Reactivation of hepatitis B in a long-term anti-HBs-positive patient with AIDS following lamivudine withdrawal

• Published in: Journal of hepatology 1998-08, Vol.29 (2), p.306-309
• Main Authors: Altfeld, Marcus, Rockstroh, Jurgen K., Addo, Marylyn, Kupfer, Bernd, Pult, Irmgard, Will, Hans, Spengler, Ulrich
• Format: Article
• Language: English
• Subjects: Acquired Immunodeficiency Syndrome - complications; Acquired Immunodeficiency Syndrome - drug therapy; AIDS; AIDS/HIV; Anti-HIV Agents - administration & dosage; Anti-HIV Agents - therapeutic use; Biological and medical sciences; DNA, Viral - blood; Drug Administration Schedule; Hepatitis B; Hepatitis B - complications; Hepatitis B - physiopathology; Hepatitis B Surface Antigens - blood; Hepatitis B virus - growth & development; Hepatitis B virus - isolation & purification; HIV; Homosexuality, Male; Human viral diseases; Humans; Infectious diseases; Lamivudine; Lamivudine - administration & dosage; Lamivudine - therapeutic use; Male; Medical sciences; Middle Aged; Reactivation; Recurrence; Viral diseases; Viral diseases of the lymphoid tissue and the blood. Aids; Virus Activation
• ISSN: 0168-8278; 1600-0641
• DOI: 10.1016/S0168-8278(98)80017-2

Background/Aims: In HIV-infected patients, who have recovered completely from an acute hepatitis B infection and become anti-HBs positive, hepatitis B infection may be reactivated after progression to AIDS. Case Report: We present the case of a homosexual male patient with AIDS who developed clinical and serological reactivation of hepatitis B with detectable HBV-DNA 18 years after complete recovery from acute hepatitis B infection. Prior to reactivation, anti-retroviral triple therapy including lamivudine was changed to therapy without lamivudine. After reintroduction of lamivudine in the triple therapy, HBV-DNA became undetectable and the patient lost HBsAg and again developed anti-HBs antibodies. Conclusion: The hepatitis B in this patient can be explained best by reactivation of persistent HBV infection, possibly because of transient decline in antibodies against HBs-antigen due to a reduction in CD4+ lymphocyte numbers and B cell dysfunction. This observation points to the clinical relevance of HBV persistence in serum and blood cells of anti-HBs-positive subjects for many years after recovery from acute hepatitis B infection. The possible role of lamivudine withdrawal which immediately preceded HBV breakthrough in our patient is noteworthy. Regular monitoring of markers of HBV infection, including HBV-DNA, in patients with AIDS appears justified after discontinuation of lamivudine.