Abstract
Pemphigus is a group of autoimmune blistering diseases including pemphigus vulgaris (PV) and pemphigus foliaceus (PF). Lesion morphology has been explained by the desmoglein compensation hypothesis (DCH), which uses the epidermal distribution of desmoglein (Dsg) proteins and autoantibody profile. The DCH theorizes 3 types of lesion morphology: mucosal PV, mucocutaneous PV, and cutaneous PF. While the DCH has been supported in the literature, logical inconsistencies have been identified and published in multiple small-scale studies.
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