Soluble adhesion molecules correlate with liver inflammation and fibrosis in chronic hepatitis C treated with interferon-α

Abstract

Background: In chronic hepatitis C the relation of circulating adhesion molecules to disease features before, during and after therapy has not been completely established. Aim: To analyse the basal levels of circulating adhesins and the changes induced by interferon in these patients. Methods: We studied, using ELISA assays, the serum levels of soluble intercellular adhesion (sICAM-1) and vascular cell adhesion (sVCAM-1) in 52 patients with chronic hepatitis C on entry, prior to finalizing a 6-month course of interferon-α therapy and at the end of the follow-up. Correlations with clinical, virological and histological features, including inflammation and fibrosis, were calculated by Pearson's r-test. Results: Liver necroinflammation was more closely related to sICAM-1 (r = 0.54, P = 0.0000) than to sVCAM-1 (r = 0.32, P = 0.02). Fibrosis, both as serum pIIIP and histological scoring, was, however, clearly related to sVCAM-1 (1071 ± 291 in patients who scored 0-2 vs. 1870 ± 458 in patients who scored 3-4; P = 0.0000). Severe fibrosis was never found below a sVCAM-1 cut-off threshold of 1300 ng/mL. Levels of both adhesins did not correlate with viraemia and were comparable among 1b and non-1b genotypes. Sustained response to interferon was significantly related to low viraemia (P = 0.03), non-1b type (P = 0.04) and low sICAM-1 (P = 0.04), but not to sVCAM-1. On finalizing therapy, patients with normal transaminases had reduced sICAM-1 (P = 0.0005), but not sVCAM-1 levels. Conclusions: In chronic hepatitis C, sICAM-1 was a marker of liver necroinflammation while sVCAM-1 reflected fibrosis. Both low sVCAM-1 and pIIIP serum concentrations were strictly linked, suggesting that measuring sVCAM-1 could give information on the degree of liver fibroplasia.