Endocrine Abstracts

Introduction: PNETs are rare with an annual incidence of 5 per million population. 75 % of pancreatic NET are functioning, PTHrP secretion regarded as a rarer entity and few case reports have been identified worldwide. Surgical resection is definitive management, however SSA treatment and Peptide Receptor Radionuclide Therapy (PRRT) have shown promising results in reducing PTHrP secretion.

Case report: Here we describe a 61 years old lady who presented with cough and clinical and features of hypercalcaemia in 2016. Biochemical evaluation revealed elevated calcium levels (2.85 mmol/l), Suppressed PTH level (0.8 pmol/l) with normal vitamin D level (59 nmol/l) and high Chromogranin A levels (49.7 nmol) with fully suppressed PTH, PTHrP was measured and found to be elevated (2.2 pmol/l, normal range 0-1.8). Radiological evaluation with CT and NM octreotide scan confirmed the presence of large pancreatic tail invasive mass measuring 8 cm with multiple Liver, splenic metastasis. USS guided biopsy confirmed ENETS grade 2 NET with Ki 67 index of 7%. She was treated with (PRRT-Lutathera™) and tumour size was reduced on follow up imaging. She discontinued her depot analogue and switched to sc octreotide with normalization of calcium level. She was plagued by side effects including day time somnolence, insomnia and mood changes on the analogue and discontinued it. She developed marked hypercalcaemia and rapid bilateral hip osteoarthrosis. She has declined re-trial with analogue therapy. Currently she is managed IV Zoledronic acid treatment for hypercalcaemia and awaits bilateral hip replacements. Current imaging is stable. National assay shortage issues have meant repeat PTHrP levels have not been possible, calcium levels have been the marker for this.

Conclusion: We report a novel case of PTHrpoma with uncontrolled hypercalcaemia and accelerated osteoarthosis with intolerance to SSA therapy. Previous biomedical studies have reported an association between PTH deficiency and the risk of OA. The function and regulation of PTHrP in OA cartilage are still poorly understood and it is unclear if loss of PTHrP hormonal control accelerates OA.