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Clinical Thrombotic Manifestations in SLE Patients With and Without Antiphospholipid Antibodies: A 5-year Follow-up

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Abstract

Objective

To analyze the association of antiphospholipid antibodies (aPL) with the development of clinical thrombotic manifestations and to characterize the efficacy of anti-thrombotic therapies used.

Methods

272 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 (aβ2GPI) antibodies, and lupus anticoagulant (LAC) were measured according to international recommendations. New thrombotic events were registered during follow-up.

Results

The 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).

Conclusion

The findings emphasize the importance of determining both aCL and aβ2GPI antibodies and LAC in SLE patients and the need for adequate anticoagulant therapy.

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Correspondence to Emese Kiss.

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Tarr, T., Lakos, G., Bhattoa, H.P. et al. Clinical Thrombotic Manifestations in SLE Patients With and Without Antiphospholipid Antibodies: A 5-year Follow-up. Clinic Rev Allerg Immunol 32, 131–137 (2007). https://doi.org/10.1007/s12016-007-0009-8

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