive patients were HBV DNA positive compared to 2 HBV DNA-positive patients of 25 HBeAg-negative patients (8%) (p less than 0.001). Four HBeAg-negative patients had serum HBV DNA initially or during follow-up; three had anti-HBe. Six of 77 patients with acute type B hepatitis (8%) became chronic HBsAg carriers, and HBV DNA was detectable from 5 months to more than 3 years after onset of symptoms. The presence of serum HBV DNA for more than 8 weeks after initial symptoms may predict development of a chronic HBsAg carrier state. In none of the chronic carriers was serum HBV DNA present after clearing of HBeAg.

Adolescent↗
PubMedDate not supplied

[Low prevalence of ant-hepatitis c virus antibodies in hepatocellular carcinoma in Senegal].

Senegal is a country with a high incidence of hepatocellular carcinoma (HCC). The role of the hepatitis B virus (HBV) in the genesis of HCC is well established. To evaluate the role of the hepatitis C virus (HCV) in the occurrence of HCC in Senegal, second-generation serologic tests were used to compare the prevalence of anti-HCV antibody in subjects with HCC and in controls without liver disease. A polymerase chain reaction assay was used to look for HCV RNA in sera from patients with HCC and anti-HCV antibody. HBV markers were assayed in all study subjects. Prevalences of anti-HCV antibody were 10.9% (7/64) in the HCC group and 5% (3/58) in the control group (NS). In the HCC group, anti-HCV antibody was found in 2.4% (1/42) of subjects positive for the hepatitis B antigen (HBsAg) versus 27.2% (6/22) of subjects negative for the HBsAg (p < 0.01). HCV RNA was detected in five of six anti-HCV-positive HCC patients. Prevalence of the HBsAg was 65.6% (42/64) in the HCC group versus 17.2% (10/58) in the control group (p < 10-8). Anti-HBV antibody was detected in 48.3% (28/58) of controls versus 6.3% (4/64) of HCC patients (p < 10-8). These data do not support a close epidemiologic association between the HCV and HCC in Senegal, where the HBV remains the main viral cause of HCC.

Adolescent↗