Gastroenterology

Gastroenterology

Volume 108, Issue 4, April 1995, Pages 1104-1109
Gastroenterology

Liver, pancreas, and biliary tract
Hepatic iron concentration as a predictor of response to interferon alfa therapy in chronic hepatitis C,☆☆

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Abstract

Background/Aims: It has been reported that hepatic iron concentration (HIC) may influence response to therapy in chronic viral hepatitis. The aim of this study was to determine the relationship between HIC and response to interferon alfa therapy in patients with chronic hepatitis C. Methods: HIC was measured in liver biopsy specimens from 58 patients with chronic hepatitis C treated at three centers. Three patients had mild chronic hepatitis C, 35 had moderate to severe chronic hepatitis C, and 20 had active cirrhosis. Serum ferritin levels were measured in 51 of these 58 patients. Response to therapy was defined as normalization of alanine aminotransferase levels at the end of treatment. Results: Twenty-four patients (41%) responded to therapy. HICs were generally within the normal range (<1500 μg/g). The mean HIC in nonresponders (860 ± 100 μg/g; range, 116–2296 μg/g) was significantly higher than in responders (548 ± 85 μg g; range, 29–1870 μg/g) (P < 0.05). Eighty-eight percent of patients with an HIC of >1100 μg/g and 87% of patients with an elevated serum ferritin concentration did not respond to interferon alfa therapy. Conclusions: HIC seems to influence response to interferon alfa therapy among patients with chronic hepatitis C. A subgroup of patients with chronic hepatitis C has been identified for which an HIC of >1100 μg/g predicted nonresponse in 88% of patients.

Abbreviations

HIC
hepatic iron concentration
HII
hepatic iron index
IFN
interferon
NIH
National Institutes of Health
SLUHSC
St. Louis University Health Sciences Center
UM
University of Miami

Cited by (0)

Supported in part by a grant from the U.S. Public Health Service (RO1-DK 41816) (to B.R.B.) and an Amy and Athelstan Saw Postgraduate Medical Research Scholarship, University of Western Australia (to J.K.O.).

☆☆

Presented at the annual meeting of the American Association for the Study of Liver Diseases, November 1993, and published in abstract form (Hepatology 1993; 18: A90).