acenocoumarol and Leg-Dermatoses

A 62-year-old woman was referred to the dermatology department for a history of fever, asthenia and cutaneous rash, which appeared after a 3-day course of digitalin and acenocoumarol for atrial fibrillation. The physical examination revealed multiple round confluent purpuric lesions over her entire legs with no blistering. Laboratory exams were all negative. Biopsy of the involved skin was compatible with leucocytoclastic vasculitis. The acenocoumarol treatment was withheld and the skin lesions resolved spontaneously over the next 10 days. The cause of this purpura was seemingly acenocoumarol because of the close temporal relationship between exposure to the drug and the onset of the symptoms, and the spontaneous resolution of the lesions after acenocoumarol was discontinued. This observation illustrates a rare association between vasculitis and acenocoumarol. Clinicians should be aware of this potential adverse effect and recommend interrupting the drug intake when temporal relation is evocative.

Topics: Acenocoumarol; Anticoagulants; Atrial Fibrillation; Diagnosis, Differential; Drug Eruptions; Female; Humans; Leg Dermatoses; Middle Aged; Vasculitis, Leukocytoclastic, Cutaneous

Cutaneous necrosis is an infrequent complication of coumarin therapy. Skin necrosis has usually been reported in patients with congenital protein C deficiency or, less commonly, protein S deficiency. However, this complication may also occur with acquired and transient protein C and/or S deficiency. In coumarin therapy there is a relatively hypercoagulable state at the start of treatment, and most lesions appear between the third and sixth days. We describe a 75-year-old man receiving coumarin therapy (acenocumarol) for 7 years who was given a nonsteroidal anti-inflammatory agent (diclofenac) for a pain in his knee. Two days later, his renal function deteriorated and skin necrosis became evident. Biopsy showed histological changes consistent with coumarin-induced necrosis. Protein C and S levels were normal. We concluded that in our patient acute renal insufficiency aggravated by diclofenac treatment probably associated with an inadvertent withdrawal could have been the precipitating factor for transient protein C deficiency.

Topics: Acenocoumarol; Acute Kidney Injury; Aged; Anti-Inflammatory Agents, Non-Steroidal; Anticoagulants; Diclofenac; Humans; Leg Dermatoses; Male; Skin