Protein C deficiency with venous and arterial thromboembolic events

Abstract

Protein C (PC) is a key component of the vitamin K-dependent coagulation pathway. It exerts anticoagulant effects by inactivating factors V and VIII. Acquired or inherited PC deficiency results in a prothrombotic state, with presentations varying from asymptomatic to venous thromboembolism. However, there has been an increasing number of reports linking PC deficiency to arterial thromboembolic events, such as myocardial infarction and ischemic stroke. This editorial focuses on the association between PC deficiency and thromboembolism, which may provide some insights for treatment strategy and scientific research.

Keywords: Protein C deficiency; Venous thromboembolism; Myocardial infarction; Editorial; Arterial thromboembolism

Core Tip: Protein C (PC) deficiency impairs the balance between the procoagulant and anticoagulant system, which results in venous thromboembolism. However, there has been an increasing number of reports linking the condition to arterial thromboembolic events. A thorough understanding of PC deficiency is essential for the development of new management strategies against PC deficiency-related thromboembolism events.