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David T. Woodley, MD

Arch Dermatol. 1990;126(2):229-231.

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

Epidermolysis bullosa acquisita (EBA) is a severe chronic subepidermal bullous disease that has been described in the medical literature since the 19th century.^1,2 Like most primary blistering diseases, EBA is decidedly rare. However, EBA may be more common than previously appreciated, especially if one includes all subepidermal blistering disorders associated with autoantibodies to type VII (anchoring fibril) collagen.^3,4

The full clinical spectrum of EBA is not known. The most well-known presentation of EBA is a noninflammatory, mechanobullous disease reminiscent of porphyria cutanea tarda or dystrophic forms of hereditary EB. These patients are plagued with marked skin fragility and chronic wounds that heal with scarring and milia formation. This "classical" presentation was well documented by Roenigk et al,² who reviewed the world literature through 1971 and added three new cases of EBA. Patients with EBA frequently have significant involvement of their mucosal surfaces, such as the mouth, genitalia, and . . . [Full Text PDF of this Article]

Author Affiliations
Department of Dermatology Edwards Bldg, Room 144 Stanford University School of Medicine Stanford, CA 94305

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