Cutaneous necrosis induced by acenocoumarol.

Abstract

Cutaneous necrosis is an infrequent but well-documented complication of oral anticoagulants. In the pathogenesis of cutaneous necrosis induced by oral anticoagulants recent hypotheses favour the combined role of local factors and a transient unbalance of coagulation mechanisms leading to an hypercoagulable state. There exists a genetic factor that determines a decreased level of two vitamin-K dependent glycoproteins, namely protein C and protein S. We present the case of an obese woman that developed an extensive cutaneous necrosis while receiving acenocoumarol for a deep venous thrombosis. She had an heterozygous deficit for protein C. The histopathologic findings of vessel thrombi and red blood cell extravasation were consistent with the clinical picture. A biopsy specimen taken from an initial lesion disclosed images of leucocytoclastic vasculitis. We reviewed the literature focusing on the pathogenesis and the histopathology of the disease.

• Authors: M Valdivielso, I Longo, M Lecona, P Lázaro
• Journal: Journal of the European Academy of Dermatology and Venereology : JEADV (J Eur Acad Dermatol Venereol) Vol. 18 Issue 2 Pg. 211-5 (Mar 2004) ISSN: 0926-9959 [Print] England
• PMID: 15009309 (Publication Type: Case Reports, Journal Article, Review)

Chemical References

• Anticoagulants
• Acenocoumarol

Topics

• Acenocoumarol (administration & dosage, adverse effects)
• Administration, Oral
• Aged
• Aged, 80 and over
• Anticoagulants (administration & dosage, adverse effects)
• Female
• Humans
• Necrosis
• Protein C Deficiency (complications)
• Skin (pathology)
• Vasculitis, Leukocytoclastic, Cutaneous (complications, pathology)