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Russell W. Eyre, MD; John R. Stanley, MD
Dermatology Branch National Cancer Institute Bldg 10, Room 12N-238 National Institutes of Health Bethesda, MD 20892

Arch Dermatol. 1988;124(1):25-27.

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

To the Editor.—

There are two major types of pemphigus, pemphigus foliaceus (PF), in which blisters form due to acantholysis in the superficial epidermis, and pemphigus vulgaris (PV), in which acantholysis occurs in the deeper epidermis, just above the basal layer.¹ Mucous membrane lesions, flaccid bullae, and extensive erosions are commonly seen in PV; whereas, in PF, superficial crusts and scales appear, often in a seborrheic distribution, and mucous membrane lesions or extensive erosions are rarely seen. Patients with each type of pemphigus have autoantibodies to different keratinocyte cell surface molecules.^2,3 Patients with PF have antibodies to a characteristic complex of polypeptides of 260 000,160 000, 110000, and 85 000 molecular weight (mol wt), as detected by immunoprecipitation of human epidermal extracts.³ These polypeptides include desmoglein I, a 160 000-mol wt core desmosomal glycoprotein and, possibly, other desmosomal proteins. Patients with PV have antibodies to a different, characteristic complex of polypeptides of 210000, 130000, and . . . [Full Text PDF of this Article]

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