## Abstract Many cases of acute hepatitis remain undiagnosed and the hepatitis E virus (HEV) is emerging in industrialized countries. The aim of this study was to assess the role HEV as causative agent in acute non‐A, non‐B, and non‐C hepatitis patients in Hungary. 10.5% of the 264 acute non‐A, non
Hepatitis C viraemia rebound after “successful” interferon therapy in patients with chronic non-A, non-B hepatitis
✍ Scribed by Dr. J. A. Garson; S. Brillanti; C. Ring; P. Perini; M. Miglioli; L. Barbara
- Publisher
- John Wiley and Sons
- Year
- 1992
- Tongue
- English
- Weight
- 449 KB
- Volume
- 37
- Category
- Article
- ISSN
- 0146-6615
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
A quantitative polymerase chain reaction (PCR) assay for hepatitis C viral RNA (HCV‐RNA) was used to monitor viraemia levels in six patients at multiple time points before, during, and after interferon therapy for chronic non‐A, non‐B hepatitis (NANBH). Prior to therapy, serum HCV‐RNA was detected in all patients at approximately 10^4^‐10^5^ HCV genomes/ml. HCV viraemia became undetectable within 1 month of commencing interferon in three of the five patients whose alanine aminotransferase (ALT) levels decreased to normal on therapy. In the remaining two responder patients, viraemia levels declined more slowly, becoming undetectable after a period of several months. Recurrence of viraemia during therapy was observed in two cases. The one patient whose serum ALT levels remained elevated throughout therapy showed no decline in viraemia. On stopping interferon after a 6 months course, HCV genome titres climbed rapidly in all patients, reaching higher levels than had been observed prior to therapy. Biochemical relapse occurred within 7 months of ending interferon treatment in all but one of the patients who demonstrated this viraemia “rebound” phenomenon. © 1992 Wiley‐Liss, Inc.
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