{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T16:15:32Z","timestamp":1762100132280,"version":"3.38.0"},"reference-count":47,"publisher":"SAGE Publications","issue":"9","license":[{"start":{"date-parts":[[2000,11,1]],"date-time":"2000-11-01T00:00:00Z","timestamp":973036800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Lupus"],"published-print":{"date-parts":[[2000,11]]},"abstract":"<jats:p> The pathogenesis of antiphospholipid antibody (aPL) related thrombosis is multifactorial and includes, amongst others, enhanced coagulation activation measured as prothrombin fragment 1 \/ 2 (F1 \/ 2), elevated plasma levels of von Willebrand factor (vWF), plasminogen activator inhibitor (PAI) and endothelin-l (ET-1) as well as heightened thromboxane generation and lipid peroxidation. To evaluate the antioxidant susceptibility of some of the above pathways, probucol (500 mg\/d orally, a cholesterol lowering agent bearing antioxidant properties) was administered for a three week period to 14 subjects with aPL and to seven healthy controls. At baseline aPL participants showed higher plasma levels of vWF (P \u2018 0.006), ET-1 (P \u2018 0.0002) and enhanced urinary excretion of 11-dehydro-thromboxane-B<jats:sub>2<\/jats:sub> (TXB<jats:sub>2<\/jats:sub>)(P \u2018 0.0004), F2-isoprostanes (marker of lipid peroxidation) (P \u2018 0.02) and albumin (P \u2018 0.04) than controls. In the aPL group baseline IgG anticardiolipin (aCL) titre positively related with urinary TXB<jats:sub>2<\/jats:sub> (r<jats:sup>2<\/jats:sup> \u2018 0.43, P \u2018 0.01) and inversely with urinary NO<jats:sub>x<\/jats:sub> (r<jats:sup>2<\/jats:sup> \u2018\u00ff0.6, P \u2018 0.005) whereas urinary NO<jats:sup>x<\/jats:sup> and TXB<jats:sup>2<\/jats:sup> were negatively correlated (r<jats:sup>2<\/jats:sup> \u2018\u00ff0.42, P \u2018 0.01). After the treatment period significant decreases from baseline values were noted for PAI (P \u2018 0.01), ET-1 (P \u2018 0.006), TXB<jats:sup>2<\/jats:sup> (P \u2018 0.02), F2-isoprostanes (P \u2018 0.01) and albuminuria (P \u2018 0.01) in aPL participants but not in controls. These pilot data support oxidative sensitive mechanisms and a potential role for antioxidant treatment in the pathogenesis of aPL induced vasculopathy. <\/jats:p>","DOI":"10.1191\/096120300677692516","type":"journal-article","created":{"date-parts":[[2003,11,12]],"date-time":"2003-11-12T12:45:16Z","timestamp":1068641116000},"page":"688-695","source":"Crossref","is-referenced-by-count":37,"title":["Antioxidant susceptibility of pathogenic pathways in subjects with                 antiphospholipid antibodies: a pilot study"],"prefix":"10.1177","volume":"9","author":[{"given":"P R J","family":"Ames","sequence":"first","affiliation":[{"name":"75 Canterbury House, Royal Street, London SE1 7EH, UK. 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