Thrombosis in systemic lupus erythematosus: Congenital and acquired risk factors

• Published in: Arthritis and rheumatism 2005-06, Vol.53 (3), p.452-459
• Main Authors: Afeltra, Antonella, Vadacca, Marta, Conti, Laura, Galluzzo, Sara, Mitterhofer, Anna P., Ferri, Giovanni M., Del Porto, Flavia, Caccavo, Domenico, Gandolfo, Giuseppe M., Amoroso, Antonio
• Format: Article
• Language: English
• Subjects: Adolescent; Adult; Antibodies, Anticardiolipin - blood; Antithrombins - analysis; Female; Fibrin Fibrinogen Degradation Products - analysis; Homocysteine - blood; Humans; Lupus Coagulation Inhibitor - blood; Lupus Erythematosus, Systemic - complications; Lupus Erythematosus, Systemic - genetics; Male; Methylenetetrahydrofolate Reductase (NADPH2) - genetics; Middle Aged; Mutation; Protein C - analysis; Prothrombin - genetics; Risk Factors; Systemic lupus erythematosus; Thrombosis; Thrombosis - congenital; Thrombosis - etiology
• ISSN: 0004-3591; 1529-0131
• DOI: 10.1002/art.21172

Objective To investigate the thrombotic tendency in patients with systemic lupus erythematosus (SLE) by evaluating congenital or acquired abnormalities associated with an increased risk of venous and/or arterial thrombosis. Methods A total of 57 patients with SLE were included in the study. Twenty‐one patients (37%) had a history of arterial and/or venous thrombosis and 36 patients (63%) did not have such a history. Sera from 50 healthy controls were examined. Protein C, protein S, antithrombin, D‐dimer, fibrinogen, homocysteine, anticardiolipin antibodies (aCL), lupus anticoagulant (LAC), prothrombin G20210A, and methylenetetrahydrofolate reductase (MTHFR) C677T gene mutation were evaluated. Results Protein C, antithrombin, fibrinogen, D‐dimer, and homocysteine levels were significantly higher in patients with SLE than in controls. A prothrombin mutation was observed in 2 (4%) of 50 controls and in 6 (11%) of 57 patients. A significantly higher prevalence (P = 0.036) of MTHFR homozygous mutation was observed in patients with SLE (14 [25%] of 57) in comparison with controls (4 [8%] of 50). IgG‐aCL and IgM‐aCL levels were significantly higher in patients with SLE than in controls (P < 0.0001). The presence of medium‐high (≥20 IgG phospholipid units/ml) IgG‐aCL antibody titers was significantly higher (P = 0.005) in patients with thrombosis (11 [52%] of 21) than in patients without (5 [14%] of 36) thrombosis. LAC was present in 22 (38.5%) of 57 patients and in none of 50 controls. Conclusion In this study, we confirm the association between thrombosis and IgG‐aCL at medium‐high titers and suggest that the coexistence of other risk factors can affect the expression of thrombosis in patients with SLE.