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.
Highlights
BackgroundProtein C (PC), a 62-kD vitamin K dependent glycoprotein, is produced by the liver [1]
This review aims to highlight the pathophysiology of PC as an anticoagulant along with its various other functions and a detailed discussion of different types of PC deficiency
The mainstay of treatment in the majority of cases has been the use of anticoagulants such as heparin, warfarin, aspirin, and clopidogrel [2,24,25,26,27,28,29,30,31,32]
Summary
Protein C (PC), a 62-kD vitamin K dependent glycoprotein, is produced by the liver [1]. It circulates in the blood as an inactive zymogen. When PC is bound to the endothelial proteoglycan thrombomodulin, thrombin catalyzes its conversion into activated PC (APC), i.e., a serine-protease-like enzyme [1]. As a part of its anticoagulant activity, APC causes inactivation of the coagulation factors Va and VIIIa, which are vital for the activation of factor X and the generation of thrombin [1]. APC exerts anti-inflammatory and cytoprotective functions owing to the endothelial PC receptor (EPCR) and the protease-activated receptor-1 (PAR-1) [1]
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