Abstract
It is well established that inflammation and thrombosis are intricately linked processes,
and there is increasing evidence of the importance of their roles in activated complement
in the pathogenesis of thromboembolism. The two systems are activated by similar stimuli
simultaneously and interact, either directly or through biochemical mediators, to
protect the host from microbial invasion. Diseases characterized by complement hyperactivity
such as paroxysmal nocturnal hemoglobinuria and atypical hemolytic uremic syndrome
have high rates of thrombosis. This review describes how disease processes where there
is excessive complement activation leads to thrombosis, and the specific interactions
between the complement and coagulation systems that lead to pathological thrombus
formation.
Keywords
inflammation - thrombosis - complement activation