Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2021) 74 NCC49 | DOI: 10.1530/endoabs.74.NCC49

SFENCC2021 Abstracts Highlighted Cases (71 abstracts)

Diagnostic and management challenges in a case of aggressive PTH-dependent hypercalcaemia associated with malignancy

Nwe Aung , Victoria Stokes & Chitrabhanu Ballav

0Stoke Mandeville Hospital NHS Trust, Aylesbury, United Kingdom

A 76 years old previously healthy gentleman presented with severe hypercalcaemia (5.19 mmol/l;, 2.1–2.55) and raised Parathyroid Hormone (PTH, 37 pmol/l, 1.6–7.2) after a three weeks history of confusion, diarrhoea, and weight loss. There were no other focal symptoms and family history was not significant. Other significant findings included mild recent hyponatraemia (132 mmol/l;, 136–145), acute kidney injury (urea 16.1 mmol/l, 3.2–7.4, creatinine 177 umol/l, 63–111), low vitamin D (30.1 nmol/l, 80–150), high CRP (39 mg/l, 0–5), and normal Thyroid Stimulating Hormone (1.96 mIU/l, 0.35–4.94). An ultrasound scan was unable to localise a parathyroid lesion, while high resolution CT scan of the neck showed a 2 cm poorly defined lesion adjacent to the right lobe of the thyroid. A CT scan of the chest, abdomen and pelvis showed three sub-centimetre nodules in the lungs and multiple lesions, including one 7.7 cm exophytic heterogenous lesion in the liver. Histology of one of the liver lesions demonstrated poorly differentiated adenocarcinoma. Immunohistochemistry staining showed high index of Ki67 with multiple mitotic figures, positivity for AE1/3, and weak staining for TTF-1. Significantly the tissue did not stain for chromogranin A, synaptophysin, and CD 56. Blood DNA analysis for CDC73, Menin, and RET was requested and results are awaited. The hypercalcaemia was refractory to treatment with intravenous hydration and bisphosphonates. The PTH increased within days from 37 to 96.5 pmol/l and liver function tests became markedly abnormal which was attributed to the burden of hepatic disease. The patient deteriorated rapidly requiring intensive care admission for intubation and ventilation. He had haemofiltration to treat his hypercalcaemia and renal impairment and required inotropic support for hypotension. He continued to decline and died before our investigations could be completed and definitive management instigated. In conclusion we describe a patient with terminal aggressive PTH dependant hypercalcaemia of uncertain aetiology. Differential diagnoses include metastatic parathyroid carcinoma or ectopic PTH secretion from another primary, such as a hepatocellular carcinoma. Parathyroid carcinomas typically follow an indolent course with the cause of death usually attributable to hypercalcaemia rather than tumour burden. This case is remarkable for the speed at which the patient deteriorated, despite his hypercalcaemia being adequately treated by haemofiltration. The absence of staining for chromogranin A on histology is also unusual for parathyroid carcinoma and raises the possibility of a diagnosis of ectopic PTH secretion from another primary.

Volume 74

Society for Endocrinology National Clinical Cases 2021

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