Protein C Deficiency as a Risk Factor for Stroke in Young Adults: A Review

Abstract

Protein C (PC) is a 62-kD vitamin K dependent glycoprotein produced by the liver as a zymogen and is activated by binding to the thrombin-thrombomodulin complex, with protein S (PS) acting as a cofactor. Among its various functions, PC acts as a naturally occurring anticoagulant and its deficiency, either homozygous or heterozygous, predisposes the individual to a state of thrombosis, particularly venous thromboembolism, and mainfests as myocardial infarction (MI), deep venous thrombosis, pulmonary embolism, or stroke. This review discusses the pathophysiology of the anticoagulatory effect of PC, mode of inheritance of its deficiency, the arterial and venous involvement in patients with stroke, and its risk factors. A detailed analysis of published case reports on PC deficiency as a causative agent of stroke in young adults has also been included along with the management of such patients.