Endocrine Abstracts (2015) 38 P159 | DOI: 10.1530/endoabs.38.P159

Use of Sunitinib in refractory hypercalcaemia in pancreatic neuroendocrine tumours

Ladan Akbarian-Tefaghi1, Jonathan Wadsley3, John Newell-Price1,2 & Alia Munir2


1University of Sheffield, Medical School, Sheffield, UK; 2Royal Hallamshire Hospital, STH NHS Foundation Trust, Sheffield, UK; 3Weston Park Hospital STH NHS Foundation Trust, Sheffield, UK.


: The orally administered targeted therapies, Sunitinib and Everolimus lengthen progression free survival in pancreatic neuroendocrine tumours (pNETs). Choice of therapy has traditionally been on avoidance of deterioration in established co-morbidities. Sunitinib has been recognised to induce hypocalcaemia and the subsequent need for calcium supplementation has been reported. However, little has been documented about the utility and therapeutic significance of this effect.

Case 1: A 45 year old lady presented with acute appendicitis and was found to have an incidental cystic pancreatic lesion, vascular liver metastases and lung metastases, pNET was confirmed. She was commenced on Lanreotide Autogel 120 mg deep sc injection monthly. Surveillance proved further progression and her corrected calcium (cCa) was 4.18 mmol/l, PTH 6.0 (NR 20–75 ng/l), PTH-rp <0.7 pmol/l (NR 0–1.8 pmol/l). Conventional treatment for hypercalcaemia failed and initiation of Sunitinib stabilised disease progression and rendered the cCa normal at 2.3mmol/l.

Case 2: An 81 year male presented with hypercalcaemia and a radiological diagnosis of pancreatic adenocarcinoma was made in 2004. Following splenectomy and distal pancreatectomy, histology confirmed pNET with a ki67 of 15%. Subsequent surveillance imaging confirmed liver and peritoneal metastases with recurrence in the tail of the pancreas. Sandostatin LAR 30 mg IM was commenced 4 weekly. The cCa was 3.24 falling to 2.5 mmol/l within 2 weeks of Sunitinib. Dose reduction from 37.5 mg to 25 mg has been made with success.

Case 3: A 73 year old male presented with hypercalcaemia. Staging CT and liver biopsy confirmed pNET. Pre-treatment cCa was 3.3 mmol/l but despite Everolimus this remained elevated at 3.34 mmol/l. Disease progression and diabetes mellitus has ensued. Sunitinib is due to be commenced and we would anticipate a calcium reduction.

Conclusion: Sunitinib induced hypocalcaemia could be given high consideration when refractory hypercalcaemia in progressive pNETs is a dominant feature of the disease.

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