Marked independent relationship between circulating interleukin-6 concentrations and endothelial activation in rheumatoid arthritis.
We examined the potential impact of conventional compared with nonconventional cardiovascular risk factors including interleukin-6 levels on endothelial activation in RA. Circulating soluble E-selectin, vascular cell adhesion molecule-1, intercellular adhesion molecule-1, and monocyte chemoattractant protein-1 concentrations were measured in 217 African patients (112 black and 105 white) with RA. In comprehensive confounder adjusted mixed regression models, 5 conventional and 4 nonconventional cardiovascular risk factors were associated (P = 0.05 to <0.0001) with endothelial activation. Interleukin-6 was the only risk factor related to each endothelial activation molecule and independently contributed by 18% and significantly more than other risk factors to the variation in overall endothelial activation as estimated by an SD (z) score of endothelial activation molecule concentrations. The independent interleukin-6-overall endothelial activation relationships were reproduced in various subgroups. Interleukin-6 concentrations relate consistently, markedly, and to a larger extent than other cardiovascular risk factors to endothelial activation in RA. Assessment of interleukin-6 concentrations may enhance cardiovascular risk stratification in RA.
Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, P.O. Box 1012 Johannesburg, Melville 2109, South Africa.
Patrick H
PH
Dessein
Department of Rheumatology, Charlotte Maxeke Johannesburg Academic Hospital, Faculty of Health Sciences, University of the Witwatersrand, South Africa.
Ahmed
A
Solomon
Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, P.O. Box 1012 Johannesburg, Melville 2109, South Africa.
Angela J
AJ
Woodiwiss
Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, P.O. Box 1012 Johannesburg, Melville 2109, South Africa.
Gavin R
GR
Norton
Milpark Hospital, Johannesburg, South Africa.
Linda
L
Tsang
Department of Rheumatology, Hospital Universitario Marques de Valdecilla, IFIMAV, Avenida de Valdecilla s/n, 39008 Santander, Spain.
Miguel A
MA
Gonzalez-Gay
D000328:Adult; D000368:Aged; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000150:complications*; D001799:Blood Sedimentation; D002318:Cardiovascular Diseases / Q000209:etiology; D018932:Chemokine CCL2 / Q000097:blood; D004730:Endothelium, Vascular / Q000502:physiology*; D066246:ErbB Receptors / Q000502:physiology; D005260:Female; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood*; D008297:Male; D008875:Middle Aged; D052243:Resistin / Q000097:blood; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
C111835:CCL2 protein, human; D018932:Chemokine CCL2; C508600:IL6 protein, human; D015850:Interleukin-6; C499624:RETN protein, human; D052243:Resistin; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D066246:ErbB Receptors