Effects of interferon therapy on fibrosis serum markers in HCV-positive chronic liver disease.

Objective To evaluate serum levels of prolyl-hydroxylase and helical domain of Type IV° collagen, markers of hepatic fibrogenesis, in patients with HCV-positive chronic liver disease and the effects of interferon therapy on these markers. Design Prolyl-hydroxylase and Type IV° collagen were determined before therapy and each month during the treatment and follow-up. Methods Fifty-seven HCV-positive patients were studied. All the subjects received α2a recombinant interferon, 6 MU subcutaneously three times a week for 4 weeks, followed by 3 MU thrice weekly for 5 months. After cessation of treatment, each patient was followed for 12 months. Prolyl-hydroxylase and helical domain of Type IV° collagen were measured by using immunoenzymatic methods. HCV-RNA and HCV genotype were determined according to the method of Okamoto. Results In the patients prolyl-hydroxylase (39.8 ± 8.9 ng/ml) was not different from controls (39.1 ± 5.9 ng/ml). On the contrary, the patients showed a mean Type IV° collagen (133.6 ± 93.3 ng/ml) significantly (P < 0.01) higher than controls (100.2 ± 10.5 ng/ml). A good relationship between the degree of liver fibrosis and the Type IV° collagen serum level was found (r = 0.68; P < 0.005). In both responders and non-responders the Type IV° collagen levels decreased during interferon therapy. During the follow-up, in responders the Type IV° collagen did not show modifications, while in non-responders/relapsers it returned rapidly to the pretreatment levels (139.1 ± 100.7 ng/ml). Conclusion In HCV-positive chronic liver disease, prolyl-hydroxylase is not a good marker of hepatic fibrosis, while Type IV° collagen is a useful tool for evaluating fibrogenic activity. Interferon seems to be able to reduce the liver fibrosis even without the inhibition of viral replication and independently from liver necrosis.