August 2004

Difficult Management of Livedoid Vasculopathy

Author Affiliations

Copyright 2004 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.2004

Arch Dermatol. 2004;140(8):1011. doi:10.1001/archderm.140.8.1011

Efficacy of low-molecular-weight heparin (LMWH) in 2 patients with livedoid vasculopathy was recently reported in the Cutting Edge section of the ARCHIVES.1 Vitamin K antagonists may also have beneficial effects. In our experience, due to the cost, compliance with the drug injections, and the potential effect of osteoporosis with long-term use of LMWH,2 we think that this treatment should be restricted for patients whose condition is refractory to treatment with platelet aggregation inhibitors and vitamin K antagonists. Since 1993, 16 patients with apparently idiopathic livedoid vasculopathy were followed up in our institution. Some of them were previously described.3 All of the patients had chronic, painful leg ulcerations followed by the development of white scars with fine borders of ectatic vessels. Diagnosis was confirmed by histopathologic findings showing fibrinous occlusion of dermal blood vessels without leukocytoclasis. Patients with abnormal continuous-wave venous Doppler findings of the legs or connective tissue disease were systematically excluded. As previously described, laboratory investigations screened standard biochemistry values, blood cell count, serum homocysteine levels, functional and immunological levels of antithrombin III protein, biological activity, antigen levels of protein C, biological and antigen activity of protein S, R506Q of factor V (Leiden) and 20210G/A of prothrombin mutations, cryoglobulin and cryofibrinogen research, detection of lupus anticoagulant, and anticardiolipin antibodies.4 Clinical data and effects of treatments were reviewed retrospectively. Complete remission was defined as disappearance of ulcerations and partial remission was defined as at least 50% decrease in the number of ulcerations. Except for 2 patients, all were treated with either LMWH (enoxaparin sodium) or a vitamin K antagonist (fluindione). A preventive dose of LMWH consisted of 1 daily subcutaneous injection of 4000 IU of anti-Xa. A curative dose of LMWH consisted of 2 daily subcutaneous injections (100 IU/kg of anti-Xa per injection). The dosage of vitamin K antagonist was adapted to achieve an international normalized ratio of 2.5 to 3.5.

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