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

Background: In chronic hepatitis C the relation of circulating adhesion mol ecules to disease features before, during and after therapy has not been co mpletely established. Aim: To analyse the basal levels of circulating adhesins and the changes in duced by interferon in these patients. Methods: We studied, using ELISA assays, the serum levels of soluble interc ellular adhesion molecule-1 (sICAM-1) and vascular cell adhesion molecule-1 (sVCAM-1) in 52 patients with chronic hepatitis C on entry, prior to final izing a 6-month course of interferon-alpha therapy and at the end of the fo llow-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 se rum 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 c ut-off threshold of 1300 ng/mL. Levels of both adhesins did not correlate w ith viraemia and were comparable among Ib and non-lb genotypes. Sustained r esponse 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 necroinf lammation while sVCAM-1 reflected fibrosis. Both low sVCAM-1 and pIIIP seru m concentrations were strictly linked, suggesting that measuring sVCAM-1 co uld give information on the degree of liver fibroplasia.