Abstract
Increasing knowledge of immunology has shown that immune mechanism, especially humoral reaction including antibody and complement, plays a part in the clotting mechanism. Fibrin clot has been demonstrated in the tissue of Arthus phenomenon or in the glomerulus of nephritic kidney. So-called acute or hyperacute rejection in tissue transplantation has been explained to be due to clot formation around the transplanted tissue. Recently, disseminated intravascular coagulation (DIC) has been reported in patients with immune complex diseases. These evidences strongly support the participation of immune reaction in coagulation mechanism.
Complement system has been demonstrated to play an important role in the coagulation mechanism, through the investigation of C6-deficient rabbit and complement-depleted animals. In order to understand the mechanism of hypercoagulable stage through the activation of complement system, it seems reasonable to explain in the following manner. (1) Destruction of vascular endothel mainly due to the deposition of immune complex results in the activation of contact system (Hageman factor) as well as the enhancement of platelets aggregation. (2) Destruction or aggregation of platelets can easily occur by the action of complement through its classical or the alternative pathway and results in the release of platelet factors. (3) Tissue factor is released when tissue damage is produced by complement. In addition, activation of plasmin or kinin through Hageman factor dependent pathway also activate complement system and enhances above mentioned coagulation mechanisms.
From the clinical standpoint, estimation of complement gives valuable informations in the managing the patients with DIC. Serum complement (CH 50) and complement components C3 and C4 revealed marked reduction after the onset of DIC, and those who survived restored their complement level. Titration of complement in patients with hypercoagulable stage was strongly recommended.
