Abstract
Bullous pemphigoid (BP) is an autoimmune bullous skin disease that causes blistering due to the presence of immunoglobulin G antibody/antigen complexes at the dermal-epidermal junction. Primarily seen in people over the age of 60, BP can be triggered by medications, infections, comorbidities, and environmental skin stressors. The clinical presentation of BP begins with non-bullous patches that may resemble eczema or urticaria; this stage is followed by the development of tense vesiculobullous lesions in flexural areas that usually heal without scarring. Erosions sometimes develop on mucous membranes such as the oral cavity or genitalia. The diagnosis is made by using direct immunofluorescence on punch biopsy samples taken from perilesional skin, which will show the linear deposits of immunoglobulin G antibody/antigen complexes along the dermal-epidermal junction. Salt-split skin testing can also confirm the direct immunofluorescence results. Treatment options include the removal of any triggering factors and the use of topical or oral corticosteroids. If prolonged treatment is required, steroid-sparing medications such as immunosuppressants, immunoglobulins, monoclonal antibody agents, or doxycycline can be combined to achieve satisfactory results. BP causes an increased risk of developing pulmonary emboli or stroke, but most patients will be able to achieve remission after 6–60 months of treatment without further complications.
Published Version
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