Eighteen patients with presumed childhood acquisition of chronic hepatitis B virus infection were initially entered into this randomized controlled trial. Twelve were treated with prednisolone for 4 weeks followed, after a 2‐week gap, by thrice weekly lymphoblastoid a‐interferon for 12 weeks. Two of these had previously acted as untreated controls. Three of the 12 patients (25%) [who were initially hepatitis B virus (HBV) surface antigen (HBsAg),‘e’ antigen (HBeAg) and HBV‐DNA positive] became HBeAg and HBV‐DNA negative during therapy and remained so after 12 months post‐therapy follow‐up. One of these also lost HBsAg. A further two patients lost HBeAg and HBV‐DNA during therapy but relapsed 6 and 9 months later. Two additional patients were HBV‐DNA negative but HBeAg positive at the end of follow‐up. None of the eight untreated control patients seroconverted during an identical follow‐up period. Two further patients were HBsAg and HBeAg positive but HBV‐DNA negative at the start of therapy. These were omitted from the final analysis: both subsequently lost HBeAg. The treatment response was associated with a rise in aspartate aminotransferase, peaking 2–6 weeks after prednisolone withdrawal, loss of HBV‐DNA 0–8 weeks later and subsequent normalization of liver function tests. Treatment was well tolerated.
|Number of pages||6|
|Journal||Alimentary Pharmacology & Therapeutics|
|Publication status||Published - 1993|