Clinical thrombotic manifestations in SLE patients with and without antiphospholipid antibodies: a 5-year follow-up.
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 (abeta2GPI) 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).


CONCLUSIONS
The findings emphasize the importance of determining both aCL and abeta2GPI antibodies and LAC in SLE patients and the need for adequate anticoagulant therapy.
Tarr
Tunde
T
Third Department of Internal Medicine, Medical and Health Science Centre, University of Debrecen, Debrecen, Hungary.
Lakos
Gabriella
G
Bhattoa
Harjit Pal
HP
Soltesz
Pal
P
Shoenfeld
Yehuda
Y
Szegedi
Gyula
G
Kiss
Emese
E
D000328:Adult; D017152:Antibodies, Antiphospholipid / Q000276:immunology*; D000918:Antibody Specificity; D000925:Anticoagulants / Q000627:therapeutic use*; D016736:Antiphospholipid Syndrome / Q000150:complications / Q000276:immunology; D001241:Aspirin / Q000627:therapeutic use; D015331:Cohort Studies; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000150:complications / Q000276:immunology; D008297:Male; D008875:Middle Aged; D013927:Thrombosis / Q000209:etiology / Q000276:immunology / Q000517:prevention & control; D013997:Time Factors
D017152:Antibodies, Antiphospholipid; D000925:Anticoagulants; D001241:Aspirin