title: Endothelial and leukocyte adhesion molecules in primary hypertriglyceridemia.
abstract: Hypertriglyceridemia is known to be associated to functional impairment of the endothelium and, consequently, to higher risk of atherosclerosis. Nevertheless, some crucial steps in the development of the atherosclerotic plaque are still unknown in primary hypertriglyceridemia. The aim of the present study was to explore the expression of soluble and leukocyte-associated cell adhesion molecules in a group of patients with primary hypertriglyceridemia, both including (n=50) and excluding (n=24) subjects with metabolic syndrome, in comparison with control normotriglyceridemic individuals (n=30). Lipid profile, CETP activity, HDL and VLDL chemical composition were evaluated. Soluble (VCAM-1, ICAM-1 and E-selectin) and leukocyte cell adhesion molecules (CD18, CD49d and CD54) were measured by enzyme-linked immunosorbent assay and flow cytometry, respectively. Patients with primary hypertriglyceridemia as compared with control subjects showed significantly higher VCAM-1 (15.6+/-4.5 ng/ml versus 13.9+/-3.8 ng/ml, respectively; p<0.05) and ICAM-1 (16.9+/-3.1 ng/ml versus 15.2+/-3.2 ng/ml, respectively; p<0.05). Regarding leukocyte cell adhesion molecules, significant increases were also detected in monocyte CD18 (398+/-180 versus 332+/-136 arbitrary units, respectively; p<0.05) and CD54 (49+/-14 versus 42+/-12 arbitrary units, respectively; p<0.05), and lymphocyte CD18 (122+/-53 versus 101+/-33 arbitrary units, respectively; p<0.05). ICAM-1 plasma levels, as well as monocyte CD18 and CD54, and lymphocyte CD18 persisted elevated even if patients with metabolic syndrome were discarded among those with hypertriglyceridemia. The increase in circulating and leukocyte cell adhesion molecules in primary hypertriglyceridemic patients would highlight the inflammatory process which is a key event in atherogenesis.
authors.affiliation: Laboratory of Lipids and Lipoprotein, Department of Clinical Biochemistry, Faculty of Pharmacy and Biochemistry, University of Buenos Aires, Junin 956, Buenos Aires 1113, Argentina.
authors.forename: María Belén
authors.initials: MB
authors.lastname: Benítez
authors.forename: Luis
authors.initials: L
authors.lastname: Cuniberti
authors.forename: María Cecilia
authors.initials: MC
authors.lastname: Fornari
authors.forename: Leonardo
authors.initials: L
authors.lastname: Gómez Rosso
authors.forename: Vanina
authors.initials: V
authors.lastname: Berardi
authors.forename: Gerardo
authors.initials: G
authors.lastname: Elikir
authors.forename: Pablo
authors.initials: P
authors.lastname: Stutzbach
authors.forename: Laura
authors.initials: L
authors.lastname: Schreier
authors.forename: Regina
authors.initials: R
authors.lastname: Wikinski
authors.forename: Fernando
authors.initials: F
authors.lastname: Brites
mesh_terms: D000328:Adult; D018821:CD18 Antigens / Q000378:metabolism*; D016022:Case-Control Studies; D006801:Humans; D015228:Hypertriglyceridemia / Q000097:blood* / Q000150:complications; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism*; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood* / Q000150:complications; D008875:Middle Aged; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism*
chemical_list: D018821:CD18 Antigens; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1