Endocrine Abstracts

A 71 year old gentleman, known to have Renal Cell Carcinoma with metastasis to lung, mediastinum, spine and liver, was transferred to our services for management of T2/T3 Spinal root impingement. On admission he was noted to have severe hypercalcemia of 3.33mmol/l, mild hypophosphatemia 0.8mmol/land an ongoing acute kidney injury. He had appropriate initial management with intravenous fluids, and was started on dexamethasone 8 mg with PPI cover for the spinal metastasis. His imaging was reviewed in the spinal MDT and medical management and radiotherapy was advised. The patient went on to have spinal radio therapy subsequently. The patient was also prescribed Denosumab at admission which he had not yet received due to availability. With the fluids his Calcium levels had appropriately started improving. On day 4 of admission his calcium had reduced to 2.8mmol/l, while his phosphate was 0.7mmol/l. His Parathormone and vitamin D3 levels were not checked. Unfortunately, at this point he went on to receive the Denosumab. On day 10 of admission patient developed symptoms of tingling, numbness and fasciculations. He was found to be profoundly hypocalcaemic at 1.68mmol/lwith characteristic corresponding ECG changes of QTc prolongation. He was then referred to Endocrinology for evaluation, and was managed with multiple Calcium Gluconate infusions, alfacalcidol, and high dose cholecalciferol in Level 2-3 care. He went on to have his Parathormone and vitamin d levels checked, which were 174ng/land 30nmol/lrespectively. His calcium levels normalised and stabilised on day 17, and his Alfacalcidol was stopped. He was switched to maintenance dose Vitamin D and oral calcium replacement. Unfortunately, the patient’s general condition deteriorated significantly during the admission and he passed away. This case demonstrates a classic presentation of Hungry Bone syndrome (HBS) secondary to Denosumab administration on background of low Vitamin D and phosphate levels, post hypercalcemia treatment. It highlights the importance of trying to determine the cause of hypercalcemia during initial resuscitation and ensuring replete vitamin D levels prior to use of bisphosphonates or denosumab, though this might seem counterintuitive. Low prevailing vitamin D, magnesium and phosphate levels while administering these medications can precipitate large calcium shifts from the blood to the bone, hence the term ’Hungry Bone Syndrome’. HBS can cause refractory hypocalcaemia, unnecessarily prolonging hospital stay and has the potential to cause significant change in electrolyte homeostasis.