Case Report: Tislelizumab-induced delayed-onset diabetic ketoacidosis and hypothyroidism in esophageal adenocarcinoma
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Le résumé fourni par la source
Immune checkpoint inhibitor-related diabetes ketoacidosis (ICI-DKA) and hypothyroidism are rare but serious adverse events of Anti-programmed cell death-1 (anti-PD-1) therapy, previously unreported in patients with EAC receiving tislelizumab. A 53-year-old man with well-controlled type 2 diabetes and human epidermal growth factor receptor 2 (HER2)-positive metastatic EAC completed 8 cycles of tislelizumab combined with trastuzumab and capecitabine-oxaliplatin (XELOX) chemotherapy, achieving a partial response. Eleven months after the last tislelizumab dose, he presented with fatigue and was diagnosed with DKA and hypothyroidism. Laboratory testing revealed severe insulin deficiency and negative diabetes-related autoantibodies. This was the first reported case of tislelizumab-induced concurrent DKA and hypothyroidism in an EAC patient. This case demonstrates the potential for severe, delayed-onset endocrine toxicity with tislelizumab, even in patients with pre-existing diabetes. It underscores the necessity for extended monitoring of glucose, C-peptide, and thyroid function beyond active therapy in programmed cell death protein 1 (PD-1) inhibitor recipients to mitigate life-threatening complications like ICI-DKA. Given the expanding global use of tislelizumab for EAC and the life-threatening nature of ICI-DKA, this case provides critical safety evidence necessitating urgent protocol revisions for long-term endocrine monitoring.
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Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- Case Report: Tislelizumab-induced delayed-onset diabetic ketoacidosis and hypothyroidism in esophageal adenocarcinoma
- Date Crossref
- 28/08/2025
- Éditeur
- Frontiers Media SA
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
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