“…Recent studies with RA patients have indeed revealed interactions between ED and disease activity; these include soluble human vascular cell adhesion protein 1, von Willebrand factor, pentraxin-3, asymmetric dimethyl-L-arginine, soluble E-selectin, monocyte chemotactic protein-1, and osteoprotegerin. 33 Many of these substances are affected by inflammatory mediators and cytokines, and as specified earlier, contribute to the mechanisms underlying RA pathogenesis. With respect to therapeutic strategies for RA treatment, especially anti-tumor necrosis factor-alpha therapies, most are effective at reducing inflammation, as well as improving endothelial function.…”