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June 1991

Protein C and Fibrinolysis-Reply

Author Affiliations

Department of Dermatology and Cutaneous Surgery University of Miami School of Medicine PO Box 016250 (R-250) Miami, FL 33101

Arch Dermatol. 1991;127(6):909. doi:10.1001/archderm.1991.01680050155025

In Reply.—  We are pleased at the interest generated by our article.1 Dr Samlaska properly warns against overinterpretation of isolated defects in hypercoagulability states. We concur with this, and wish to point out that we were cautious in the interpretation of our results. It is indeed quite possible that the endothelial surface is partially at fault in the full expression of venous disease. There are observations suggesting that the endothelium is damaged in the course of venous hypertension. It has also been hypothesized that the damage to the endothelium causes trapping of leukocytes, which could lead to further endothelial cell activation or damage.2 It is obvious that no single hypothesis presently explains the full expression of venous disease, but that many steps may be required in the pathogenesis. We do concur with Dr Samlaska, however, that venous hypertension is most likely the initial event.Newman describes the interesting relationship between

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