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Abstract
Bullous pemphigoid is an autoimmune subepidermal blistering condition in which autoantibodies target components of the hemidesmosomal proteins. It typically presents as pruritic bullous lesions in a generalized distribution. Certain drugs such as diuretics, NSAIDs, antibiotics, and ACE inhibitors have been implicated in the development of bullous pemphigoid. Recently, a class of medications for type II diabetes, dipeptidyl peptidase-4 (DPP-4) inhibitors (commonly called gliptins) have been implicated in drug-induced bullous pemphigoid. We report a case of a 73-year-old female with type II diabetes mellitus who presented with biopsy-proven bullous pemphigoid after being treated with linagliptin. After discontinuing linagliptin and receiving first-line treatment, the patient achieved remission by her five-week follow-up. It is imperative that dermatologists and primary care physicians remain aware of this association when diagnosing and treating bullous pemphigoid, particularly in diabetic patients.
Highlights
Bullous pemphigoid (BP) is an autoimmune disease characterized by subepidermal blisters and autoantibodies against hemidesmosomal proteins of the basement membrane, BP 180 and BP 230.1 It predominantly affects the elderly and typically presents as tense vesicles and bullae in normal-appearing skin or over erythematous or urticarial plaques.[1]
DPP4-I withdrawal combined with firstline treatment results in complete clinical response in almost all patients
DPP4-I - Dipeptidyl peptidase-4 inhibitor; BP – bullous pemphigoid, SD – standard deviation; PO – per oral case-controlled cohort study found linagliptin to be significantly associated with BP, to a lower extent than vildagliptin.[5]
Summary
Bullous pemphigoid (BP) is an autoimmune disease characterized by subepidermal blisters and autoantibodies against hemidesmosomal proteins of the basement membrane, BP 180 and BP 230.1 It predominantly affects the elderly and typically presents as tense vesicles and bullae in normal-appearing skin or over erythematous or urticarial plaques.[1]. A 73-year-old woman with a history of diabetes mellitus II and hypertension presented for evaluation of intermittent blisters. She reported the lesions appeared mostly on her scalp, mouth, upper chest, arms, and, occasionally, on her legs (Figure 1). Drug-induced bullous pemphigoid associated with either linagliptin or ramipril was suspected. Fluocinonide gel twice a day to mucosal lesions. She had full resolution of her lesions and pruritus at her five-week follow-up, with no recurrence. Had the lesions not resolved past four months, after allowing sufficient time for IgG antibodies to decay, discontinuation of the ACE inhibitor would have been attempted
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