Interactions between human immunodeficiency virus-1, hepatitis delta virus and hepatitis B virus infections in 260 chronic carriers of hepatitis B virus
Article first published online: 5 DEC 2005
Copyright © 1992 Wiley Subscription Services, Inc.
Volume 15, Issue 4, pages 578–583, April 1992
How to Cite
Housset, C., Pol, S., Carnot, F., Dubois, F., Nalpas, B., Housset, B., Berthelot, P. and Brechot, C. (1992), Interactions between human immunodeficiency virus-1, hepatitis delta virus and hepatitis B virus infections in 260 chronic carriers of hepatitis B virus. Hepatology, 15: 578–583. doi: 10.1002/hep.1840150404
- Issue published online: 5 DEC 2005
- Article first published online: 5 DEC 2005
- Manuscript Accepted: 12 APR 1991
- Manuscript Received: 4 SEP 1990
- Commission Recherche Clinique A.P
To evaluate the factors determining the severity of chronic hepatitis B virus infection and the interactions of human immunodeficiency virus and hepatitis delta virus infections, we retrospectively analyzed 260 patients, 146 of whom were followed for a mean of 31.4 ± 1.8 mo. Human immunodeficiency virus, hepatitis B virus, and hepatitis delta virus status and aminotransferase activities, histological activity index, alcohol consumption and the prevalence of cirrhosis were investigated. The patients included 54 homosexuals, 19 parenteral drug abusers and 187 subjects with other or unidentified risk factors for exposure to hepatitis B virus.
Thirty-five patients (13%) were positive for antibody to human immunodeficiency virus; 27 were homosexual and 8 were drug abusers. The mean aminotransferase activities, histological activity index and the prevalence of cirrhosis were similar in the human immunodeficiency virus–positive and human immunodeficiency virus–negative subgroups. Actuarial survival was significantly lower in the human immunodeficiency virus–positive group than in the human immunodeficiency virus–negative subjects (p = 0.004); the cause of death was clearly related to liver failure in four of the five human immunodeficiency virus–positive patients and two of the six human immunodeficiency virus–negative subjects who died. To evaluate the factors determining the severity of liver disease, we compared homogeneous subgroups of subjects. Among the homosexual patients, the prevalence of HBeAg and hepatitis B virus DNA, aminotransferase activities and the histological activity index did not differ according to human immunodeficiency virus antibody status. By contrast, human immunodeficiency virus–positive drug abusers had a higher histological activity index than their human immunodeficiency virus–negative counterparts (14.3 vs. 11.1; p = 0.02), despite a similar prevalence of hepatitis delta virus (around 70%) and similar alcohol consumption.
In a stepwise logistic regression analysis, risk factor for exposure to hepatitis B virus was the most reliable variable for predicting the histological activity index (p = 0.0002). Age (p < 0.0001), excessive alcohol consumption (p = 0.0002) and risk factor for exposure to hepatitis B virus (p = 0.01) were independently predictive of cirrhosis. The group of drug abusers showed both the highest histological activity index and the highest rate of cirrhosis.
In contrast to previous studies, these results show the potential severity of chronic hepatitis B virus–related liver disease in human immunodeficiency virus–positive subjects. Indeed, they suggest that human immunodeficiency virus infection does not attenuate and may even worsen hepatitis B virus–related chronic liver damage. They also show the importance of the type of risk factor for exposure to hepatitis B virus in the outcome of chronic hepatitis B virus infection (Hepatology 1992;15:578–583).