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Vincent Falanga, MD; Franklin A. Bontempo, MD; William H. Eaglstein, MD

Arch Dermatol. 1990;126(9):1195-1197.

Abstract
• Lipodermatosclerosis of the lower extremity, with or without ulceration, is a common manifestation of severe venous disease and the result of sustained venous hypertension. The latter is generally a sequela of deep vein thrombosis. Factors that enhance clot formation or impair fibrinolysis contribute to the pathogenesis of venous disease. It is already established that faulty fibrinolysis may play a pathogenic role in patients with venous disease. We examined the possibility that patients with venous disease have abnormally low plasma levels of proteins C and S, two proteins whose deficiencies have been reported to cause an increased frequency of thromboembolic disease. Using immunologic and functional assays for plasma proteins C and S, we found that 4 (21%) of 19 patients with lipodermatosclerosis and leg ulcers had abnormally low levels of protein C or protein S. One of 7 patients with lipodermatosclerosis without ulceration had a profoundly depressed level of protein C and a history of cerebral stroke at a young age. Plasma levels of protein C were normal in five patients with arterial insufficiency severe enough to cause leg ulceration. We conclude that abnormally low plasma levels of proteins C and S may be found in patients with lipodermatosclerosis and venous ulceration. As with the abnormally low fibrinolytic activity in these patients, our findings indicate a possible propensity for increased thrombotic disease.

(Arch Dermatol. 1990;126:1195-1197)

Author Affiliations
From the Department of Dermatology and Cutaneous Surgery, University of Miami (Fla) School of Medicine. Dr Bontempo is now with the University of Pittsburgh (Pa).

Footnotes
Accepted for publication March 28, 1990.

Reprint requests to Department of Dermatology and Cutaneous Surgery, University of Miami School of Medicine, PO Box 016250 (R-250), Miami, FL 33101 (Dr Falanga).

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