title: Soluble intercellular cell adhesion molecule-1 and vascular cell adhesion molecule-1 in asymptomatic dyslipidemic subjects.
abstract: OBJECTIVE
  The plasma levels of soluble intercellular cell adhesion molecule-1 (s-ICAM-1) and soluble vascular cell adhesion molecule-1 (s-VCAM-1) were assessed in clinically asymptomatic subjects to compare them between normolipidemic and various dyslipidemic phenotypes. The associations between soluble cell adhesion molecules (s-CAMs) and risk factors for atherosclerosis, markers of insulin resistance, and the intima-media thickness of the common carotid artery (IMT) were evaluated, too.
  
  
  METHODS
  Thwo hundred and thirty-four asymptomatic subjects were divided into four dyslipidemic phenotypes (DLP) according to apolipoprotein B (apoB) and triglycerides (TG): DLP1 (N.=58, apoB<1.2 g/L and TG<1.5 mmol/L), DLP2 (N.=47, apoB<1.2 g/L and TG≥1.5 mmol/L), DLP3 (N.=31, apoB≥1.2 g/L and TG<1.5 mmol/L) and DLP4 (N.=98, apoB≥1.2 g/L and TG≥1.5 mmol/L). DLP1 (normo-apoB /normo-TG) served as a control group.
  
  
  RESULTS
  A significant difference in s-ICAM-1 between DLP1 (502.0 [457.1-568.2] ng/mL) and DLP4 (567.9 [502.8-692.1] ng/mL, P<0.001) was found. No significant differences in s-VCAM-1 between DLPs were apparent. S-ICAM-1 was independently predicted by HDL-cholesterol, non-HDL-cholesterol, proinsulin, C-peptide, waist, systolic and diastolic blood pressure. S-VCAM-1 was predicted only by age and systolic blood pressure. Both s-CAMs were detected as independent predictors for IMT, which was significantly increased in DLP 4.
  
  
  CONCLUSIONS
  The elevation of s-ICAM-1 was presented only in patients with simultaneously elevated TG and apoB (DLP4) in comparison with normolipidemic subjects. Patients with DLP 4 had significantly increased IMT, which was independently predicted by levels of s-ICAM-1 and of s-VCAM-1. These findings pointed out DLP4 subjects as individuals with the highest risk for early manifestation of atherosclerosis.
authors.affiliation: 3rd Department of Internal Medicine, University Hospital, Olomouc, Czech Republic. david.karasek@fnol.cz
authors.forename: D
authors.initials: D
authors.lastname: Karasek
authors.forename: H
authors.initials: H
authors.lastname: Vaverkova
authors.forename: Z
authors.initials: Z
authors.lastname: Frysak
authors.forename: M
authors.initials: M
authors.lastname: Halenka
authors.forename: D
authors.initials: D
authors.lastname: Jackuliakova
authors.forename: D
authors.initials: D
authors.lastname: Novotny
authors.forename: J
authors.initials: J
authors.lastname: Lukes
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D001055:Apolipoproteins B / Q000097:blood; D058070:Asymptomatic Diseases; D015415:Biomarkers / Q000097:blood; D002339:Carotid Arteries / Q000000981:diagnostic imaging; D002340:Carotid Artery Diseases / Q000097:blood / Q000000981:diagnostic imaging / Q000209:etiology*; D002784:Cholesterol / Q000097:blood; D018153:Czech Republic; D005260:Female; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood* / Q000150:complications / Q000175:diagnosis; D007124:Immunoenzyme Techniques; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood*; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D012044:Regression Analysis; D018570:Risk Assessment; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood; D014463:Ultrasonography; D015854:Up-Regulation; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood*
chemical_list: D001055:Apolipoproteins B; D015415:Biomarkers; D014280:Triglycerides; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D002784:Cholesterol