[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address 54.197.124.106. Please contact the publisher to request reinstatement.
[Skip to Content Landing]
Article
October 1992

Livedo Vasculitis With Protein C System Deficiency

Author Affiliations

Policlinique de dermatologie Hôpital Saint Louis 1 ave Claude Vellefaux 75475 Paris Cedex 10, France

Arch Dermatol. 1992;128(10):1410-1411. doi:10.1001/archderm.1992.01680200122031
Abstract

To the Editor.—  Protein C is a vitamin K—dependent plasma glycoprotein synthetized in the liver. Thrombomodulin (the endothelial receptor for thrombin) catalyzes the thrombin activation of protein C. Activated protein C has anticoagulant activity. Protein C deficiency is responsible for a hypercoagulable state that can be symptomatic.1Protein C deficiency is either acquired or is transmitted in an autosomal dominant fashion.1 Homozygous deficiency is responsible for neonatal purpura fulminans and disseminated intravascular coagulation within the first days of life. Heterozygous deficiency is responsible for deep-vein thrombosis in young adults. Development of skin necrosis in these patients during the initiation of oral anticoagulant therapy is also well known. It is probably caused by a rapid drop in protein C concentration, which has a shorter life than most of the procoagulant vitamin K—dependent factors, thus resulting in a transient hypercoagulable state.We report a case of livedo reticularis with superficial

First Page Preview View Large
First page PDF preview
First page PDF preview
×