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 molecule-1 (sICAM-1) and vascular cell adhesion molecule-1 (sVCAM-1) in 52 patients with chronic hepatitis C on entry, prior to finalizing a 6-month course of interferon-alpha 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-lb 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.
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 molecule-1 (sICAM-1) and vascular cell adhesion molecule-1 (sVCAM-1) in 52 patients with chronic hepatitis C on entry, prior to finalizing a 6-month course of interferon-alpha 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-lb 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.
Authors: G Montalto; L Giannitrapani; M Soresi; L Virruso; D D Martino; R Gambino; A Carroccio; M Cervello Journal: Inflammation Date: 2001-04 Impact factor: 4.092