Review on Bullous Pemphigoid: Fixed Drug Eruption or Autoimmune Disorder

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dc.contributor.authorAdarsh Keshari
dc.contributor.authorKriti Jain
dc.contributor.authorRoshan Pandey
dc.contributor.authorAyush Mishra
dc.contributor.authorSarita Jangra
dc.contributor.authorAmit Sharma
dc.contributor.authorBhavesh Dharmani
dc.contributor.authorBisman
dc.contributor.authorThakur Gurjeet Singh
dc.date.accessioned2025-12-19T09:43:21Z
dc.date.available2025-12-19T09:43:21Z
dc.date.issued2024-11-20
dc.description.abstractBackground: Bullous pemphigoid is a blistering disease of autoimmune nature predominantly affecting the geriatric population. It is characterized by blister formation at the subepidermal level, due to autoantibodies at the dermo-epidermal junction targeting proteins BP180XV11 and BP230. Mainly an autoimmune condition, diagnosis and treatment get complicated as it overlaps with drug-induced hypersensitivity reactions, including fixed drug eruption. Unlike Bullous Pemphigoid, it is a condition of localized hypersensitivity mediated by T cells. Purpose: The review tries to establish Bullous Pemphigoid as an autoimmune condition separate from fixed drug eruption. It is centered on the causative role of medications, which include diuretics, antibiotics, and dipeptidyl peptidase-4 inhibitors, in drug-induced bullous pemphigoid. Besides, it examines genetic, immunological, and environmental etiologies of the disease and delineates clinical and diagnostic characteristics of Bullous Pemphigoid and fixed drug eruptions. Method: A systematic analysis of current literature was performed, focusing on the pathophysiology, immunological mechanisms, and histopathological differences between Bullous Pemphigoid and fixed drug eruptions. The review also examines the role of medications, genetic predispositions such as specific human leukocyte antigen haplotypes, and the diagnostic utility of histopathological and immunological methods like direct immunofluorescence. Results: Autoantibodies against BP180 and BP230 in bullous pemphigoid initiate inflammatory cascades, causing subepidermal blistering and eosinophilic infiltration. Fixed drug eruption involves basal cell necrosis and localized lymphocytic infiltration. Drugs like dipeptidyl peptidase-4 inhibitors exacerbate bullous pemphigoid through immune modulation and oxidative stress. Genetic susceptibility plays a significant role, and immunological tests such as direct immunofluorescence help distinguish the two conditions. Conclusion: Bullous pemphigoid is a distinct autoimmune disease with unique immunopathological mechanisms compared to fixed drug eruption. Understanding its pathogenesis, drug interactions, and diagnostic methods enhances accurate diagnosis and management of both spontaneous and drug-induced bullous pemphigoid.
dc.identifier.issn2321-2217
dc.identifier.issn2321-2225
dc.identifier.otherhttps://doi.org/10.15415/jptrm.2024.122002
dc.identifier.urihttps://demodspace.chitkara.edu.in/handle/123456789/299
dc.language.isoen
dc.publisherChitkara University Publications
dc.subjectBullous pemphigoid
dc.subjectFixed drug eruption
dc.subjectBasement membrane zone (BMZ)
dc.subjectDrug induced Bullous pemphigoid
dc.subjectAutoantibodies.
dc.titleReview on Bullous Pemphigoid: Fixed Drug Eruption or Autoimmune Disorder
dc.typeArticle

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JPTRM Vol. 12 No. 2 (November 2024)