Bullous pemphigoid: An immune disorder related to aging (Review)

Bullous pemphigoid (BP) is the most frequent subepidermal autoimmune blistering disease and is caused by autoantibodies directed against two principal antigens of the hemidesmosome, BP antigen 180 and BP antigen 230. The pathogenesis of BP is dependent upon the interaction between genetic predisposition, physiological skin alterations due to aging and specific triggers. Several triggers have already been reported to induce this disease and include drugs, thermal or electrical burns, surgical procedures, trauma, UV radiation, radiotherapy, chemicals and infections. Data from the current literature support the hypothesis that alterations of the skin barrier associated with aging increase individual susceptibility to these aforementioned triggers. Consequently, this has been reported to lead to the attack of autoantibodies, demonstrating the predilection of BP for the elderly population. The identification of triggering factors and comorbidities may aid in understanding the pathogenesis of BP and improve clinical management by encouraging their prompt recognition and removal. Moreover, the present review has indicated that current management of BP should be aimed at counteracting the detrimental effects of aging on the skin by restoring skin barrier integrity and maintaining cutaneous homeostasis, for example with systematic applications of topical emollients and photoprotection. This strategy could prove even more beneficial in the elderly, in which frequent comorbidities associated with age often narrow available immunosuppressive treatment options. Furthermore, the safety of treatment regimens may significantly affect outcome and prognosis.