Lupus anticoagulant and increased thrombin generation in patients with systemic lupus erythematosus.

Ginsberg et all have reported that in patients with systemic lupus erythematosus (SLE) the presence of high circulating levels of anticardiolipin antibodies (ACA) is associated with an ongoing prothrombotic state. This was documented by finding significantly higher values of F 1+2, a marker of thrombin generation, in ACA (+) patients than in ACA (-) ones.’ We have data supporting the association between antiphospholipid antibodies (APLA) and an ongoing prothrombotic state. but we do not confirm that this is closely related to ACA positivity. We studied 45 patients (39 women, 6 men, ages 20 to 58 years) having SLE according to ARA criteria.2 Fifteen (33%) (12 women, 3 men, ages 21 to 58 years) had a history of thromboembolism: 7 venous thrombosis, 2 arterial thrombosis, 2 venous and arterial thrombosis, 3 recurrent fetal loss, and I recurrent fetal loss and venous thrombosis. All but 9 were under treatment with prednisone ( 5 to 25 mg/d) or methyl prednisolone (4 to 24 mg/d). Patients were not treated by anticoagulants in the month preceding the study. No patients had active infection, surgery, or trauma in the previous 3 months. Between 8 AM and 9 AM a blood sample was taken from each patient fasting from at least 12 hours to evaluate lupus anticoagulant (LA), ACA, and F 1 +2. LA was defined by the prolongation of at least two coagulation tests and by the positivity of confirmatory test with phosphatidylserine-phosphatidylcoline liposome^.^ ACA levels were measured by an enzyme-linked immunosorbent assay (ELISA) method, validated in an international workshop,“ with the upper limit of I O GPL (antiphospholipid IgG) U/mL, as being 3 SD above the mean of 40 healthy volunteers. Patients were considered LA(+) or ACA(+) if positivity persisted on two separate occasions at least 2 months apart. Plasma F I +2 levels were assayed by an ELBA method (ENZIGNOST F 1 +2; Behringwerke, Marburg, Germany); 30 healthy subjects matched for sex and age (25 women, 5 men, ages 23 to 56 years) were used as control (ref val 0.6 f 0.2 nmol/L, range 0.3 to 1.2 nmol/L). Statistical analysis was performed by Mann-Whitney U-test and Fisher exact test. Sixteen (35%) and 20 (44%) were LA(+) or ACA(+), respectively. Twelve (27%) were LA(+) and ACA(+). The disease activity, defined as previously d~scr ibed,~ was similar in LA(+) and LA(-), or ACA(+) and ACA(-) subgroups. The Odds ratio for the association