Organ specific complement proteins inhibition can reduce the risk of antiphospholipid antibodies mediated fetal loss

Antiphospholipid syndrome is a pregnancy related, systemic autoimmune disorder in which antibodies directed against cell membrane phospholipids with multiple venous/arterial thromboses. Though the etiology of antiphospholipid syndrome has not been identified exactly, experimental evidences suggest the possible mechanisms involved in the pathogenicity of this syndrome. Antiphospholipid antibodies mediate deposition of complement proteins in placenta and over expression of tissue factor on the surface of neutrophils which are reported to be the prominent cause of prothrombotic phenotype. The activation complement components C3 and C5 by antiphospholipid antibodies would eventually activates blood coagulation pathway that leads to thrombosis. Inhibition of activated complement components C3a and C5a by anticomplement agents protects from antiphospholipid antibody mediated fetal loss. Since the interference of complement pathway may lead to deleterious effects, we hypothesis that local inhibition of complement proteins C3a and C5a at placenta would reduce the risk of antiphospholipid antibody mediated placental thrombosis and pregnancy complications.