Levels of soluble cell adhesion molecules in patients with dyslipidemia.
BACKGROUND
Increased expression of cell adhesion molecules (CAMs) on the vascular endothelium has been postulated to play an important role in atherogenesis. Both in vitro and in vivo studies have suggested that dyslipidemia may increase expression of CAMs.


RESULTS
To determine whether dyslipidemia is associated with increased expression of CAMs, we examined the levels of soluble intercellular adhesion molecule 1 (sICAM-1), soluble vascular cell adhesion molecule 1 (sVCAM-1), and soluble E-selectin (sE-selectin) in individuals with either hypercholesterolemia or hypertriglyceridemia and in control subjects matched for age and sex. Patients with hypertriglyceridemia had significantly higher levels of sVCAM-1 (739 +/- 69 ng/mL) compared with patients with hypercholesterolemia (552 +/- 63 ng/mL) and control subjects (480 +/- 56 ng/mL). Levels of sICAM-1 were significantly increased in both the hypercholesterolemic and hypertriglyceridemic groups (298 +/- 29 and 342 +/- 31 ng/mL, respectively) compared with the control group (198 +/- 14 ng/mL). Levels of sE-selectin were significantly increased in hypercholesterolemic patients (74 +/- 9 ng/mL) compared with control subjects (48 +/- 5 ng/mL). Ten hypercholesterolemic patients were treated aggressively with atorvastatin alone or a combination of colestipol and either atorvastatin or simvastatin for a mean of 42 weeks and had an average LDL cholesterol reduction of 51%. Comparison of soluble CAMs before and after treatment showed a significant reduction only in sE-selectin (77 +/- 11 versus 56 +/- 6 ng/mL, P < or = .03) but not for sVCAM-1 or sICAM-1.


CONCLUSIONS
Although severe hyperlipidemia is associated with increased levels of soluble CAMs, aggressive lipid-lowering treatment had only limited effects on the levels. Increased levels of soluble CAMs in patients with hyperlipidemia may be a marker for atherosclerosis.
Hackman
A
A
Department of Medicine, Baylor College of Medicine, Houston, Tex., USA.
Abe
Y
Y
Insull
W
W
Pownall
H
H
Smith
L
L
Dunn
K
K
Gotto
A M
AM
Ballantyne
C M
CM
D000924:Anticholesteremic Agents / Q000627:therapeutic use; D001161:Arteriosclerosis / Q000097:blood / Q000453:epidemiology; D000069059:Atorvastatin; D015815:Cell Adhesion Molecules / Q000097:blood*; D003084:Colestipol / Q000008:administration & dosage / Q000627:therapeutic use; D004359:Drug Therapy, Combination; D019040:E-Selectin / Q000097:blood; D004730:Endothelium, Vascular / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000627:therapeutic use; D005260:Female; D006538:Heptanoic Acids / Q000008:administration & dosage / Q000627:therapeutic use; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D006937:Hypercholesterolemia / Q000097:blood* / Q000188:drug therapy; D015228:Hypertriglyceridemia / Q000097:blood*; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D008148:Lovastatin / Q000008:administration & dosage / Q000031:analogs & derivatives / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D011758:Pyrroles / Q000008:administration & dosage / Q000627:therapeutic use; D012307:Risk Factors; D019821:Simvastatin; D012995:Solubility; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
D000924:Anticholesteremic Agents; D015815:Cell Adhesion Molecules; D019040:E-Selectin; D004791:Enzyme Inhibitors; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D000960:Hypolipidemic Agents; D011758:Pyrroles; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D008148:Lovastatin; D000069059:Atorvastatin; D019821:Simvastatin; D003084:Colestipol