Endothelial dysfunction is present in established rheumatoid arthritis, but it is not clear at what stage of the disease this abnormality develops. We set out to determine whether endothelial damage/dysfunction is present in a group of patients with early arthritis (EA) (new onset inflammatory arthritis, EA).
Eighteen patients with EA, 48 healthy controls and 25 disease controls were recruited. Plasma was obtained for endothelial [von Willebrand factor (vWF) and soluble E-selectin] and angiogenesis markers (vascular endothelial growth factor and its receptor sFlt-1), adhesion molecules (intercellular adhesion molecule 1 and vascular cell adhesion molecule 1) and circulating endothelial cells (CECs, as a marker of endothelial damage). Microvascular endothelial function was assessed using laser Doppler perfusion imaging and macrovascular function using flow-mediated dilatation of the brachial artery.
von Willebrand factor and CECs (both P < 0.05) were significantly elevated in EA suggesting endothelial dysfunction and damage but were unrelated to classical laboratory markers of inflammation C-reactive protein, erythrocyte sedimentation rate or IL6. No other biomarkers was elevated in EA. Microvascular and macrovascular abnormalities were confined to endothelium-independent (smooth muscle cell) responses.
Endothelial damage/dysfunction is present early in the course of inflammatory arthritis but is not directly related to inflammation markers.