The Variable Nature of Biopsy-Proven Vildagliptin-Induced Bullous Pemphigoid in an Elderly Patient: A Case Series
https://doi.org/10.15605/jafes.041.S1
- Author:
Mohd Fyzal Bahrudin
1
;
Chin Voon Tong
1
;
Raja Nurazni Raja Azwan
1
;
Hazleen Zainal
2
;
Zanariah Hussein
1
Author Information
1. Institut Endokrin, Hospital Putrajaya
2. Unit Dermatologi, Hospital Putrajaya
- Publication Type:Journal Article
- From:
Journal of the ASEAN Federation of Endocrine Societies
2026;41(S1):51-52
- CountryPhilippines
- Language:English
-
Abstract:
Introduction:Bullous pemphigoid (BP) is the most common autoimmune
blistering disease. Drug-induced BP has been increasingly
reported, with dipeptidyl peptidase-4 (DPP-4) inhibitors,
particularly vildagliptin, emerging as a notable cause.
The pathogenesis is thought to involve the disruption of
immune tolerance and epitope spreading, leading to a
broader autoimmune response against basement membrane
antigens beyond the classic NC16A domain of BP180. This
case series highlights the variable clinical spectrum and
therapeutic challenges in vildagliptin-induced BP.
Case:A 74-year-old male with type 2 diabetes mellitus (T2DM),
hypertension, dyslipidemia, and a history of stroke
presented with a 2-month history of recurrent, pruritic,
tense bullae. He had been on vildagliptin for 36 months.
Histopathology confirmed subepidermal blistering, and
direct immunofluorescence demonstrated linear IgG/C3
deposition at the dermo-epidermal junction, with positive
anti-BP180 antibodies, diagnosing BP. Discontinuation
of vildagliptin and initiation of systemic corticosteroids
resulted in significant clinical improvement, allowing a
rapid prednisolone taper to 5 mg daily without new bullae
formation.
A 62-year-old female with T2DM and dyslipidemia
presented with bullous eruptions 3 months after initiating
vildagliptin. Skin biopsy confirmed BP, revealing
subepidermal blistering with eosinophils and linear C3/IgG
deposition at the basement membrane zone. Vildagliptin was discontinued. Despite initial management with
systemic corticosteroids, the disease course was refractory.
The patient experienced a flare upon steroid taper and
had persistent blistering on prednisolone 20 mg daily,
necessitating the addition of azathioprine as a steroidsparing agent.
Conclusion:This case series illustrates the variable clinical course
of vildagliptin-induced BP in which the therapeutic
trajectories diverged significantly. Recognition of BP as a
potential adverse effect of DPP-4 inhibitors is critical, and
management should be individualized.
- Full text:2026073014075642273EP_A059.pdf
