title: Thrombosis in systemic lupus erythematosus: congenital and acquired risk factors.
abstract: 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 (> or = 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: University Campus Bio-Medico, Rome, Italy. a.afeltra@unicampus.it
authors.forename: Antonella
authors.initials: A
authors.lastname: Afeltra
authors.forename: Marta
authors.initials: M
authors.lastname: Vadacca
authors.forename: Laura
authors.initials: L
authors.lastname: Conti
authors.forename: Sara
authors.initials: S
authors.lastname: Galluzzo
authors.forename: Anna P
authors.initials: AP
authors.lastname: Mitterhofer
authors.forename: Giovanni M
authors.initials: GM
authors.lastname: Ferri
authors.forename: Flavia
authors.initials: F
authors.lastname: Del Porto
authors.forename: Domenico
authors.initials: D
authors.lastname: Caccavo
authors.forename: Giuseppe M
authors.initials: GM
authors.lastname: Gandolfo
authors.forename: Antonio
authors.initials: A
authors.lastname: Amoroso
mesh_terms: D000293:Adolescent; D000328:Adult; D017153:Antibodies, Anticardiolipin / Q000097:blood; D000991:Antithrombins / Q000032:analysis; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D006710:Homocysteine / Q000097:blood; D006801:Humans; D016682:Lupus Coagulation Inhibitor / Q000097:blood; D008180:Lupus Erythematosus, Systemic / Q000150:complications* / Q000235:genetics; D008297:Male; D042965:Methylenetetrahydrofolate Reductase (NADPH2) / Q000235:genetics; D008875:Middle Aged; D009154:Mutation; D011486:Protein C / Q000032:analysis; D011516:Prothrombin / Q000235:genetics; D012307:Risk Factors; D013927:Thrombosis / Q000151:congenital / Q000209:etiology*
chemical_list: D017153:Antibodies, Anticardiolipin; D000991:Antithrombins; D005338:Fibrin Fibrinogen Degradation Products; D016682:Lupus Coagulation Inhibitor; D011486:Protein C; C036309:fibrin fragment D; D006710:Homocysteine; D011516:Prothrombin; D042965:Methylenetetrahydrofolate Reductase (NADPH2)