ALPHA-INTERFERON FOR CHRONIC ACTIVE HEPATITIS-B IN HUMAN IMMUNODEFICIENCY VIRUS-INFECTED PATIENTS

Citation
H. Zylberberg et al., ALPHA-INTERFERON FOR CHRONIC ACTIVE HEPATITIS-B IN HUMAN IMMUNODEFICIENCY VIRUS-INFECTED PATIENTS, Gastroenterologie clinique et biologique, 20(11), 1996, pp. 968-971
Citations number
17
Categorie Soggetti
Gastroenterology & Hepatology
ISSN journal
03998320
Volume
20
Issue
11
Year of publication
1996
Pages
968 - 971
Database
ISI
SICI code
0399-8320(1996)20:11<968:AFCAHI>2.0.ZU;2-C
Abstract
Objectives.-A pilot study was conducted to evaluate the efficiency of alpha-interferon treatment in chronic active hepatitis B in anti-HIV-p ositive patients. Methods.-Twenty-five patients with chronic active he patitis (23 men and 2 women, mean age: 33 years) were included in the study Viral infections were acquired by intravenous drug addiction in 2, homosexual relations in 22, and multiple heterosexual contacts in o ne. The mean CD4 cell count was 480 +/- 234/mL, 7 patients had p24 ant igenemia, but none belonged to class C of the CDC classification. All patients were sei-um HBs Ag and HBV DNA-positive, and delta antigen an d antibody negative. patients received a 6-month course of alpha-inter feron 2a, 6 MU subcutaneously three times per week. The mean follow-re p after treatment was 15 months. Eighteen patients with serum anti-HIV antibodies, HBsAg and HBV DNA-positive, and chronic active hepatitis, who were not treated with interferon, were included as controls (mean follow-up : 29 months). Results.-Nine of the 25 patients (36%) lost s erum HBV DNA (1, 2, 4, 6, and 8 months after the beginning of treatmen t in 1, 4, 1, 2 and 1 cases, respectively), and were considered respon ders. Only one of the responders developed serum anti-HBe during follo w-up, despite the disappearance of HBe Ag in 2 and of HBs Ag in one. L oss of HBV DNA was not clearly associated with the immune status, sinc e 3 of the 9 responders had p24 antigenemia and the 9 responders had a lower mean CD4 count (283 +/- 246/mm(3)) than non responders (454 +/- 437/mm(3), NS). Three of the 18 patients (16.7%) in the control group had spontaneous loss of serum HBV DNA during follow-up. Thus, there w as a 2.15-fold increase in HBV DNA loss in the anti-HIV-positive patie nts who received alpha interferon, compared to those who did not. Conc lusion.-In HIV-positive patients treated with alpha interferon, the ra te of HBV DNA loss was not clearly different front that reported in im munocompetent patients. As severe HBV-related liver disease has previo usly been described in anti-HIV positive patients, at least in drug us ers, these results suggest that this treatment may be proposed whateve r the immune status, at least in the absence of AIDS.