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What It Is and How the Patient Should Be Evaluated and Treated

Arch Dermatol. 2006;142:1481-1482.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

In this issue of the ARCHIVES are 2 articles that aid us in defining associated conditions in patients with livedoid vasculopathy (LV). Hairston et al¹ demonstrate that thrombophilic conditions occur frequently in patients with LV, including inherited abnormalities and acquired disease. In addition, they note a wide variety of associated conditions, including connective tissue diseases and neoplasia. Deng et al² used tissue plasminogen activator (tPA) to successfully manage LV in a patient who was found to have elevated levels of plasminogen activator inhibitor-1 owing to a homozygous mutation of the plasminogen activator inhibitor-1 promoter. They note that patients with elevated levels of plasminogen activator inhibitor-1 have a propensity for thrombotic disorders. Their patient experienced 4 relapses of LV generally associated with discontinuation of antithrombotic therapy. In each instance, the lesions responded to reinstitution of tPA infusions.

In 1998, Jorizzo,³ in an editorial about an article by Papi et al,⁴ . . . [Full Text of this Article]

AUTHOR INFORMATION
Jeffrey P. Callen, MD

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Livedoid Vasculopathy: Further Evidence for Procoagulant Pathogenesis
Bethany R. Hairston, Mark D. P. Davis, Mark R. Pittelkow, and Iftikhar Ahmed
Arch Dermatol. 2006;142(11):1413-1418.
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Livedoid Vasculopathy Associated With Plasminogen Activator Inhibitor-1 Promoter Homozygosity (4G/4G) Treated Successfully With Tissue Plasminogen Activator
April Deng, Christopher D. Gocke, John Hess, Meyer Heyman, Michael Paltiel, and Anthony Gaspari
Arch Dermatol. 2006;142(11):1466-1469.
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