SERUM INTERCELLULAR-ADHESION MOLECULE-1 IN ALCOHOLIC LIVER-DISEASE AND ITS RELATIONSHIP WITH HISTOLOGICAL DISEASE SEVERITY

Citation
Ac. Douds et al., SERUM INTERCELLULAR-ADHESION MOLECULE-1 IN ALCOHOLIC LIVER-DISEASE AND ITS RELATIONSHIP WITH HISTOLOGICAL DISEASE SEVERITY, Journal of hepatology, 26(2), 1997, pp. 280-286
Citations number
22
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
0168-8278
Volume
26
Issue
2
Year of publication
1997
Pages
280 - 286
Database
ISI
SICI code
0168-8278(1997)26:2<280:SIMIAL>2.0.ZU;2-I
Abstract
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 o f alcoholic liver disease subjects and as a circulating soluble form ( sICAM-1). The origin of sICAM-1 and its relationship to disease severi ty is unknown, although it has been postulated that it may arise from activated T lymphocytes and is an inflammatory marker. Aims: The aim o f the study was to determine the relationship of sICAM-1 to clinical a nd histological severity of alcoholic liver disease and to serum T-cel l (soluble interleukin-2 receptor (sIL-2R), beta(2)-microglobulin) and monocyte (neopterin) immune activation markers. Methods: Serum from 4 8 outpatients with biopsy proven alcoholic liver disease (steatosis=9, cirrhosis=28, hepatitis+/-cirrhosis = 11), 31 with primary biliary ci rrhosis and 27 normals was assayed for sICAM-1, sIL-2R, beta(2)-microg lobulin, and neopterin. Results: sICAM-1 was significantly elevated, p =0.0001, in alcoholic liver disease and primary biliary cirrhosis pati ents compared to normals, Circulating sIL-2R (p=0.0001) and beta(2)-mi crogloblin (p=0.0034) were significantly elevated in alcoholic liver d isease compared to controls, There was a highly significant correlatio n between levels of sICAM-1 and histological grade of disease, Rs=0.80 (p=0.0001), but no significant correlation with clinical correlates o f disease severity or circulating immune activation markers. Conclusio ns: sICAM-1 is elevated in alcoholic liver disease, is a marker of his tological severity of disease and does not appear to originate from ac tivated T lymphocytes. Measurements of sICAM-1 may be useful in assess ing histological severity of alcoholic liver disease.