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Correspondence
June 2002

Livedoid Vasculitis With Ulcerations: The Role of Antithrombin III Deficiency and Its Therapeutic Consequences

Author Affiliations
 

Copyright 2002 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.2002

Arch Dermatol. 2002;138(6):841-842. doi:10.1001/archderm.138.6.838

Livedoid vasculitis (LV) is a descriptive and still indistinct clinical term that includes considerable "semantic confusion."1 It covers localized cutaneous vasculopathies presenting a clinical pattern of livedoid discoloration mainly in distal parts of the lower extremities, eventually eliciting long-lasting painful ulcers particularly after exposure to heat or cold.1,2 Histologically, microthromboses and segmental hyalinization of the subendothelial intima in blood vessels of the middle and lower dermis are significant findings.2 Besides local factors, systemic hypercoagulopathies (protein C or factor XII deficiencies, deficient release of tissue plasminogen activator, elevated tissue plasminogen inhibitor, and increased platelet aggregation) are under discussion as copathogenetic factors.3-5 Herein, we report, for the first time, 2 cases of LV relating to antithrombin III (AT-III) deficiency.

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