{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T16:13:18Z","timestamp":1791216798085,"version":"4.1.0"},"reference-count":29,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2011,10,10]],"date-time":"2011-10-10T00:00:00Z","timestamp":1318204800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Clin Investigation"],"published-print":{"date-parts":[[2012,5]]},"abstract":"<jats:sec><jats:label\/><jats:p>Eur J Clin Invest 2012; 42 (5): 510\u2013516<\/jats:p><\/jats:sec><jats:sec><jats:title>Abstract<\/jats:title><jats:p><jats:bold>Background\u2002<\/jats:bold> 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).<\/jats:p><jats:p><jats:bold>Materials and methods\u2002<\/jats:bold> 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\u2010selectin] and angiogenesis markers (vascular endothelial growth factor and its receptor sFlt\u20101), 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\u2010mediated dilatation of the brachial artery.<\/jats:p><jats:p><jats:bold>Results\u2002<\/jats:bold> von Willebrand factor and CECs (both <jats:italic>P<\/jats:italic>\u2003&lt;\u20030\u00b705) were significantly elevated in EA suggesting endothelial dysfunction and damage but were unrelated to classical laboratory markers of inflammation C\u2010reactive protein, erythrocyte sedimentation rate or IL6. No other biomarkers was elevated in EA. Microvascular and macrovascular abnormalities were confined to endothelium\u2010independent (smooth muscle cell) responses.<\/jats:p><jats:p><jats:bold>Conclusions\u2002<\/jats:bold> Endothelial damage\/dysfunction is present early in the course of inflammatory arthritis but is not directly related to inflammation markers.<\/jats:p><\/jats:sec>","DOI":"10.1111\/j.1365-2362.2011.02607.x","type":"journal-article","created":{"date-parts":[[2011,9,27]],"date-time":"2011-09-27T20:36:18Z","timestamp":1317155778000},"page":"510-516","source":"Crossref","is-referenced-by-count":29,"title":["An observational study of endothelial function in early arthritis"],"prefix":"10.1111","volume":"42","author":[{"given":"Will","family":"Foster","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gregory Y. 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