Endocrine, metabolic & immune disorders drug targets · 2026
The Liraglutide-Induced Pemphigus Vulgaris: A First Case Report Highlighting Autoimmune Risks of GLP-1 Receptor Agonists.
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Cai Shuning, Zhang Zhenyu, Ding Wei, Zhou Shuting, Qiu Xuemei, Hou Feifei, Wu Chuanji, Shen Zhengzhong, Feng Xiaodong, Jiang Lu
Аннотация
INTRODUCTION: Pemphigus vulgaris (PV) is a rare autoimmune blistering disorder that primarily affects the skin and mucous membranes. Drug-induced pemphigus (DIP) is an uncommon variant that is triggered by certain medications. The introduction of novel hypoglycemic agents, such as glucagon-like peptide-1 receptor agonists (GLP-1RA), has been associated with an increase in drug-induced bullous diseases. However, reports of pemphigus induced by these agents remain exceedingly rare.
CASE PRESENTATION: We report the first case of liraglutide-induced PV in a 40-year-old female patient with type 2 diabetes mellitus. The patient developed erosive lesions on the palatal and buccal mucosa three months after initiating liraglutide therapy. Histopathological examination confirmed the diagnosis of PV. The temporal association with liraglutide use, combined with positive results from in vitro gamma-interferon release assays, supports the diagnosis of DIP. The patient showed partial remission after liraglutide discontinuation and topical glucocorticoid therapy, but lesions recurred when liraglutide was reintroduced.
CONCLUSION: The precise mechanism behind liraglutide-induced pemphigus is not yet fully understood. Potential mechanisms include interference with immune modulation or direct effects on keratinocytes. This case underscores the importance of careful monitoring for autoimmune reactions in patients treated with GLP-1RAs and highlights the need for further research into the underlying mechanisms and management strategies for DIP.
CASE PRESENTATION: We report the first case of liraglutide-induced PV in a 40-year-old female patient with type 2 diabetes mellitus. The patient developed erosive lesions on the palatal and buccal mucosa three months after initiating liraglutide therapy. Histopathological examination confirmed the diagnosis of PV. The temporal association with liraglutide use, combined with positive results from in vitro gamma-interferon release assays, supports the diagnosis of DIP. The patient showed partial remission after liraglutide discontinuation and topical glucocorticoid therapy, but lesions recurred when liraglutide was reintroduced.
CONCLUSION: The precise mechanism behind liraglutide-induced pemphigus is not yet fully understood. Potential mechanisms include interference with immune modulation or direct effects on keratinocytes. This case underscores the importance of careful monitoring for autoimmune reactions in patients treated with GLP-1RAs and highlights the need for further research into the underlying mechanisms and management strategies for DIP.