Key result
Warfarin skin necrosis recurs despite stopping anticoagulation, linked to factors causing vitamin K deficiency.
Case Report (n=1)
This case highlights that lesions typical of warfarin skin necrosis can recur in the absence of anticoagulant therapy, potentially driven by vitamin K deficiency.
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Vitamin K deficiency may trigger recurrent necrosis-like lesions off anticoagulants; case report leaves open broader mechanisms and monitoring needs.
Skin necrosis is a well-known yet rare complication of oral anticoagulant therapy. We report the unusual recurrence of lesions typical of warfarin skin necrosis in the absence of anticoagulant therapy. A 59-year-old woman developed skin necrosis while receiving prophylactic warfarin following the detection of a large left ventricular thrombus. The warfarin was discontinued and the lesions improved. One month later new areas of skin necrosis developed although the patient had received no further warfarin. Progressive congestive heart failure, poor nutrition, and prolonged oral antibiotic therapy preceded the recurrence. Vitamin K deficiency was present on admission. The potential role of vitamin K-dependent coagulation factors in the pathogenesis of anticoagulant-associated skin necrosis is discussed.
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Humphries et al. (1991) conducted a case report in Warfarin skin necrosis (n=1). Warfarin was evaluated on Recurrence of skin necrosis. Warfarin skin necrosis recurred in a 59-year-old woman despite the absence of further anticoagulant therapy, preceded by factors contributing to vitamin K deficiency.
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