De Novo Hypercalcaemia in a Patient With Chronic Hypoparathyroidism

Calcium Homeostasis in the human body is regulated by hormones, including parathyroid hormone and vitamin D3. Dysfunction in the form of hypoparathyroidism causes hypocalcaemia. In patients treated for primary hypoparathyroidism with activated vitamin D replacement, iatrogenic hypercalcaemia can occur. This must be investigated to exclude other aetiologies, such as malignancy and granulomatous disease. In this case report, we describe a 73-year-old man with a distant history of chronic hypoparathyroidism treated with vitamin D3 who presented with lethargy, confusion, polyuria, and polydipsia. On admission, he was found to be hypercalcaemic at 3.22 mmol/L. He presented on two previous occasions with symptomatic hypocalcaemia that resulted in a reduction and subsequent cessation of his vitamin D supplementation. This hypercalcaemia persisted, prompting investigations of non-iatrogenic causes. Computer tomography (CT) and positron emission tomography (PET) scans showed bilateral hilar lymphadenopathy and ruled out malignancy. Serum angiotensin-converting enzyme was three times the normal range while calcitriol levels were inappropriately raised, suggesting sarcoidosis as the likely aetiology of the hypercalcaemia. The patient was very responsive to steroid therapy, with serum calcium dropping to normal levels over a four-week admission. The patient developed hypocalcaemia within weeks of discharge, eventually requiring the recommencement of his vitamin D replacement, which has been titrated to maintain normal serum calcium levels. This case highlights a rare occurrence of two infiltrative disorders with simultaneous differential adverse effects on calcium metabolism, leading to a series of acute hospitalisations often alternating between severe hypocalcaemia or severe hypercalcaemia.