History, Diagnosis, Pathogenesis, and Nomenclature in Sublamina Densa-Type Linear IgA Disease

In this issue of JAMA Dermatology, Becker et al1 report an extensive retrospective study of 300 patients who received diagnoses of IgA epidermolysis bullosa acquisita (EBA), IgG EBA, or linear IgA disease (LAD) at a single institution. They identified cohorts of 3 different autoimmune bullous diseases (AIBDs), including 222 cases of lamina lucida (LL)-type LAD with IgA autoantibodies reactive with the epidermal side in indirect immunofluorescence (IIF) using 1M sodium chloride–split normal human skin (ssIIF), which they designate as linear IgA bullous dermatosis (LABD), 57 cases of classical EBA with IgG autoantibodies to type VII collagen (COL7), and 21 cases of sublamina densa (SD)-type LAD with IgA antibodies reactive with the dermal side in ssIIF, which they designate as IgA EBA.1