Antiphospholipid antibodies and thrombosis: association with acquired activated protein C resistance in venous thrombosis and with hyperhomocysteinemia in arterial thrombosis.
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-beta(2)-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.
Kassis
Jeannine
J
Department of Hematology, Hôpital Maisonneuve-Rosemont, Université de Montréal, Montreal, Quebec, Canada.
Neville
Carolyn
C
Rauch
Joyce
J
Busque
Lambert
L
Chang
Erika R
ER
Joseph
Lawrence
L
Le Comte
Martine
M
Subang
Rebecca
R
Fortin
Paul R
PR
D020016:Activated Protein C Resistance / Q000097:blood / Q000276:immunology*; D000328:Adult; D017153:Antibodies, Anticardiolipin / Q000097:blood / Q000276:immunology; D017152:Antibodies, Antiphospholipid / Q000276:immunology*; D016736:Antiphospholipid Syndrome / Q000276:immunology; D001772:Blood Cell Count; D002341:Carotid Artery Thrombosis / Q000097:blood; D015331:Cohort Studies; D005165:Factor V / Q000235:genetics; D005260:Female; D006023:Glycoproteins / Q000097:blood; D006801:Humans; D020138:Hyperhomocysteinemia / Q000097:blood / Q000276:immunology*; D016015:Logistic Models; D016682:Lupus Coagulation Inhibitor / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009154:Mutation; D016017:Odds Ratio; D010641:Phenotype; D012044:Regression Analysis; D012307:Risk Factors; D019851:Thrombophilia / Q000276:immunology; D013927:Thrombosis / Q000097:blood / Q000276:immunology*; D020246:Venous Thrombosis / Q000097:blood / Q000276:immunology*; D053482:beta 2-Glycoprotein I
D017153:Antibodies, Anticardiolipin; D017152:Antibodies, Antiphospholipid; D006023:Glycoproteins; D016682:Lupus Coagulation Inhibitor; D053482:beta 2-Glycoprotein I; C095381:factor V Leiden; D005165:Factor V