Previous research has highlighted multiple interactions between the inflammatory response and the coagulation system.[30] Infection elevates C-reactive protein, enhancing tissue factor expression on leukocytes and promoting platelet reactivity and generation.[31] Esmon et al posit that infection-induced inflammation activates complement, apoptosis, and necrosis, crucial processes in clotting reactions, thereby promoting thrombus formation and potentially damaging venous endothelium.[32]. Here, CRP is linked to infection.