Review on Bullous Pemphigoid: Fixed Drug Eruption or Autoimmune Disorder

Home > 2024, Vol. 12 No. 02 > Review on Bullous Pemphigoid: Fixed Drug Eruption or Autoimmune Disorder

Published: November 20, 2024

Authors

Adarsh Keshari, Roshan Pandey, Sarita Jangra, Amit Sharma, Bhavesh Dharmani, Bisman, and Thakur Gurjeet Singh

DOI Number
https://doi.org/10.15415/jprtm.2024.122002

Keywords
Bullous pemphigoid, Fixed drug eruption, Basement membrane zone (BMZ), Drug induced Bullous pemphigoid, Autoantibodies.

Abstract

Background: 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.

References

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How to Cite

Adarsh Keshari, Roshan Pandey, Sarita Jangra, Amit Sharma, Bhavesh Dharmani, Bisman, and Thakur Gurjeet Singh. Review on Bullous Pemphigoid: Fixed Drug Eruption or Autoimmune Disorder. J. Pharm. Technol. Res. Manag.. 2024, 12, 15-24

Review on Bullous Pemphigoid: Fixed Drug Eruption or Autoimmune Disorder

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