INTERFERON ANTIBODIES IN PATIENTS WITH CHRONIC HEPATITIC-C VIRUS-INFECTION TREATED WITH RECOMBINANT INTERFERON ALPHA-2-ALPHA

Citation
P. Bonetti et al., INTERFERON ANTIBODIES IN PATIENTS WITH CHRONIC HEPATITIC-C VIRUS-INFECTION TREATED WITH RECOMBINANT INTERFERON ALPHA-2-ALPHA, Journal of hepatology, 20(3), 1994, pp. 416-420
Citations number
13
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
01688278
Volume
20
Issue
3
Year of publication
1994
Pages
416 - 420
Database
ISI
SICI code
0168-8278(1994)20:3<416:IAIPWC>2.0.ZU;2-U
Abstract
Patients treated with alpha-2a interferon for chronic hepatitis C may produce anti-interferon antibodies whose effect, if any, on the indivi dual response to therapy has not been fully clarified. The prevalence and kinetics of anti-interferon, including those of neutralizing type, have been studied in 60 patients with chronic hepatitis C enrolled in a randomized controlled trial of recombinant alpha-2a interferon. Thi rty patients received interferon while 30 were untreated controls. Two different methods, an enzyme immunoassay and an antiviral neutralizat ion bioassay, were used and serial serum. samples from each patient we re analyzed. Enzyme immunoassay-positive anti-interferon appeared in 6 0.7% of treated patients within 6 months of therapy; antiviral neutral ization bioassay-positive anti-interferon appeared in 52.9% of these e nzyme immunoassay-positive patients, and was associated with high enzy me immunoassay reactivity and long-term persistence. Anti-interferon w as detected in 75% of patients showing no response to interferon. Anti bodies were also detected in three out of six patients who showed alan ine aminotransferase normalization persisting up to the end of treatme nt and in 8 out of 14 patients who showed an initial marked reduction or even normalization of alanine aminotransferase, followed by reactiv ation of liver damage during treatment. Interestingly, patients who be came anti-interferon positive before complete alanine aminotransferase normalization later showed reactivation of liver damage independently of interferon dose reduction, while patients who became positive for anti-interferon after complete alanine aminotransferase normalization either did not reactivate or did so only after interferon dose reducti on. These results seem to indicate that anti-interferon may interfere with the biochemical response to interferon in some patients with chro nic hepatitis C and that this interference is closely dependent on whe ther anti-interferon appears before or after a response. (C) Journal o f Hepatology.