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Michel Baccard, MD; Marie Dominique Vignon-Pennamen, MD; Michel Janier, MD; Marie Lorraine Scrobohaci, MD; Louis Dubertret, MD
Policlinique de dermatologie Hôpital Saint Louis 1 ave Claude Vellefaux 75475 Paris Cedex 10, France

Arch Dermatol. 1992;128(10):1410-1411.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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.¹

Protein 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 . . . [Full Text PDF of this Article]

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