Z Gastroenterol 2009; 47 - P154
DOI: 10.1055/s-0029-1241404

Characteristics of HBeAg-positive patients chronically infectedwith hepatitis b virus (HBV) who achieved hbsag loss/seroconversion following tenofovir disoproxil fumarate (TDF) treatment

J Petersen 1, M Manns 2, S Mauss 3, S Zeuzem 4, G Teuber 4, B Möller 5, J Heathcote 6, P Marcellin 7, J Sorbel 8, F Rousseau 8
  • 1IFI Institut für Interdisziplinäre Medizin, Leberzentrum Hamburg, Hamburg, Germany
  • 2Medizinische Hochschule Hannover, Gastroenterologie, Hepatologie und Endokrinologie, Hannover, Germany
  • 3Gemeinschaftspraxis, Düsseldorf, Germany
  • 4Johann Wolfgang Goethe-Universität, Zentrum für Innere Medizin, Frankfurt am Main, Germany
  • 5Internistische Gemeinschaftspraxis, Berlin, Germany
  • 6University of Toronto, Toronto, Canada
  • 7Universite de Paris, Clichy, France
  • 8Gilead Sciences, Durham, United States

Aims: HBsAg loss was observed in significantly more TDF-treated patients versus adefovir dipivoxil (ADV) at Week (W) 48 in HBeAg-positive patients enrolled in the pivotal, phase 3 study 103 (3.2% TDF versus 0% ADV; p=0.02).

Goal: To characterize the TDF-treated patients who achieved HBsAg loss by W96 in study 103.

Methods: Patients with HBeAg-positive chronic hepatitis B (CHB) were randomized to double-blind, once daily TDF 300mg (N=176) or adefovir dipivoxil 10mg (ADV) (N=90). After W48, eligible patients (with a W48 liver biopsy) initiated open-label TDF for an additional 7 years. Two year data are presented.

Results: Overall, 6% of patients (10 TDF-TDF and 5 ADV-TDF) experienced HBsAg loss and 4% experienced seroconversion to anti-HBs by W96 (11/15 anti-HBs). Demographics of the patients who lost HBsAg revealed that 100% were Caucasian, 80% men and 80% from Europe with a median (min, max) age of 35 years (20, 64). No patient had prior interferon experience. Baseline disease characteristics included median baseline HBsAg levels of 5.11 log10IU/mL (4.62, 5.38), HBV DNA levels of 9.48 log10 copies/mL (8.47, 9.64), median ALT levels 150 U/L (75, 425) and a median pretreatment Knodell necroinflammatory score of 9.4 (5.0, 12.0). Sixty-seven percent had bridging fibrosis or cirrhosis prior to treatment. Sixty percent harbored genotype A and 40% harbored genotype D virus. Although more patients lost HBeAg prior to HBsAg loss, this pattern was not uniform. Although no patient in the ADV arm achieved HBsAg loss within the first 48 weeks, by week 96 (after 48 weeks of open label TDF) the same percentage of patients achieved HBsAg loss. However, these patients did not achieve HBsAg loss until week 80 or later. Patients with HBsAg loss had high HBV DNA and HBsAg levels at baseline however there was no clear correlation between baseline ALT levels and HBsAg loss.

Conclusion: TDF-treated patients who achieved HBsAg loss by W96 were Caucasian patients infected with genotypes A or D hepatitis B virus and with high HBV DNA and high HBsAg levels prior to treatment.