Bullous pemphigoid
Akbarialiabad, Hossein; Schmidt, Enno; Patsatsi, Aikaterini; Lim, Yen Loo; Mosam, Anisa; Tasanen, Kaisa; Yamagami, Jun; Daneshpazhooh, Maryam; De, Dipankar; Cardones, Adela Rambi G; Joly, Pascal; Murrell, Dedee F (2025-02-20)
Avaa tiedosto
Sisältö avataan julkiseksi: 20.08.2025
Springer
20.02.2025
Akbarialiabad, H., Schmidt, E., Patsatsi, A. et al. Bullous pemphigoid. Nat Rev Dis Primers 11, 12 (2025). https://doi.org/10.1038/s41572-025-00595-5
https://rightsstatements.org/vocab/InC/1.0/
© 2025 Springer Nature Limited. This version of the article has been accepted for publication, after peer review (when applicable) and is subject to Springer Nature’s AM terms of use, but is not the Version of Record and does not reflect post-acceptance improvements, or any corrections. The Version of Record is available online at: https://doi.org/10.1038/s41572-025-00595-5
https://rightsstatements.org/vocab/InC/1.0/
© 2025 Springer Nature Limited. This version of the article has been accepted for publication, after peer review (when applicable) and is subject to Springer Nature’s AM terms of use, but is not the Version of Record and does not reflect post-acceptance improvements, or any corrections. The Version of Record is available online at: https://doi.org/10.1038/s41572-025-00595-5
https://rightsstatements.org/vocab/InC/1.0/
Julkaisun pysyvä osoite on
https://urn.fi/URN:NBN:fi:oulu-202505273979
https://urn.fi/URN:NBN:fi:oulu-202505273979
Tiivistelmä
Abstract
Bullous pemphigoid is a chronic, subepidermal autoimmune blistering disease characterized by tense blisters on erythematous or normal skin that predominantly affects the older population. The disease arises from autoantibodies targeting hemidesmosomal proteins BP180 and BP230, which are crucial for dermal–epidermal adhesion. The incidence of bullous pemphigoid is increasing, attributed to an ageing population and improved diagnostic recognition. Genetic predisposition, environmental triggers and associations with other autoimmune disorders underline its multifactorial nature. Diagnosis involves clinical presentation, histopathology, direct immunofluorescence and serological tests. Treatment aims to reduce symptoms and prevent new blister formation, using corticosteroids, immunosuppressive agents and biologics such as rituximab and omalizumab. Despite therapeutic advancements, challenges persist in long-term management, especially in older patients with comorbidities. Ongoing research into molecular mechanisms and novel therapeutic targets and clinical trials are crucial for the development of safer and more effective treatments.
Bullous pemphigoid is a chronic, subepidermal autoimmune blistering disease characterized by tense blisters on erythematous or normal skin that predominantly affects the older population. The disease arises from autoantibodies targeting hemidesmosomal proteins BP180 and BP230, which are crucial for dermal–epidermal adhesion. The incidence of bullous pemphigoid is increasing, attributed to an ageing population and improved diagnostic recognition. Genetic predisposition, environmental triggers and associations with other autoimmune disorders underline its multifactorial nature. Diagnosis involves clinical presentation, histopathology, direct immunofluorescence and serological tests. Treatment aims to reduce symptoms and prevent new blister formation, using corticosteroids, immunosuppressive agents and biologics such as rituximab and omalizumab. Despite therapeutic advancements, challenges persist in long-term management, especially in older patients with comorbidities. Ongoing research into molecular mechanisms and novel therapeutic targets and clinical trials are crucial for the development of safer and more effective treatments.
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