{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,23]],"date-time":"2026-08-23T18:00:58Z","timestamp":1787508058056,"version":"build-2736575974"},"reference-count":0,"publisher":"S. Karger AG","issue":"5-6","license":[{"start":{"date-parts":[[2015,1,1]],"date-time":"2015-01-01T00:00:00Z","timestamp":1420070400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2015,1,1]],"date-time":"2015-01-01T00:00:00Z","timestamp":1420070400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cerebrovasc Dis"],"published-print":{"date-parts":[[2015]]},"abstract":"<b><i>Background:<\/i><\/b> There are very limited prospective data on the significance of persistent antiphospholipid antibodies (aPL) and recurrent thrombo-occlusive events (TOEs). We investigated the prognostic value of (1) 2 newer aPL assays, (2) an aPL portfolio and (3) persistent aPL positivity following stroke. <b><i>Methods:<\/i><\/b> A total of 1,770 subjects from the APASS-WARSS study underwent further aPL testing for antibodies to phosphatidylserine (aPS) and anti-\u03b2<sub>2<\/sub>-glycoprotein-I (anti-\u03b2<sub>2<\/sub>GPI) from stored sera. Follow-up aPL status was also tested in a subset of subjects. Primary analysis was based on time to any TOE (ischemic stroke, myocardial infarction, transient ischemic attack, deep vein thrombosis, pulmonary embolism or systemic arterial occlusion)\/death at 2 years. Cox proportional hazard analyses assessed whether aPL independently related to outcome. <b><i>Results:<\/i><\/b> Persistent anti-\u03b2<sub>2<\/sub>GPI decreased the time to TOE\/death after adjustment for potential confounders (hazards ratio (HR) 2.86, 95% CI 1.21-6.76, p = 0.017). When persistent anti-\u03b2<sub>2<\/sub>GPI was combined with another persistently positive aPL, time to TOE\/death was also reduced (HR 3.79, 95% CI 1.18-12.14, p = 0.025). Neither persistent anticardiolipin antibodies nor persistent aPS alone nor a single positive anti-\u03b2<sub>2<\/sub>GPI nor aPS was associated with decreased time to TOE\/death. No single positive aPL, portfolio of baseline aPL or any persistent aPL increased the rate of TOE\/death. <b><i>Conclusions:<\/i><\/b> Rates of TOE\/death were not influenced by aPL results at baseline or follow-up. Persistent anti-\u03b2<sub>2<\/sub>GPI alone, and with persistent second aPL, was independently associated with decreased time to TOE\/death. Persistent aPL, an aPL portfolio and newer aPL in ischemic stroke patients are not helpful in predicting an increased rate of recurrent TOEs.<\/jats:p>","DOI":"10.1159\/000441362","type":"journal-article","created":{"date-parts":[[2015,10,29]],"date-time":"2015-10-29T18:01:24Z","timestamp":1446141684000},"page":"293-300","source":"Crossref","is-referenced-by-count":28,"title":["Antiphospholipid Antibodies and Recurrent Thrombotic Events: Persistence and Portfolio"],"prefix":"10.1159","volume":"40","author":[{"given":"Colum F.","family":"Amory","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7451-7534","authenticated-orcid":false,"given":"Steven R.","family":"Levine","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robin L.","family":"Brey","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mulugeta","family":"Gebregziabher","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stanley","family":"Tuhrim","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Barbara C.","family":"Tilley","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ann-Catherin C.","family":"Simpson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ralph L.","family":"Sacco","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jay P.","family":"Mohr","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"name":"for the APASS-WARSS Collaborators","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"127","published-online":{"date-parts":[[2015,10,29]]},"container-title":["Cerebrovascular Diseases"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/441362","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/441362","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/441362","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,23]],"date-time":"2025-04-23T13:59:45Z","timestamp":1745416785000},"score":1,"resource":{"primary":{"URL":"https:\/\/karger.com\/article\/doi\/10.1159\/000441362"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2015]]},"references-count":0,"journal-issue":{"issue":"5-6","published-online":{"date-parts":[[2015,11,1]]},"published-print":{"date-parts":[[2015,11,26]]}},"URL":"https:\/\/doi.org\/10.1159\/000441362","archive":["Portico"],"relation":{},"ISSN":["1015-9770","1421-9786"],"issn-type":[{"value":"1015-9770","type":"print"},{"value":"1421-9786","type":"electronic"}],"subject":[],"published":{"date-parts":[[2015]]}}}