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The Need for More Evidence

Linda K. Martin, BA, BSc(Med), MBBS, MMed(ClinEpi); Dedee F. Murrell, MA, BM BCh, FAAD, MD

Arch Dermatol. 2008;144(1):100-101.

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

Pemphigus vulgaris is a prototype antibody-mediated autoimmune disorder in which autoantibodies against desmosomal intraepidermal adhesion proteins lead to acantholysis and blister formation. Although our understanding of the molecular pathogenesis of pemphigus and other autoimmune bullous diseases has increased markedly in recent decades, similar progress regarding effective treatment has not been made.

There are a large number of potential interventions for pemphigus.¹ The cornerstone of treatment is corticosteroids, although use of immunosuppressive agents, immunomodulatory agents, plasmapheresis, intravenous immunoglobulin, and biological agents has also been described. The efficacy and role of each of these agents has not been established.

The advent of synthetic glucocorticosteroids in the 1950s revolutionized the treatment and prognosis of pemphigus, with mortality rates improving from 90% to 10%. Unfortunately, in the ensuing 5 decades, there has been little advancement in treatment, and the . . . [Full Text of this Article]

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