Case report: Glycemic instability despite fasting C-peptide recovery during sequential somatostatin receptor ligand therapy in acromegaly with diabetes

Background Somatostatin receptor ligands (SRLs) may improve glucose metabolism by reducing growth hormone excess, but they can also suppress insulin secretion. Severe hyperglycemia is well recognized with pasireotide. Less is known about glycemic stability after recovery from severe decompensation and during later changes in SRL therapy. Case presentation A 32-year-old woman with diabetes had persistent acromegaly despite transsphenoidal surgery, Gamma Knife radiosurgery, cabergoline, octreotide, and lanreotide. Pasireotide long-acting release 40 mg lowered growth hormone and insulin-like growth factor 1, but approximately 1 month later was followed by diabetic ketoacidosis and a fasting C-peptide of 0.38 ng/mL. Pasireotide was stopped, insulin-based treatment was given, and octreotide was resumed. Fasting C-peptide increased to 3.09 ng/mL within 2 months. During lanreotide re-exposure in 2025, HbA1c was 9.3% despite fasting C-peptide within the reference interval and no parallel deterioration in biochemical disease control. After lanreotide withdrawal and adjustment of diabetes therapy, intermittent hyperglycemia continued, although HbA1c decreased to 6.3% by July 2026. Conclusions Return of fasting C-peptide into the reference interval after pasireotide-associated diabetic ketoacidosis did not predict sustained glycemic stability in this patient. The later deterioration during lanreotide therapy was temporally associated with treatment but does not establish causality. The overall course is more consistent with persistent metabolic vulnerability despite normalization of fasting C-peptide than with confirmed recurrent SRL-induced dysglycemia. Glucose monitoring should be intensified when an SRL is started or changed in patients with diabetes or previous ketosis.