PROLONGED AND HIGH-DOSE RECOMBINANT INTERFERON-ALPHA-2B ALONE OR AFTER PREDNISONE PRIMING ACCELERATES TERMINATION OF ACTIVE VIRAL REPLICATION IN CHILDREN WITH CHRONIC HEPATITIS-B INFECTION

Background, There is no generally accepted treatment for chronic hepat itis B (HB) infection in children. Objectives, To evaluate the efficac y of a prolonged course of high dose interferon alone or after prednis one priming in children with chronic HB infection. Methods, The outcom e of 31 children with HB e antigen (HBeAg)-positive chronic hepatitis who randomly received either no treatment (n = 9) or 10 million units of interferon alpha-2b/m(2), alone (n = 13) or after prednisone primin g (n = 9), three times weekly for 1 year was studied. Results. One pat ient withdrew from treatment, By the end of the first year treatment i nduced a loss of HB virus DNA and HBeAg from serum in 10 of 21 patient s (48%), and a loss of HB surface antigen (HBsAg) in 4 (19%), Alanine aminotransferase values became normal in one patient (4.8%), Response rates in the two groups of treated patients were similar, In controls only one patient lost HBeAg and HBV DNA (11%; P = 0.05), and none lost HBsAg or showed alanine aminotransferase normalization (P = 0.21 and 0.70, respectively), After a posttreatment 2-year follow-up there were still no differences in the response rates of the two treatments; of the 21 pooled treated patients, 61% lost HBeAg and DNA and 67% normali zed alanine aminotransferase (US, 33 and 44% of controls, respectively ; P = 0.32 and 0.40), Reversion to HBeAg and HBV DNA negativity in tre ated patients occurred significantly earlier (P = 0.02 and 0.006, resp ectively) than in controls, No further patient lost HBsAg, but one rea cquired HBsAg. Treated patients had posttreatment histologic scores be tter than controls (P = 0.03). Conclusions. Our medium term follow-up results indicate that a prolonged course of high dose interferon in ch ildren with chronic HE infection, regardless of prednisone priming, po orly affects response rates but significantly speeds termination of ac tive viral replication.