title: High antiphospholipid antibody levels are associated with statin use and may reflect chronic endothelial damage in non-autoimmune thrombosis: cross-sectional study.
abstract: OBJECTIVE
  Persistently elevated antiphospholipid antibodies and positive lupus anticoagulant (LAC) are associated with an increased risk of thrombosis. The objective of this study was to explore whether antiphospholipid antibody and/or LAC positivity were associated with the traditional risk factors for thrombosis or with medication use in patients without autoimmune diseases hospitalised with arterial or venous thrombosis.
  
  
  METHODS
  Cross-sectional study.
  
  
  METHODS
  Montefiore Medical Center, a large urban tertiary care centre.
  
  
  METHODS
  270 patients (93 with deep vein thrombosis (DVT) or pulmonary embolism (PE), and 177 with non-haemorrhagic stroke (cerebrovascular accident (CVA)) admitted between January 2006 and December 2010 with a discharge diagnosis of either DVT, PE or CVA, who had LAC and antiphospholipid antibodies measured within 6 months from their index admission. Patients with lupus or antiphospholipid syndrome were excluded.
  
  
  METHODS
  The main dependent variable was antiphospholipid antibodies of 40 units or greater (antiphospholipid antibody positivity) and/or LAC positivity. Independent variables were traditional thrombosis risk factors, statin use, aspirin use and warfarin use.
  
  
  RESULTS
  31 (11%) patients were LAC positive and/or antiphospholipid antibody positive. None of the traditional risk factors at the time of DVT/PE/CVA was associated with antiphospholipid antibody positivity. Current statin use was associated with an OR of 3.2 (95% CI 1.3 to 7.9, p=0.01) of antiphospholipid antibody positivity, adjusted for age, ethnicity and gender. Aspirin or warfarin use was not associated with antiphospholipid antibody levels.
  
  
  CONCLUSIONS
  If statin therapy reflects the history of previous hyperlipidaemia, high levels of antiphospholipid antibodies may be a marker for earlier endothelial damage caused by hyperlipidaemia.
authors.affiliation: Division of Rheumatology, Albert Einstein College of Medicine/Montefiore Medical Center, Bronx, New York, USA. abroder@montefiore.org
authors.forename: Anna
authors.initials: A
authors.lastname: Broder
authors.forename: Jonathan N
authors.initials: JN
authors.lastname: Tobin
authors.forename: Chaim
authors.initials: C
authors.lastname: Putterman
mesh_terms: D000368:Aged; D017152:Antibodies, Antiphospholipid / Q000097:blood*; D001241:Aspirin / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D002908:Chronic Disease; D003430:Cross-Sectional Studies; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000473:pathology; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000009:adverse effects*; D006949:Hyperlipidemias / Q000188:drug therapy; D016682:Lupus Coagulation Inhibitor / Q000097:blood*; D008297:Male; D008875:Middle Aged; D011655:Pulmonary Embolism / Q000097:blood* / Q000473:pathology; D012307:Risk Factors; D020521:Stroke / Q000097:blood / Q000473:pathology; D020246:Venous Thrombosis / Q000097:blood* / Q000473:pathology; D014859:Warfarin / Q000627:therapeutic use
chemical_list: D017152:Antibodies, Antiphospholipid; D015415:Biomarkers; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D016682:Lupus Coagulation Inhibitor; D014859:Warfarin; D001241:Aspirin