title: Thrombotic events in systemic lupus erythematosus. Its association with acquired and inherited thrombophilic defects.
abstract: Systemic lupus erythematosus (SLE) is characterised by increased venous and arterial thrombotic risk. Although antiphospholipid antibodies (APAs) have been shown to be related with thrombotic tendency in these patients, in more than 40% of them, thrombosis occurs without the presence of such antibodies. We analysed the association of venous and arterial thrombotic events with acquired (anticardiolipin antibodies (ACAs) and lupus anticoagulant (LA)) and inherited (antithrombin (AT), protein C (PC), protein S (PS) deficiencies, factor V Leiden and the prothrombin G20210A mutation), thrombophilic risk factors in 86 SLE patients and 89 healthy controls. Patients showed a higher significant percentage of ACAs titres IgG>41 GPL u/ml and LA than controls (P=0.009; P<0.001, respectively), although no differences in AT, PC, PS deficiencies, factor V Leiden and prothrombin G20210A mutation was observed (P>0.05). When patients with and without thrombosis were compared, those with thrombosis showed a statistically higher percentage of ACAs IgG>41 GPL u/ml and LA (P=0.048; P=0.001, respectively), OR 4.33; 95% CI 1.01-18.50 and OR 11.57; 95% CI 3.28-40.75, respectively. When venous and arterial thrombotic events were considered separately, the presence of LA constituted a risk factor for arterial thrombosis (P=0.010), OR 11.33; 95% CI 1.86-68.89, as well as for venous thrombosis (P=0.005), OR 10.15; 95% CI 2.12-48.64, while ACAs IgG>41 GPL u/ml on their own, were not associated with arterial or venous thrombosis (P=0.142, P=0.233, respectively). In addition inherited thrombophilic risk factors AT, PC, PS deficiencies, factor V Leiden and PT G20210A mutation do not seem to increase thrombotic risk in SLE patients.
authors.affiliation: Hemorheology and Thrombosis Unit, Department of Clinical Pathology, La Fe University Hospital, and Department of Preventive Medicine, School of Medicine, University of Valencia, Valencia, Spain. vaya_amp@gva.es
authors.forename: Amparo
authors.initials: A
authors.lastname: Vayá
authors.forename: Marisa
authors.initials: M
authors.lastname: Santaolaria
authors.forename: Luisa
authors.initials: L
authors.lastname: Micó
authors.forename: Javier
authors.initials: J
authors.lastname: Calvo
authors.forename: Roberto
authors.initials: R
authors.lastname: Oropesa
authors.forename: Piedad
authors.initials: P
authors.lastname: Villa
authors.forename: Jose
authors.initials: J
authors.lastname: Todoli
authors.forename: María
authors.initials: M
authors.lastname: Simó
authors.forename: Dolores
authors.initials: D
authors.lastname: Corella
authors.forename: Jose M
authors.initials: JM
authors.lastname: Ricart
mesh_terms: D000328:Adult; D017153:Antibodies, Anticardiolipin / Q000097:blood*; D001798:Blood Proteins / Q000032:analysis / Q000235:genetics*; D005260:Female; D006801:Humans; D016682:Lupus Coagulation Inhibitor / Q000097:blood*; D008180:Lupus Erythematosus, Systemic / Q000097:blood* / Q000150:complications / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D009154:Mutation; D012307:Risk Factors; D013927:Thrombosis / Q000097:blood* / Q000209:etiology / Q000235:genetics*
chemical_list: D017153:Antibodies, Anticardiolipin; D001798:Blood Proteins; D016682:Lupus Coagulation Inhibitor