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Chronic hepatitis C and interferon alfa therapy: predictors of long term response
Author(s) -
Jenkins Peter J,
Cromie Suzanne L,
Finch Caroline F,
Dudley Francis J,
Bowden D Scott
Publication year - 1996
Publication title -
medical journal of australia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 131
eISSN - 1326-5377
pISSN - 0025-729X
DOI - 10.5694/j.1326-5377.1996.tb122013.x
Subject(s) - medicine , steatosis , gastroenterology , viral load , viral hepatitis , alanine transaminase , hepatitis c , ribavirin , univariate analysis , interferon alfa , interferon , immunology , fibrosis , hepatitis c virus , liver disease , alpha interferon , multivariate analysis , virus
Objective To identify independent patient, disease and viral characteristics that predict a sustained biochemical or viral response to interferon alfa therapy in patients with chronic hepatitis C. Design Comparison of interferon responders and non‐responders by univariate and multivariate analysis. Setting The hepatitis clinic of the Alfred Hospital, Melbourne (a tertiary referral hospital), between July 1989 and June 1994. Subjects All patients with chronic hepatitis C who were treated with interferon alfa (IFN‐α; 3 million IU, three times a week or more) for at least 12 weeks. Outcome measures Patient demographic and epidemiologic characteristics, pretreatment serum alanine aminotransferase (ALT) and γ‐glutamyl transpeptidase (GGT) levels, histological grading of hepatic steatosis, necroinflammatory activity and fibrosis, serum hepatitis C virus (HCV) RNA titres and genotype and post‐treatment serum ALT levels and presence of HCV RNA. Results Of 58 patients, 13 (22%) had a sustained (six months or longer) biochemical response to IFN‐α therapy, including 12 (21%) with a sustained viral response. Univariate analysis showed that young patients with a normal serum GGT level, grade 0–1 steatosis and fibrosis, low viral titre and infection with genotypes 3a and 2a were more likely to have a sustained response. Infection with genotypes other than 1a and 1b was the only independent variable associated with both a sustained biochemical and viral response. After adjusting for genotype, a hepatic fibrosis grade of 0–1 was also independently associated with viral response. This logistic regression model accurately predicted the virological response in 80% of cases. Conclusion In Australian patients with chronic hepatitis C, a sustained viral response to IFN‐α therapy is most likely in those infected with a genotype other than 1a or 1b and with minimal hepatic fibrosis.