Protein C deficiency in splanchnic venous thrombosis

Abstract

Deficiencies of protein C activity and antigen were observed in eight consecutive patients with splanchnic venous thrombosis. There was a significant reduction in the ratio of protein C to factor X. Six of the eight patients had a decrease in antithrombin III, but free protein S antigen was within normal limits in all but two subjects. It is proposed that a thrombogenic stimulus such as stasis, altered hormonal milieu, or failure of hepatic clearance of activated coagulants results in consumption of protein C and antithrombin III, predisposing to splanchnic venous occlusion. This further impairs hepatic function, prevents restitution of protein C and antithrombin levels, and promotes continuing venous thrombosis. Thus, a vicious cycle of thrombosis and hepatic damage is perpetuated.