title: [Necrotic leg ulcers induced by vitamin K antagonists: five cases].
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
  
  
  CONCLUSIONS
  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.
authors: Service de dermatologie, hôpital Robert-Debré, Reims, France. maudbezier@hotmail.com
authors: M
authors: M
authors: Bezier
authors: G
authors: G
authors: Perceau
authors: Z
authors: Z
authors: Reguiai
authors: V
authors: V
authors: Remy-Leroux
authors: T
authors: T
authors: Tchen
authors: A
authors: A
authors: Durlach
authors: F
authors: F
authors: Grange
authors: P
authors: P
authors: Nguyen
authors: P
authors: P
authors: Bernard
mesh_terms: D000074:Acenocoumarol / Q000009:adverse effects* / Q000627:therapeutic use; D020016:Activated Protein C Resistance / Q000150:complications / Q000235:genetics; D000368:Aged; D000369:Aged, 80 and over; D000925:Anticoagulants / Q000009:adverse effects* / Q000627:therapeutic use; D003925:Diabetic Angiopathies / Q000150:complications; D005165:Factor V / Q000235:genetics; D005260:Female; D006801:Humans; D020138:Hyperhomocysteinemia / Q000150:complications; D007871:Leg Ulcer / Q000139:chemically induced* / Q000209:etiology / Q000473:pathology; D008297:Male; D009336:Necrosis; D010630:Phenindione / Q000009:adverse effects / Q000031:analogs & derivatives* / Q000627:therapeutic use; D010488:Polyarteritis Nodosa / Q000139:chemically induced / Q000473:pathology; D011183:Postoperative Complications / Q000139:chemically induced / Q000517:prevention & control; D011693:Purpura / Q000139:chemically induced; D019851:Thrombophilia / Q000150:complications*; D014647:Varicose Ulcer / Q000139:chemically induced / Q000473:pathology; D018366:Vasculitis, Leukocytoclastic, Cutaneous / Q000139:chemically induced* / Q000473:pathology; D014812:Vitamin K / Q000037:antagonists & inhibitors*
chemical_list: D000925:Anticoagulants; C095381:factor V Leiden; D014812:Vitamin K; D010630:Phenindione; D005165:Factor V; C017673:fluindione; D000074:Acenocoumarol