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Predictors of HBeAg status and hepatitis B viraemia in HIV-infected patients with chronic hepatitis B in the HAART era in Brazil

DOI: 10.1186/1471-2334-11-247

Keywords: hepatitis B virus, HIV, virological outcome, tenofovir

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Abstract:

A retrospective cross-sectional study was performed, of HBsAg-positive HIV-infected patients in treatment between 1994 and 2007 in two AIDS outpatient clinics located in the S?o Paulo metropolitan area, Brazil. The baseline data were age, sex, CD4 T+ cell count, ALT level, HIV and HBV viral load, HBV genotype, and duration of antiretroviral use. The variables associated to HBeAg status and HBV viremia were assessed using logistic regression.A total of 86 HBsAg patients were included in the study. Of these, 48 (56%) were using combination therapy that included lamivudine (LAM) and tenofovir (TDF), 31 (36%) were using LAM monotherapy, and 7 patients had no previous use of either one. Duration of use of TDF and LAM varied from 4 to 21 and 7 to 144 months, respectively. A total of 42 (48. 9%) patients were HBeAg positive and 44 (51. 1%) were HBeAg negative. The multivariate analysis revealed that the use of TDF for longer than 12 months was associated with undetectable HBV DNA viral load (serum HBV DNA level < 60 UI/ml) (p = 0. 047). HBeAg positivity was associated with HBV DNA > 60 UI/ml (p = 0. 001) and ALT levels above normality (p = 0. 038).Prolonged use of TDF containing HAART is associated with undetectable HBV DNA viral load. HBeAg positivity is associated with HBV viremia and increased ALT levels.Hepatitis B virus (HBV) and human immunodeficiency virus (HIV) co-infection is a frequent event because both viruses share the same routes of transmission. Studies conducted in North America, Europe, and Australia have shown that between 5% and 10% of all HIV-infected patients are also infected with HBV [1]. In Brazil, this prevalence ranges from 1. 6% to 8. 5% [2-8].HIV infection has a negative impact in all phases of the natural history of hepatitis B, leading to increased rates of persistent infection, higher HBV DNA levels, and lower rates of hepatitis B and antigen loss [9-11]. Progression of fibrosis, development of cirrhosis, and liver-related mortality are more

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