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Published on: May 23, 2025
Recurrent thrombosis in antiphospholipid syndrome may be associated with cardiovascular risk factors and inflammatory
Sabrina da Silva Saraiva1, Isadora Fernandes Custódio1, Bruna de Moraes Mazetto1
1Hematology and Hemotherapy Center, University of Campinas, Rua Carlos Chagas, 480, Cidade Universitária "Zeferino Vaz", Campinas, SP CEP: 13083-970, Brazil.
Introduction:
Antiphospholipid syndrome (APS) is a pro-thrombotic autoimmune disease that affects different vascular beds, with potential risk for recurrence. Systemic lupus erythematosus (SLE), specific autoantibodies profile and atherogenic disorders have been described as risk factors for the occurrence of first thrombosis in patients with antiphospholipid antibodies (aPL). However, factors associated with recurrent thrombosis have not yet been completely elucidated in APS. The aim of this study was to evaluate the association of recurrent thrombosis with markers of inflammation, autoimmunity and the presence of atherogenic disorders in APS patients.
Materials And Methods:
We performed a retrospective evaluation of a cohort of APS patients in order to determine if markers of inflammation, autoimmunity and cardiovascular risk were associated with recurrence of thrombosis.
Results:
One hundred fifteen patients with APS were included, 60% had primary APS. History of recurrent thrombosis was positive in 38.3% of patients, and 40% of them were on oral anticoagulants at the time of recurrence. Independent risk factors associated with recurrent thrombosis were arterial hypertension (OR = 3.7, 95% CI = 1.6–8.5, P = 0.002) and monocytosis above 500 u/mm(3) (OR = 2.4, 95% CI = 1.2–5.3, P = 0.02). These factors were particularly relevant in cases of venous index event.
Conclusion:
The results suggest that arterial hypertension and monocyte counts may be independent factors for thrombosis recurrence in APS. Given the morbidity of recurrent cases, the results may support the evaluation of therapeutic measures to a rigid control of blood pressures and modulation of inflammatory response in APS, as additional prophylaxis against the recurrence of vascular events.
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