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Thromb Haemost. Author manuscript; available in PMC Oct 26, 2012.
Published in final edited form as:
PMCID: PMC3482245
Antiphospholipid antibodies and thrombosis: association with acquired activated protein C resistance in venous thrombosis and with hyperhomocysteinemia in arterial thrombosis
Jeannine Kassis,1 Carolyn Neville,2 Joyce Rauch,3 Lambert Busque,1 Erika R. Chang,4 Lawrence Joseph,2,5 Martine Le Comte,2 Rebecca Subang,3 and Paul R. Fortin4,6
1Department of Hematology, Hôpital Maisonneuve-Rosemont, Université de Montréal, Montreal, Quebec, Canada
2Division of Clinical Epidemiology, The Montreal General Hospital, McGill University Health Centre, Montreal, Quebec, Canada
3Division of Rheumatology, The Research Institute of the McGill University Health Centre, Montreal, Quebec, Canada
4Division of Outcomes and Population Health, University Health Network, University of Toronto, Toronto, Ontario, Canada
5Department of Epidemiology and Biostatistics, McGill University, Montreal, Quebec, Canada
6Division of Rheumatology, University Health Network, University of Toronto, Toronto, Ontario, Canada
Correspondence to: Paul R. Fortin MD, MPH, FRCP(C), Director of Clinical Research, Arthritis Centre of Excellence, Toronto Western Hospital, Room ECW 5-044, 399 Bathurst Street, Toronto, Ontario, Canada M5T 2S8, Tel.: + 416 603-5664, Fax: + 416 603-6288, paul.fortin/at/
Although antiphospholipid antibodies (aPL) are associated with thrombosis, it is not known who with aPL is at higher risk for thrombosis. It was the aim of this cross-sectional study to investigate how thrombophilic factors contribute to venous or arterial thrombosis in aPL-positive individuals. In outpatient test centres at two tertiary care hospitals, two hundred and eight (208) persons requiring aPL testing were matched by age, gender and centre to 208 persons requiring a complete blood count. Persons were classified as aPL-positive (having anticardiolipin, lupus anticoagulant and/or anti-β2-glycoprotein I antibodies) or aPL-negative. Several thrombophilic factors were studied using logistic regression modelling. Results showed that the aPL-positive group had three-fold more events (37%) than the aPL-negative group (12%). In unadjusted analyses, clinically important associations were observed between factor V Leiden and venous thrombosis, hyperhomocysteinemia and arterial thrombosis, and activated protein C resistance (APCR) and venous thrombosis (OR, 95% CI = 4.00, 1.35–11.91; 4.79, 2.03–11.33; and 2.03, 1.03–3.97, respectively). After adjusting for recruitment group, persons with both APCR and aPL had a three-fold greater risk (OR, 95% CI = 3.31, 1.30–8.41) for venous thrombosis than those with neither APCR nor aPL. Similarly, after adjusting for hypertension, family history of cardiovascular disease, gender and recruitment group, persons with both hyperhomocysteinemia and aPL had a five-fold increased risk (OR, 95% CI = 4.90, 1.37–17.37) for arterial thrombosis compared to those with neither risk factor. In conclusion, APCR phenotype and hyperhomocysteinemia are associated with a higher risk of venous and arterial thrombosis, respectively, in the presence of aPL.
Keywords: Antiphospholipid antibodies, antiphospholipid syndrome, thrombosis, activated protein C resistance, hyperhomocysteinemia