Abstract
Endothelial cells are thought to play a central role in the pathogenesis of antiphospholipid syndrome (APS). Omega-3 polyunsaturated fatty acid (n-3 PUFA) supplementation has been shown to improve endothelial function in a number of diseases; thus, it could be of high clinical relevance in APS. The aim of this study was to evaluate the efficacy of n-3 PUFA supplementation on endothelial function (primary outcome) of patients with primary APS (PAPS). A 16-week randomized clinical trial was conducted with 22 adult women with PAPS. Patients were randomly assigned (1:1) to receive placebo (PL, n = 11) or n-3 PUFA (ω-3, n = 11) supplementation. Before (pre) and after (post) 16 weeks of the intervention, patients were assessed for endothelial function (peripheral artery tonometry) (primary outcome). Patients were also assessed for systemic markers of endothelial cell activation, inflammatory markers, dietary intake, international normalized ratio (INR), and adverse effects. At post, ω-3 group presented significant increases in endothelial function estimates reactive hyperemia index (RHI) and logarithmic transformation of RHI (LnRHI) when compared with PL (+13 vs. −12%, p = 0.06, ES = 0.9; and +23 vs. −22%, p = 0.02, ES = 1.0). No changes were observed for e-selectin, vascular adhesion molecule-1, and fibrinogen levels (p > 0.05). In addition, ω-3 group showed decreased circulating levels of interleukin-10 (−4 vs. +45%, p = 0.04, ES = −0.9) and tumor necrosis factor (−13 vs. +0.3%, p = 0.04, ES = −0.95) and a tendency toward a lower intercellular adhesion molecule-1 response (+3 vs. +48%, p = 0.1, ES = −0.7) at post when compared with PL. No changes in dietary intake, INR, or self-reported adverse effects were observed. In conclusion, 16 weeks of n-3 PUFA supplementation improved endothelial function in patients with well-controlled PAPS. These results support a role of n-3 PUFA supplementation as an adjuvant therapy in APS. Registered at http://ClinicalTrials.gov as NCT01956188.
Highlights
Antiphospholipid syndrome (APS) is a systemic autoimmune disease characterized by recurrent thrombotic episodes and/ or obstetric morbidities and persistent serum antiphospholipid antibodies
Previous studies propose that endothelial cells play a central role in the pathogenesis of APS [4]. aPLs have been shown to bind to endothelial cell beta-2 glycoprotein I (β2GPI) receptors leading to endothelial malfunction and formation of thrombosis [5]
Five patients withdrew from the study for personal reasons, three patients became pregnant, one patient entered menopause, one patient was diagnosed with another autoimmune disease, and three patients experienced disease complications not related to APS
Summary
Antiphospholipid syndrome (APS) is a systemic autoimmune disease characterized by recurrent thrombotic episodes and/ or obstetric morbidities and persistent serum antiphospholipid antibodies (aPL). APS can be classified as primary or secondary if concurrent with another autoimmune disease, tumor, or hematologic disorder [1]. Primary APS (PAPS) is significantly associated with high morbidity and mortality from vascular thrombotic events [2] and an increased risk of cardiovascular diseases (CVDs) [3]. Previous studies propose that endothelial cells play a central role in the pathogenesis of APS [4]. Endothelial dysfunction is the earliest detectable stage predisposing to the formation of atherosclerotic lesions and cardiovascular events [10]. Strategies capable of minimizing endothelial dysfunction may be of high clinical relevance in APS
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
