icon_folder.gif   Conference Reports for NATAP  
  AASLD ( American Association for the Study of Liver Diseases)
November 9-13, 2001, Dallas
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Reported by Jules Levin
  see NATAP website for more AASLD coverage www.natap.org
Mark Swain, Univ of Calgary, Calgary, AB Canada; E J Heathcote, Toronto Western Hosp, Toronto, ON Canada; Ming-Yang Lai, National Taiwan Univ Hosp, Taipei Taiwan; Vincent Bain, Univ of Alberta Hosp, Edmonton, AB Canada; Victor Feinman, Univ of Toronto, Toronto, ON Canada; Morris Sherman, Toronto Gen Hosp, Toronto, ON Canada; Kelly D Kaita, Univ of Manitoba, Winnipeg, MB Canada; Edward Gane, Auckland Hosp, Auckland New Zealand; Kevork Peltekian, Queen Elizabeth Hosp, Halifax, NS Canada; Karen Lindsay, Univ of Southern CA, Los Angeles, CA; Joseph Hoffman, Michael Brunda, Hoffmann-La Roche, Nutley, NJ
Background: Treatment of chronic hepatitis C (CHC) patients with 40 kDa peginterferon alfa-2a (PEGASYS) results in superior antiviral efficacy compared to patients treated with interferon alfa-2a (IFN a-2a) in both a general CHC population and in a population of CHC patients with cirrhosis (Zeuzem S et al. N Engl J Med. 2000;343:1666-1672; Heathcote EJ et al. N Engl J Med. 2000;343:1673-1680; Pockros PJ et al. Hepatology. 2000;32(suppl):442A). In these studies, the sustained virological response was determined at the end of a 24-week treatment-free follow-up period. With other anti-HCV therapies, long-term virological responses have been reported at time points beyond 24 weeks of follow-up. To date there has been no long-term follow-up on patients who were treated in studies evaluating the effects of 40 kDa peginterferon alfa-2a.
Objective: To investigate the long-term virological effects of treatment with 40 kDa peginterferon alfa-2a in patients with CHC.
Methods: CHC patients who previously participated in one of 3 phase III studies comparing the safety and efficacy of 40 kDa peginterferon alfa-2a and IFN a-2a were included in this study if they had completed the 24 week follow-up period in the original study. Patients could not be on any anti-HCV therapy subsequent to their original treatment and were tested yearly for HCV RNA. All patients were off original therapy for 2 to 3 years. HCV RNA was measured using AMPLICOR HCV” Test v 2.0, with a lower limit of detection of 50 IU/mL.
Results: To date, over 300 patients have been enrolled into the study. Study enrollment and data collection are ongoing. Approximately two-thirds of the patients were originally infected with HCV genotype 1 and 25% were cirrhotic. Seventy percent of patients entering this trial were treated with 40 kDa peginterferon alfa-2a. Patients were evenly divided, with approximately 50% of patients being HCV RNA negative and 50% HCV RNA positive at the last assessment in the original protocol.
--Of the patients who were originally HCV RNA negative, > 99% remained HCV RNA negative 2 to 3 years after the end of their original therapy.
--In this population, all patients who were of HCV genotype 1 or cirrhotic remained HCV RNA negative.
In the patient population that was HCV RNA positive at the end of follow-up of the original study, all but one patient remained HCV RNA positive. Interestingly, the one patient who became HCV RNA negative was a virological responder until week 24 of follow-up in the original trial. No HCV RNA could be quantified in this patient, consistent with the possibility of a false positive HCV RNA test at the last evaluation in the original study.
Conclusions:The sustained virological response achieved with 40 kDa peginterferon alfa-2a results in a durable response in all patients, including those with more difficult-to-treat disease (genotype 1 and patients with cirrhosis). The data demonstrate that CHC patients originally treated with 40 kDa peginterferon alfa-2a and were HCV RNA negative at the end of 24 weeks of treatment-free follow-up remain HCV RNA negative 2 to 3 years after the end of treatment. Future evaluations of this patient population will determine the long-term effects of 40 kDa peginterferon alfa-2a on virological response.