Necrotic leg ulcers induced by vitamin K antagonists: five cases

• Published in: Annales de dermatologie et de vénéréologie 2011-10, Vol.138 (10), p.657-663
• Main Authors: Bezier, M, Perceau, G, Reguiai, Z, Remy-Leroux, V, Tchen, T, Durlach, A, Grange, F, Nguyen, P, Bernard, P
• Format: Article
• Language: fre
• Subjects: Acenocoumarol - adverse effects; Acenocoumarol - therapeutic use; Activated Protein C Resistance - complications; Activated Protein C Resistance - genetics; Aged; Aged, 80 and over; Anticoagulants - adverse effects; Anticoagulants - therapeutic use; Diabetic Angiopathies - complications; Factor V - genetics; Female; Humans; Hyperhomocysteinemia - complications; Leg Ulcer - chemically induced; Leg Ulcer - etiology; Leg Ulcer - pathology; Male; Necrosis; Phenindione - adverse effects; Phenindione - analogs & derivatives; Phenindione - therapeutic use; Polyarteritis Nodosa - chemically induced; Polyarteritis Nodosa - pathology; Postoperative Complications - chemically induced; Postoperative Complications - prevention & control; Purpura - chemically induced; Thrombophilia - complications; Varicose Ulcer - chemically induced; Varicose Ulcer - pathology; Vasculitis, Leukocytoclastic, Cutaneous - chemically induced; Vasculitis, Leukocytoclastic, Cutaneous - pathology; Vitamin K - antagonists & inhibitors
• ISSN: 0151-9638
• DOI: 10.1016/j.annder.2011.06.008

Vitamin K antagonists (VKAs) are widely used in thromboembolic diseases. We report five cases of necrotic leg ulcers having a particularly severe course and in which withdrawal of VKA treatment alone enabled healing. Five patients presented with necrotic leg ulcers clinically evocative of necrotic angiodermatitis or vasculitis. Histological features were variable, including inconstantly inflammatory lesions (leukocytoclastic vasculitis) and microthrombosis. None of the patients had laboratory signs of autoimmune disease. Healing occurred in all patients only after withdrawal of VKA therapy (fluindione or acenocoumarol). Associated vascular diseases included superficial venous, distal arterial insufficiency and postphlebitic disease. In three cases, thrombotic factors were observed: hyperhomocysteinaemia or heterozygous Factor V Leiden mutation. Although the causative role of VKAs is based solely on chronological criteria, this potential side effect deserves publication because of its practical therapeutic consequences. The physiopathological mechanisms accounting for the role of VKAs, including immunoallergic phenomena and, above all, microcirculatory thrombotic processes, are hypothetical and not universally accepted.