Bullous pemphigoid (BP) is an acquired non-scarring autoimmune subepidermal bullous disease characterised by tense blisters. Circulating IgG autoantibodies (rarely IgA and IgE) bind to BP230 and BP180 antigens, which are components of the hemidesmosome adhesion complex found in the basement membrane zone of the skin. Direct antibody and antigen interaction, local activation of complement and release of cytokines lead to loss of dermoepidermal adherence and formation of subepidermal blisters.1 Blistering typically occurs on the flexures although BP may be generalised or localised to one site such as the lower legs. Erosions and blisters occur on the mucous membranes, particularly the mouth, in about 50% of cases. Blister formation may be preceded by pruritus or an urticarial or eczematous rash, which may precede the blistering rash for many months.
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