Anticoagulant-induced skin necrosis in a patient with hereditary deficiency of protein S

Skin necrosis is a rare but debilitating complication of treatment with vit amin K antagonist anticoagulants such as warfarin, A clinically similar syn drome has been reported less frequently with heparin therapy. We recently m anaged a thirty-year-old female patient who developed skin necrosis on her left lower extremity while on warfarin for postpartum DVT. The lesions star ted to develop 48 hr after stopping heparin therapy. Discontinuation of war farin and reinstitution of heparin was complicated by a rapid decrease in p latelet count consistent with heparin-induced thrombocytopenia (HIT) end it s associated risk of platelet activation and thrombosis. The diagnosis was supported by the identification of antibodies against heparin/platelet fact or 4 complexes in the patient's serum. The platelet count recovered and the patient improved after switching to therapy with the heparinoid danaparoid . Evaluation for a hypercoagulable state revealed a partial deficiency of p rotein S, a condition that previously was identified in two of her family m embers. It is not clear if this patient suffered from warfarin-induced skin necrosis, a manifestation of heparin-mediated platelet activation, or a co mplex condition in which both drugs contributed. HIT may affect 1-3% of pat ients who receive unfractionated heparin, and this case raises the possibil ity that heparin may contribute to, or cause, some episodes of skin necrosi s attributed to warfarin. Because many patients who develop warfarin-induce d skin necrosis have been treated initially with heparin, it would seem pru dent to consider HIT in these situations. Am. J. Hematol, 60:231-236, 1999. (C) 1999 Wiley-Liss, Inc.