Endocrine Abstracts (2002) 3 P126

Treatment options for refractory hypercalcaemia in a patient with PTHrP-secreting neuroendocrine tumour and primary hyperparathyroidism

MT Barakat1, A Hameed1, C Goodlad1, P Tait2, K Meeran1, JK Howard1 & GR Williams1

1Imperial College School of Medicine Endocrine Unit, Hammersmith Hospital, London, UK; 2Department of Radiology, Hammersmith Hospital, London, UK.

A 47 year-old woman was referred with hypercalcaemia. She was receiving lithium, haloperidol and olanzapine for a schizo-affective disorder. Five years previously she had been diagnosed with liver metastases and a biopsy confirmed a neuroendocrine tumour. She had been told that her life-expectancy was limited, and she was discharged. Her calcium was 2.7mmol/l three years ago. At presentation to her local hospital, her calcium was >6.0mmol/l. She was treated aggressively with intravenous fluids and pamidronate, and following transfer, her corrected calcium was 3.51mmol/l with a phosphate of 0.75mmol/l. Primary hyperparathyroidism was suspected, and the serum PTH concentration was 3.1pmol/l, inappropriately within the normal range (1.1-6.8). However, given the diagnosis of metastatic neuroendocrine tumour, serum PTHrP was also measured and found to be markedly elevated at 5.2pmol/l (0.7-1.8), suggesting the presence of coexisting primary hyperparathyroidism and PTHrP-secreting neuroendocrine tumour as the cause of her hypercalcaemia. Abnormal uptake in the mediastinum was demonstrated by Sestamibi scanning, whereas an octreotide scan showed abnormal uptake in the liver corresponding to hepatic metastases. Venous sampling for PTH and PTHrP suggested that PTHrP production originated from the liver metastases and not the mediastinum. Despite repeated intravenous pamidronate and continuous intravenous fluids, the serum corrected calcium concentration continued to rise to 5.0mmol/l and there was no improvement following subcutaneous octreotide administration. Hepatic embolisation, was performed with some improvement of her serum calcium concentration (3.0-3.5mmol/l) and a second embolisation was performed. Since then she has continued on subcutaneous octreotide and lanreotide, has been treated with alendronate and is currently independent of intravenous fluids. Her calcium has stabilised at 2.8mmol/l. Her serum PTHrP concentration is awaited post-embolisation, and interestingly, her PTH concentration has remained between 3-4pmol/l. Although she remains hypercalcaemic, hepatic embolisation has significantly ameliorated her hypercalcaemia, and is a safe and effective treatment in patients with hepatic metastases.

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