ALT and viral load decline during PEG-IFN alpha-2b treatment for HBeAg-positive chronic hepatitis B
Background: Alanine aminotransferase (ALT) is one of the main indicators for inflammatory activity in chronic hepatitis B. During interferon-based therapy, approximately 25%-40% of patients exhibit an ALT flare. Objectives and study design: To analyze the relation between ALT and HBV-DNA during pegylated interferon alpha-2b (PEG-IFN) treatment and compare different patterns of on-treatment viral load decline with the occurrence of ALT flares. Results: Of the 123 patients included in this study 31 (25%) exhibited an ALT flare during treatment or follow-up. Six out of 8 (75%) host-induced flares, i.e. ALT flares which were followed by a HBV-DNA decrease associated with a favorable treatment outcome, occurred in patients with a delayed HBV-DNA decline pattern (delayed vs. non-delayed decline, p = .022); 5 of these 8 patients exhibited HBeAg loss and 4 even HBsAg loss at the end of follow-up. The prediction of ALT normalization was possible using on-treatment viral load. Based on the difference from baseline, the evolution of viral load and ALT level were strongly interrelated during treatment and follow-up. With a joint model we estimated a correlation coefficient of 0.38 (p < 0.001) during the first 4 weeks of the treatment and of 0.72 (p < 0.0001) thereafter. Conclusion: There was a strong relation between ALT and viral load in HBeAg-positive chronic hepatitis B patients treated with PEG-IFN alpha-2b, especially after 4 weeks of treatment. Patients with a delayed decline in viral load often exhibited a host-induced flare associated with a favorable outcome.
|Keywords||ALT, Chronic hepatitis B, HBV-DNA, HBeAg-positive|
|Persistent URL||dx.doi.org/10.1016/j.jcv.2008.02.007, hdl.handle.net/1765/30257|
|Journal||Journal of Clinical Virology|
ter Borg, M.J, Hansen, B.E, Bigot, G, Haagmans, B.L, & Janssen, H.L.A. (2008). ALT and viral load decline during PEG-IFN alpha-2b treatment for HBeAg-positive chronic hepatitis B. Journal of Clinical Virology, 42(2), 160–164. doi:10.1016/j.jcv.2008.02.007