{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T18:52:05Z","timestamp":1791139925199,"version":"4.1.0"},"reference-count":59,"publisher":"Wiley","license":[{"start":{"date-parts":[[2014,1,1]],"date-time":"2014-01-01T00:00:00Z","timestamp":1388534400000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"funder":[{"name":"Ministry of Science and Higher Education, Warsaw, Poland","award":["N N402 267636"],"award-info":[{"award-number":["N N402 267636"]}]},{"name":"Ministry of Science and Higher Education, Warsaw, Poland","award":["2012\u20132017"],"award-info":[{"award-number":["2012\u20132017"]}]},{"DOI":"10.13039\/100009045","name":"Jagiellonian University Medical College","doi-asserted-by":"crossref","award":["N N402 267636"],"award-info":[{"award-number":["N N402 267636"]}],"id":[{"id":"10.13039\/100009045","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100009045","name":"Jagiellonian University Medical College","doi-asserted-by":"crossref","award":["2012\u20132017"],"award-info":[{"award-number":["2012\u20132017"]}],"id":[{"id":"10.13039\/100009045","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Leading National Research Centre (KNOW)","award":["N N402 267636"],"award-info":[{"award-number":["N N402 267636"]}]},{"name":"Leading National Research Centre (KNOW)","award":["2012\u20132017"],"award-info":[{"award-number":["2012\u20132017"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Mediators of Inflammation"],"published-print":{"date-parts":[[2014]]},"abstract":"<jats:p><jats:italic>Objectives<\/jats:italic>. To estimate endothelial dysfunction in patients with rheumatoid arthritis (RA) of short duration in relation to disease activity based on the assessment of 28 joints (DAS28).<jats:italic>Methods<\/jats:italic>. We studied 29 patients (22 women, mean age 41 (SD, 9) years) with RA of short duration and 29 healthy controls. The RA subjects were divided into those with low (DAS28: 2.6\u20135.1,<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M1\"><mml:mi>n<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn>18<\/mml:mn><\/mml:math>) or high (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M2\"><mml:mtext>D<\/mml:mtext><mml:mtext>A<\/mml:mtext><mml:mtext>S<\/mml:mtext><mml:mn>28<\/mml:mn><mml:mo>&gt;<\/mml:mo><mml:mn>5.1<\/mml:mn><\/mml:math>,<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M3\"><mml:mi>n<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn>11<\/mml:mn><\/mml:math>) disease activity. Exclusion criteria included clinically overt atherosclerosis and other coexistent diseases. Biochemical markers of inflammatory activation and endothelial dysfunction were measured.<jats:italic>Results<\/jats:italic>. There were no significant intergroup differences in the majority of classical cardiovascular risk factors. High-sensitivity C-reactive protein, tumor necrosis factor-<jats:italic>\u03b1<\/jats:italic>, and interleukin-6 were increased in RA subjects. Compared to the controls, levels of soluble vascular cell adhesion molecule-1, von Willebrand factor, and pentraxin-3 were significantly elevated in RA subjects with low disease activity, exhibiting no further significant rises in those with high disease activity. Asymmetric dimethyl-L-arginine, soluble E-selectin, monocyte chemotactic protein-1, and osteoprotegerin were increased only in RA patients with high disease activity.<jats:italic>Conclusions<\/jats:italic>. Our findings might suggest a dissociation of pathways governing generalized and joint-specific inflammatory reactions from those involved in endothelial activation and inflammation within the vascular wall.<\/jats:p>","DOI":"10.1155\/2014\/681635","type":"journal-article","created":{"date-parts":[[2014,3,3]],"date-time":"2014-03-03T16:01:38Z","timestamp":1393862498000},"page":"1-11","source":"Crossref","is-referenced-by-count":51,"title":["Differential Associations of Inflammatory and Endothelial Biomarkers with Disease Activity in Rheumatoid Arthritis of Short Duration"],"prefix":"10.1155","volume":"2014","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4582-3425","authenticated-orcid":true,"given":"Ewa","family":"Klimek","sequence":"first","affiliation":[{"name":"Department of Internal Medicine and Gerontology, Jagiellonian University Medical College\/University Hospital, ul. \u015aniadeckich 10, 31-531 Cracow, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5560-3632","authenticated-orcid":true,"given":"Anna","family":"Skalska","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine and Gerontology, Jagiellonian University Medical College\/University Hospital, ul. \u015aniadeckich 10, 31-531 Cracow, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Beata","family":"Kwa\u015bny-Krochin","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Balneology, Jagiellonian University Medical College\/University Hospital, ul. \u015aniadeckich 10, 31-531 Cracow, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrzej","family":"Surdacki","sequence":"additional","affiliation":[{"name":"2nd Department of Cardiology, Jagiellonian University Medical College\/University Hospital, ul. 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