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Hepatitis B and C virus co-infection and the risk for hepatotoxicity of highly active antiretroviral therapy in HIV-1 infection

den Brinker, Mariekea; Wit, Ferdinand W. N. M.a; Wertheim-van Dillen, Pauline M. E.b; Jurriaans, Suzannec; Weel, Janb; van Leeuwen, Remkoa; Pakker, Nadine G.a; Reiss, Petera,d; Danner, Sven A.d; Jan Weverling, Gerrita,e; Lange, Joep M. A.a,d

Clinical Science

Objective: To investigate the risk of hepatotoxicity after initiation of protease inhibitor-containing highly active antiretroviral therapy (HAART) for HIV-1 infected patients with chronic hepatitis B virus (HBV) or hepatitis C virus (HCV) co-infection.

Design: Retrospective study with 394 HIV-1-infected patients initiating HAART at a single university clinic.

Methods: Liver enzyme elevation (LEE) was defined as alanine aminotransferase or aspartate aminotransferase at least five times the upper limit of normal and an absolute increase of > 100 U/l. Relative risks for time to LEE were estimated using Cox proportional hazards models.

Results: Of 394 patients 7% were hepatitis B surface antigen (HBsAg)-positive and 14% were anti-HCV-positive. Patients with chronic hepatitis had a higher risk for LEE compared with patients without co-infection: 37% versus 12% respectively. After adjustment for higher baseline transaminases, the presence of HBsAg or anti-HCV remained associated with an increased risk of LEE – relative risk 2.78 (95% confidence interval, 1.50–5.16) and 2.46 (95% confidence interval, 1.43–4.24) respectively. In patients with LEE, transaminases declined whether HAART was continued or modified. Of patients with chronic HBV infection 38% lost HBeAg or developed anti-HBe after initiation of HAART, and one seroconverted from HBsAg-positive to anti-HBs-positive. However, there was no clear relationship with LEE.

Conclusions: HIV-1-infected patients co-infected with HBV or HCV were at considerably higher risk of developing LEE when HAART was initiated compared with patients without co-infection, but it is usually not necessary to modify antiretroviral therapy.

Author Information

From the aNational AIDS Therapy Evaluation Center (NATEC), Department of Internal Medicine, the bDepartment of Medical Microbiology, the cDepartment of Human Retrovirology, the dDivision of Infectious Diseases, Tropical Medicine and AIDS, Department of Internal Medicine and the eDepartment of Clinical Epidemiology and Biostatistics, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.

Requests for reprints to: J. M. A. Lange, National AIDS Therapy Evaluation Center (NATEC), Department of Internal Medicine, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands.

Received: 13 March 2000;

revised: 26 September 2000; accepted: 10 October 2000.

© 2000 Lippincott Williams & Wilkins, Inc.