Erratum to Acute β-cell failure induced by selpercatinib in RET fusion–positive non-small cell lung cancer: A case report [Respir. Med. Case Rep. 59 (2026) 102372]

Background Selpercatinib, a highly selective RET tyrosine kinase inhibitor, has demonstrated remarkable efficacy in patients with RET fusion–positive non-small cell lung cancer (NSCLC). The underlying mechanisms of rare metabolic adverse events such as hyperglycemia remain poorly understood. Case presentation A 66-year-old man with type 2 diabetes mellitus (baseline HbA1c: 6.7%) and stage IVB, KIF5B–RET fusion–positive lung adenocarcinoma commenced selpercatinib 320 mg once daily. On day 30, he developed grade 3 hepatotoxicity, prompting a 24-day treatment interruption; therapy was restarted at 160 mg/day. Twenty days after reinitiation, he experienced polydipsia and polyuria. Laboratory evaluation revealed random plasma glucose of 556 mg/dL, HbA1c 11.1 %, and serum C-peptide 0.5 ng/mL. Adrenocorticotropic hormone and cortisol levels were within reference ranges, and he tested negative for anti–glutamic acid decarboxylase antibodies. A glucagon stimulation test demonstrated a blunted C-peptide response, confirming profound insulin secretory failure. Intensive insulin therapy rapidly normalized glycaemia, allowing selpercatinib to be resumed at 240 mg/day with ongoing tumor control. Conclusion This case suggests that selpercatinib may precipitate acute β-cell failure, potentially through off-target inhibition of fibroblast growth factor receptors. Regular monitoring of plasma glucose and C-peptide concentrations should be considered, particularly in patients with preexisting diabetes treated with selpercatinib.