Endocrine Abstracts

We present the case of a 69-year-old male with a rare progression of neuroendocrine tumor, initially presenting with hypoglycemia and ultimately leading to multi-organ failure. The patient, an ex-smoker with a history of alcohol use (80 units/month), was incidentally found to have a solid lesion in the pancreatic tail on CT during lung cancer screening. Referred to hepatobiliary team and underwent a distal pancreatectomy. Histology confirmed a well-differentiated neuroendocrine tumor, WHO stage 2, with a Ki-67 index of 10% and no secretory activity. Postoperative imaging showed no residual disease, and the patient recovered well, later developing type 2 diabetes, managed with metformin. Approximately six months post-surgery, the patient presented with hypoglycaemic collapse (blood glucose 1.7 mmol/l). Repeat imaging revealed recurrence in the pancreas and new hepatic lesions. MRI and biopsy confirmed recurrence of well differentiated neuroendocrine tumor with gross hepatic metastasis. Biochemical analysis showed a marked elevated C-peptide (3190 pmol/l) with paired serum glucose of 1.7mmol/l, corresponding with severe, refractory hypoglycaemia requiring continuous dextrose 20% infusion, diazoxide, and octreotide. Surgical intervention was not feasible due to metastatic disease. peptide receptor radionuclide therapy was considered keeping in view non-surgical neuroendocrine tumor but the patient succumbed to sepsis secondary to hospital-acquired infection. This case underscores the rare progression of a non-secretory neuroendocrine tumor into a secretory phenotype, a phenomenon not widely documented. It highlights the importance of ongoing surveillance for functional transformation in neuroendocrine tumors, even after initial presentation as non-secretory, and the significant challenges posed in managing metastatic insulinomas with high hypoglycaemic burden.