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Introduction

Dermatitis herpetiformis is a cutaneous manifestation of gluten sensitivity that is characterized by clusters of erythematous papules, vesicles, and bullae on the extensor surfaces (eg, elbows, knees), buttocks, and back.  Herpetiformis refers to the resemblance of the clustered vesicles to those of herpes simplex.  Most patients (ie, ~90%) have underlying gluten-sensitive enteropathy (ie, celiac disease), even if asymptomatic.

Pathogenesis and risk factors

The pathogenesis of dermatitis herpetiformis involves gluten exposure in a genetically susceptible patient.

Following the absorption of gluten, gliadin peptides elicit a T-cell–mediated inflammatory cascade ( Figure 1).  Gliadin is absorbed into the intestinal mucosa and deaminated by tissue transglutaminase in a process involving formation of covalent crosslinks between them.  Because of this, the subsequent immune response against gliadin also targets tissue transglutaminase.  The deaminated gliadin then binds to the surface of antigen-presenting cells (primarily

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