ObjectiveTo analyze the association of antiphospholipid antibodies (aPL) with the
development of clinical thrombotic manifestations and to characterize the efficacy
of anti-thrombotic therapies used.Methods272 systemic lupus erythematosus (SLE) patients
participated in the study. Patient files and a cumulative database were used to collect
patients' medical histories. Anti-cardiolipin (aCL), anti-beta2-glycoprotein I (abeta2GPI)
antibodies, and lupus anticoagulant (LAC) were measured according to international
recommendations. New thrombotic events were registered during follow-up.ResultsThe
patients were prospectively studied for 5 years, of whom 107 were aPL negative (aPL-
group). Criteria for antiphospholipid syndrome (APS) were fulfilled by 84 of 165 aPL-positive
patients (APS+ group) indicating that SLE patients with aPL have around 50% risk to
develop thrombotic complications. The aPL+ group (n = 81) consisted of aPL+ but APS-
patients. LAC was the most common aPL (n = 27, 32.1%) in patients with APS. The cumulative
presence of aPL further increased the prevalence of thrombotic events. During the
follow-up period, aPL developed in 8 of 107 patients (7.5%) from the aPL- group, of
whom 3 (2.8%) presented with thrombotic complications. Other types of aPL developed
in 7 of 165 (4.2%) aPL+ patients within 5 years. New thrombotic events occurred in
3.7% of aPL+ (n = 3) and 8.3% (n = 7) of the APS group. During follow-up, 52 of 81
aPL+ patients received primary prophylaxis, and 1 (1.9%) had transient ischemic attack
(TIA). In the non-treatment group, 2 (6.9%) had stroke. Seventy-nine of 84 of the
APS patients received secondary prophylaxis, and myocardial infarction occurred in
2 patients (on cumarine therapy maintaining an international normalized ratio around
2.5-3.0), and 5 suffered a stroke/TIA (1 on aspirin and 4 on aspirin + cumarine).ConclusionThe
findings emphasize the importance of determining both aCL and abeta2GPI antibodies
and LAC in SLE patients and the need for adequate anticoagulant therapy.
