{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T05:24:38Z","timestamp":1777440278946,"version":"3.51.4"},"reference-count":23,"publisher":"Portland Press Ltd.","issue":"2","content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2005,8,1]]},"abstract":"<jats:p>Men with AS (ankylosing spondylitis) are at elevated risk for CHD (coronary heart disease) but information on risk factors is sparse. We compared a range of conventional and novel risk factors in men with AS in comparison with healthy controls and, in particular, determined the influence of systemic inflammation. Twenty-seven men with confirmed AS and 19 controls matched for age were recruited. None of the men was taking lipid-lowering therapy. Risk factors inclusive of plasma lipids, IL-6 (interleukin-6), CRP (C-reactive protein), vWF (von Willebrand factor), fibrin D-dimer, ICAM-1 (intercellular cell-adhesion molecule-1) and fibrinogen were measured, and blood pressure and BMI (body mass index) were determined by standard techniques. A high proportion (70%) of men with AS were smokers compared with 37% of controls (P=0.024). The AS patients also had a higher BMI. In analyses adjusted for BMI and smoking, men with AS had significantly higher IL-6 and CRP (approx.\u00a09- and 6-fold elevated respectively; P&amp;lt;0.001), fibrinogen (P=0.013) and vWF (P=0.008). Total cholesterol and HDL-C (high-density lipoprotein cholesterol) were lower (P&amp;lt;0.05 and P=0.073 respectively) in AS and thus the ratio was not different. Pulse pressure was also significantly higher in AS (P=0.007). Notably, adjustment for IL-6 and CRP levels rendered all case-control risk factor differences, except pulse pressure, non-significant. In accordance with this finding, IL-6 correlated positively (r=0.74, P&amp;lt;0.001) with fibrinogen, but negatively (r=\u22120.46, P=0.016) with total cholesterol concentration. In conclusion, men with AS have perturbances in several CHD risk factors, which appear to be driven principally by systemic inflammatory mediators. Inflammation-driven atherogenesis potentially contributes to the excess CHD risk in AS.<\/jats:p>","DOI":"10.1042\/cs20040326","type":"journal-article","created":{"date-parts":[[2005,7,25]],"date-time":"2005-07-25T11:23:02Z","timestamp":1122290582000},"page":"171-176","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":108,"title":["Cardiovascular risk parameters in men with ankylosing spondylitis in comparison with non-inflammatory control subjects: relevance of systemic inflammation"],"prefix":"10.1042","volume":"109","author":[{"given":"Hiren","family":"Divecha","sequence":"first","affiliation":[{"name":"Centre for Rheumatic Diseases, Glasgow Royal Infirmary, Glasgow G31 2ER, Scotland, U.K."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Naveed","family":"Sattar","sequence":"additional","affiliation":[{"name":"University Department of Vascular Biochemistry, Glasgow Royal Infirmary, G31 2ER, Scotland, U.K."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ann","family":"Rumley","sequence":"additional","affiliation":[{"name":"University Department of Medicine, Glasgow Royal Infirmary, Glasgow G31 2ER, Scotland, U.K."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lynne","family":"Cherry","sequence":"additional","affiliation":[{"name":"University Department of Vascular Biochemistry, Glasgow Royal Infirmary, G31 2ER, Scotland, U.K."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gordon\u00a0D.\u00a0O.","family":"Lowe","sequence":"additional","affiliation":[{"name":"University Department of Medicine, Glasgow Royal Infirmary, Glasgow G31 2ER, Scotland, U.K."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Roger","family":"Sturrock","sequence":"additional","affiliation":[{"name":"Centre for Rheumatic Diseases, Glasgow Royal Infirmary, Glasgow G31 2ER, Scotland, U.K."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"288","published-online":{"date-parts":[[2005,7,25]]},"reference":[{"key":"2021120120421649200_B1","doi-asserted-by":"crossref","first-page":"2957","DOI":"10.1161\/01.CIR.0000099844.31524.05","article-title":"Explaining how \u2018high-grade\u2019 systemic inflammation accelerates vascular risk in rheumatoid arthritis","volume":"108","author":"Sattar","year":"2003","journal-title":"Circulation"},{"key":"2021120120421649200_B2","doi-asserted-by":"crossref","first-page":"862","DOI":"10.1002\/art.10089","article-title":"Accelerated atherogenesis: an extraarticular feature of rheumatoid arthritis","volume":"46","author":"Van\u00a0Doornum","year":"2002","journal-title":"Arthritis Rheum."},{"key":"2021120120421649200_B3","doi-asserted-by":"crossref","first-page":"640","DOI":"10.1093\/rheumatology\/40.6.640","article-title":"Cardiovascular risk factors, including thrombotic variables, in a population with rheumatoid arthritis","volume":"40","author":"McEntegart","year":"2001","journal-title":"Rheumatology"},{"key":"2021120120421649200_B4","doi-asserted-by":"crossref","first-page":"8","DOI":"10.1136\/ard.61.suppl_3.iii8","article-title":"Ankylosing spondylitis: an overview","volume":"61","author":"Sieper","year":"2002","journal-title":"Ann. 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