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High rates of HBeAg seroconversion and HBsAg loss
with Tenofovir + Emtricitabine in patients with HBV-HIV co-infection irrespective of CD4+ cell count
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High rates of HBeAg seroconversion and HBsAg loss with Tenofovir + Emtricitabine in patients with HBV-HIV co-infection irrespective of CD4+ cell count
Reported by Jules Levin
AASLD Oct 31-Nov 3 2009, Boston, MA
L. M. Kosi1; T. Reiberger1; K. Rutter1; K. Pfistershammer2; A. Rieger2; M. Peck-Radosavljevic1
1. Gastroenterology & Hepatology, Medical University of Vienna, Vienna, Austria.
2. Dermatology, Div. of Immunodermatology & Infectious Diseases, Medical University of Vienna, Vienna, Austria.
Background: Due to overlapping routes of transmission co-infection with hepatitis B virus (HBV) can be found in approximately 10% of HIV patients. The efficacy safety of lamivudine (3TC), tenofovir (TDF) or emtricitabine (FTC) used for highly active antiretroviral therapy (HAART) has not been completely evaluated in HBV-HIV co-infected patients.
Methods: Clinical and laboratory data of all HBV-HIV co-infected patients treated at the HIV outpatient clinic at the Medical University of Vienna between 1998 and 2009 were retrospectively analysed.
Results: A total of 107 patients (78% male, age: 41±11 years) with HBV-HIV co-infection were identified with 81% receiving HAART and 65% being initially HBV e-Antigen (HBeAg) positive. 3TC, TDF and FTC were included in 46%, 62% and 30% of used HAART regimens, respectively. HBV genotype distribution was predominantly A (56%) and D (38%). Mean liver stiffness was 4.7±0.8kPa at 7±6 years after HBV diagnosis (n=19). Mean HBV viral load was 4.35±2.29 x109 IU/mL before initiation of HAART. HBeAg-positive patients had significantly higher HBV-DNA levels (6.45±2.91 x109 IU/mL) compared to HBeAg-negative patients (2.12±3.90 x109 IU/mL; p<0.01). Over a median observation period of 61 month (range: 2-171) 90% achieved a complete suppression of HBV replication (<350 IU/mL).
HBeAg seroconversion was found in 57% of patients with a cumulative annual probability of 12.0%. Cumulative annual HBV surface-antigen (HBsAg) loss was 6.6% in HBeAg-positive patients and 7.9% in HBeAg-negative patients. Higher annual HBeAg seroconversion rates were found under TDF+FTC compared to 3TC or TDF: 14.5% vs. 9.2% (p=0.287) vs. 11.4% (p=0.436). Patients under TDF+FTC had higher annual HBsAg loss rates with TDF+FTC compared to 3TC or TDF: 10.3% vs. 6.0% (p=0.229) vs. 7.9% (p=0.334). These trends were not statistically significant. Patients with pre-treatment CD4+ counts >500/µL, 200-500/µL and <200/µL had similar annual HBeAg seroconversion rates of 11.3%, 13.3% and 12.1%, respectively (p=n.s.). Annual rates of HBsAg loss did not differ in patients with pre-treatment CD4+ counts >500/µL, 200-500/µL and <200/µL, respectively (10.3%, 8.3% and 9.1%; p=n.s.). Transient elevation of aminotransferases after initiation of HAART was found in 12% without a single case of hepatotoxicity grade III or IV.
Conclusion: HBV-HIV co-infected patients treated with HBV-active HAART show rapid suppression of HBV replication despite high baseline viremia and low levels of liver stiffness without significant hepatoxicity. TDF+FTC based HAART leads to high rates of HBeAg seroconversion (14.5%/year) and HBsAg loss (10.3%/year) irrespective of CD4+ cell counts.
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