title: Antiphospholipid Antibodies and Recurrent Thrombotic Events: Persistence and Portfolio.
abstract: BACKGROUND
  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.
  
  
  METHODS
  A total of 1,770 subjects from the APASS-WARSS study underwent further aPL testing for antibodies to phosphatidylserine (aPS) and anti-β2-glycoprotein-I (anti-β2GPI) 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.
  
  
  RESULTS
  Persistent anti-β2GPI 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-β2GPI 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-β2GPI 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.
  
  
  CONCLUSIONS
  Rates of TOE/death were not influenced by aPL results at baseline or follow-up. Persistent anti-β2GPI 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.
authors.affiliation: Department of Neurology, Albany Medical Center, Albany, N.Y., USA.
authors.forename: Colum F
authors.initials: CF
authors.lastname: Amory
authors.forename: Steven R
authors.initials: SR
authors.lastname: Levine
authors.forename: Robin L
authors.initials: RL
authors.lastname: Brey
authors.forename: Mulugeta
authors.initials: M
authors.lastname: Gebregziabher
authors.forename: Stanley
authors.initials: S
authors.lastname: Tuhrim
authors.forename: Barbara C
authors.initials: BC
authors.lastname: Tilley
authors.forename: Ann-Catherin C
authors.initials: AC
authors.lastname: Simpson
authors.forename: Ralph L
authors.initials: RL
authors.lastname: Sacco
authors.forename: Jay P
authors.initials: JP
authors.lastname: Mohr
mesh_terms: D000368:Aged; D017152:Antibodies, Antiphospholipid / Q000097:blood*; D016736:Antiphospholipid Syndrome / Q000150:complications / Q000276:immunology; D001324:Autoantigens / Q000276:immunology; D002545:Brain Ischemia / Q000209:etiology; D015986:Confounding Factors, Epidemiologic; D004311:Double-Blind Method; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D053208:Kaplan-Meier Estimate; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000209:etiology; D010718:Phosphatidylserines / Q000276:immunology; D011655:Pulmonary Embolism / Q000209:etiology; D012008:Recurrence; D012307:Risk Factors; D019851:Thrombophilia / Q000097:blood / Q000453:epidemiology* / Q000276:immunology; D013927:Thrombosis / Q000209:etiology*; D053482:beta 2-Glycoprotein I / Q000276:immunology
chemical_list: D017152:Antibodies, Antiphospholipid; D001324:Autoantigens; D010718:Phosphatidylserines; D053482:beta 2-Glycoprotein I