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, antiretroviral 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.
BACKGROUND/AIMS: In HIV-infectedpatients, 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, antiretroviral 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.
Authors: Russell B Van Dyke; Nicole Ngo-Giang-Huong; David E Shapiro; Lisa Frenkel; Paula Britto; Anuvat Roongpisuthipong; Ingrid A Beck; Praparb Yuthavisuthi; Sinart Prommas; Thanyawee Puthanakit; Jullapong Achalapong; Nantasak Chotivanich; Wirawan Rasri; Tim R Cressey; Robert Maupin; Mark Mirochnick; Gonzague Jourdain Journal: Clin Infect Dis Date: 2011-12-05 Impact factor: 9.079
Authors: Philip Meuleman; Louis Libbrecht; Stefan Wieland; Rita De Vos; Nagy Habib; Anna Kramvis; Tania Roskams; Geert Leroux-Roels Journal: J Virol Date: 2006-03 Impact factor: 5.103
Authors: Tara N Palmore; Neeral L Shah; Rohit Loomba; Brian B Borg; Uri Lopatin; Jordan J Feld; Farooq Khokhar; Glen Lutchman; David E Kleiner; Neal S Young; Richard Childs; A John Barrett; T Jake Liang; Jay H Hoofnagle; Theo Heller Journal: Clin Gastroenterol Hepatol Date: 2009-07-01 Impact factor: 11.382