Fig. 3.

Representation of the dysregulated coagulation system in the ME/CFS group as inferred from the results of this study (Table 2). The ME/CFS group exhibits an increased propensity for clotting due to decreased levels of vitamin K-dependent protein S (an endogenous anticoagulant). Increased levels of thrombospondin-1 (originating from endothelial cells and platelets) activate platelets, as well as contribute to endothelial dysfunction via proinflammatory and oxidative/nitrosative mechanisms – as does increased levels of platelet factor 4 and P-selectin [8]. The end result is a prothrombotic state, potentially resulting from and contributing to endothelial dysfunction