Dabrafenib and trametinib-induced hyperglycemia with decreased insulin secretion in a patient with lung adenocarcinoma.

Hyperglycemia is an adverse effect of targeted cancer therapies; however, the mechanisms underlying B-Raf proto-oncogene, serine/threonine kinase (BRAF)/mitogen-activated protein kinase kinase (MEK) inhibitor-associated hyperglycemia remain unclear. We describe an 80-year-old man who developed severe hyperglycemia during combination therapy with dabrafenib and trametinib for BRAF V600E-positive lung adenocarcinoma. Before treatment, he was obese and had unrecognized mild diabetes. Seven months after treatment initiation, he presented with hyperglycemia accompanied by a reduced insulin secretory capacity. Serial measurements of the C-peptide index revealed that the temporary withdrawal of dabrafenib-trametinib resulted in the recovery of insulin secretion, which gradually decreased again upon reinitiation. This case underscores the clinical importance of monitoring both the glycemic status and insulin secretion in patients receiving BRAF/MEK inhibitors.