Dupilumab-related type 1 diabetes in a patient with atopic dermatitis: a case report.
Adolescent
Autoimmune disease
Dupilumab
Human leukocyte antigen
Type 1 diabetes
Journal
Diabetology international
ISSN: 2190-1678
Titre abrégé: Diabetol Int
Pays: Japan
ID NLM: 101553224
Informations de publication
Date de publication:
Jan 2022
Jan 2022
Historique:
received:
20
05
2021
accepted:
27
07
2021
entrez:
21
1
2022
pubmed:
22
1
2022
medline:
22
1
2022
Statut:
epublish
Résumé
Dupilumab, a humanized monoclonal antibody that inhibits both interleukin (IL)-4 and IL-13 signals, is used as a treatment for a variety of allergic diseases including atopic dermatitis. We experienced a case of dupilumab-related type 1 diabetes in a patient with atopic dermatitis. An 18-year-old female presented with thirst and polydipsia seven months after initiating dupilumab therapy for atopic dermatitis and was found to have marked hyperglycemia with ketosis. She was positive for anti-glutamic acid decarboxylase antibody, leading to the diagnosis of type 1 diabetes. She carried human leukocyte antigen (HLA) genes associated with type 1 diabetes. Most type 1 diabetes is considered a T-helper (Th) 1 type autoimmune disease, whereas IL-4 and IL-13, which are Th2 cytokines, play inhibitory roles in the pathogenesis of type 1 diabetes. This case implies that dupilumab might contribute to the development of type 1 diabetes in individuals with a genetic background of type 1 diabetes via relative Th1 dominance. To our knowledge, this is the first case of the development of type 1 diabetes during dupilumab therapy. As dupilumab therapy might accelerate the development of type 1 diabetes, it is important to note cases like this case to clarify the pathogenic mechanisms underlying dupilumab-related type 1 diabetes.
Identifiants
pubmed: 35059267
doi: 10.1007/s13340-021-00526-1
pii: 526
pmc: PMC8733041
doi:
Types de publication
Case Reports
Langues
eng
Pagination
300-303Informations de copyright
© The Japan Diabetes Society 2021.
Déclaration de conflit d'intérêts
Conflict of interest A.S. received lecture fees from Novo Nordisk Pharma Ltd., Tokyo, Japan, and Sanofi K.K., Tokyo, Japan. Other authors have no potential conflicts of interest relevant to this article.
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