Serum intercellular adhesion molecule-1 in alcoholic liver disease and its relationship with histological disease severity

Background: Infiltration of the liver by leukocytes is a histological feature of alcoholic liver disease. Intercellular adhesion molecule-1 (ICAM-1) mediates the migration of lymphocytes from the circulation to target sites of inflammation. It has been demonstrated in the liver of alcoholic liver disease subjects and as a circulating soluble form (sICAM-1). The origin of sICAM-1 and its relationship to disease severity is unknown, although it has been postulated that it may arise from activated T lymphocytes and is an inflammatory marker. Aims: The aim of the study was to determine the relationship of sICAM-1 to clinical and histological severity of alcoholic liver disease and to serum T-cell (soluble interleukin-2 receptor (sIL-2R), beta(2)-microglobulin) and monocyte (neopterin) immune activation markers. Methods: Serum from 48 outpatients with biopsy proven alcoholic liver disease (steatosis=9, cirrhosis=28, hepatitis+/-cirrhosis = 11), 31 with primary biliary cirrhosis and 27 normals was assayed for sICAM-1, sIL-2R, beta(2)-microglobulin, and neopterin. Results: sICAM-1 was significantly elevated, p=0.0001, in alcoholic liver disease and primary biliary cirrhosis patients compared to normals, Circulating sIL-2R (p=0.0001) and beta(2)-microgloblin (p=0.0034) were significantly elevated in alcoholic liver disease compared to controls, There was a highly significant correlation between levels of sICAM-1 and histological grade of disease, Rs=0.80 (p=0.0001), but no significant correlation with clinical correlates of disease severity or circulating immune activation markers. Conclusions: sICAM-1 is elevated in alcoholic liver disease, is a marker of histological severity of disease and does not appear to originate from activated T lymphocytes. Measurements of sICAM-1 may be useful in assessing histological severity of alcoholic liver disease.