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Endocrine Abstracts (2024) 100 P15 | DOI: 10.1530/endoabs.100.P15

1West Hertfordshire Teaching Hospitals NHS Trust, Watford, United Kingdom; 2Imperial College Healthcare NHS Trust, London, United Kingdom


Case history: We present the case of a 59-year-old gentleman admitted to our hospital in February 2023 with severe hypercalcaemia. He had a background of mild intermittent hypercalcaemia since 2018 (highest 2.73 mmol/l), chronic kidney disease, hypertension, and a recently climbing prostate-specific antigen that had warranted a 2-week-wait Urology referral. On admission, his only symptom was constipation, without weight loss or constitutional symptoms. His parathyroid hormone (PTH) level was inappropriately high at 17.9 pmol/l with adjusted serum calcium of 3.43 mmol/l, 25-hydroxyvitamin D was 51 nmol/l. He was started on intravenous fluids and cinacalcet for hypercalcaemia presumed secondary to primary hyperparathyroidism. However, his chest X-ray (CXR) revealed bulky bilateral hilar lymphadenopathy. His calcium levels improved with this treatment, and he was discharged on cinacalcet with outpatient endocrinology follow up. He subsequently required re-admission on four separate occasions between March and July 2023 with hypercalcaemia.

Investigations: During this time, he had an ultrasound of his neck and technetium-99 m sestamibi scan which confirmed a right inferior parathyroid adenoma. In view of the hilar lymphadenopathy found on CXR, computed tomography was arranged and revealed extensive symmetrical mediastinal and hilar lymphadenopathy, peribronchial nodules and splenomegaly, raising the possibility of sarcoidosis or lymphoma. His endobronchial ultrasound-guided biopsy showed non-necrotising granulomas consistent with sarcoidosis. He had magnetic resonance imaging and biopsy of his prostate which confirmed low grade adenocarcinoma. No skeletal metastases were found on his bone isotope scan, thus excluding this as a contributor to his hypercalcaemia.

Results and treatment: He was initially treated with intravenous fluids, bisphosphonates and cinacalcet with short-lived improvement in his calcium levels. On confirmation of his diagnosis of sarcoidosis, he was commenced on a weaning regime of oral prednisolone. He underwent a right superior and inferior parathyroidectomy in August 2023, with excellent response in his PTH levels postoperatively. However, he developed recurrent severe hypercalcaemia shortly after and oral steroids were restarted, with subsequent normalisation in his calcium levels since. He currently remains under both respiratory and endocrine follow up and under active surveillance for prostate cancer.

Conclusion and points for discussion: The outcome raises the question to what extent, in hindsight, the parathyroid surgery was necessary. Our case illustrates that PTH-dependent hypercalcaemia can present concomitantly with multiple PTH-independent causes. In such instances, it can be difficult to establish the main driver for the symptoms and a systematic approach to addressing each aetiology is key to achieving a successful outcome.

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