Abstract
Cell adhesion molecules (intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1)) and hyaluronic acid, markers of inflammation and fibrosis were monitored in hepatitis C patients to determine whether changes in plasma levels, during antiviral treatment, can predict long-term response to therapy. In 55 patients with chronic hepatitis C virus (HCV), 33 treated with interferon (IFN) and 22 treated with IFN + ribavirin, sera was collected prior to treatment, at 3 + 6 months of therapy and 6 months post-treatment. Levels of ICAM-1, VCAM-1 and hyaluronic acid were correlated with alanine aminotransferase levels, HCV-RNA-polymerase chain reaction status and histological fibrosis scoring. A decrease in ICAM-1 levels at 3 and 6 months of therapy, compared with pretreatment levels, was observed in responders to IFN + ribavirin therapy but this decrease in ICAM-1 levels was not evident following cessation of treatment. Hyaluronic acid levels, in both treatment groups, did not differ significantly between responders and non-responders. Hyaluronic acid levels did correlate, significantly, with degree of fibrosis whereas VCAM-1 levels were marginally increased only in patients with moderate (grade III) fibrosis. Monitoring of VCAM-1 and hyaluronic acid, during antiviral therapy, does not differentiate between responders and non-responders. A decrease in ICAM-1 levels during IFN + ribavirin treatment is associated with response to therapy, and its efficacy in predicting long-term response should be further substantiated.
Highlights
Leukocyte adhesion molecules, among them intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), play an integral role in infiltration, activation and binding of effector cells to tissues
ICAM-1 expression on biliary epithelium occurs in both primary sclerosing cholangitis (PSC) and primary biliary cirrhosis (PBC), and while it is less frequently observed in PBC patients, in PSC its occurrence correlates with advanced stages of the disease.[2]
ICAM-1, VCAM-1 & hyaluronic acid during HCV therapy transfusion, previous surgery, jaundice, family history of chronic liver disease (CLD) and hepatocellular carcinoma were recorded with similar frequency in both groups
Summary
Among them intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), play an integral role in infiltration, activation and binding of effector cells to tissues. During inflammation, activated vascular endothelial cells and other cell types express various adhesion molecules that facilitate binding of circulating leukocytes. Serum concentrations of these circulating adhesion molecules are thought to reflect the degree of this activation. These adhesion molecules play a major role in mediating tissue damage during allograft rejection.[1,2,3,4] In the liver of healthy controls, there is low basal expression of ICAM-1 on endothelial cells (liver sinusoidal cells) and low basal expression of VCAM-1 on both sinusoidal and Kupffer cells. In patients with chronic hepatitis C, serum ICAM-1 levels are believed to correlate with degree of active inflammation, whereas VCAM-1 levels reflect degree of fibrosis.[5]
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