Endocrine Abstracts

Section 1: Case history: A 78 years old lady presented to Emergency Department with two weeks history of lethargy and confusion. She had background of advanced destructive Rheumatoid Arthritis diagnosed 30 years ago, multiple joint fractures, osteoporosis, long-term urinary catheter, recurrent UTI and renal calculi. She was recently discharged from hospital for urosepsis. She was bed-bound for the last 15 years after crushing vertebrae C2 C3 pressing on spinal cord. Her regular medicines included gabapentin, methenamine, senna and paracetamol. On admission, her observations and physical examination were unremarkable apart from features of long-standing rheumatoid arthritis.

Section 2: Investigations: Her biochemical profile on admission revealed marked hypercalcaemia with adjusted Calcium 3.88 mmol/l (2.20–2.60), phosphate 1.2 mmol/l (0.65–1.50) ALP 162 U/l (40–150), 25 OH Vitamin D 87 nmol/l (70–150), PTH 0.8 pmol/l (1.6–7.2), TSH 3.13 mU/l; (0.30–4.20), Free T4 12.3 pmol/l (7.0–17.0), urea 6.4 mmol/l (2.5–7.8). Myeloma screen and urine MSU were negative, ACE levels were <12 U/l. CT TAP did not reveal any evidence of malignancy. No clear cause for hypercalcaemia was identified after these investigations apart from prolong immobilisation.

Section 3: Results and treatment: Aggressive IV fluid replacement was commenced with close monitoring of calcium levels. Later on, intravenous pamidronate was added which resolved hypercalcaemia and she improved clinically. She was assessed by physiotherapy but had no rehabilitation potential and needed hoist transfers. She was discharged home with routine electrolyte monitoring as outpatient.

Section 4: Conclusion and points for discussion: Hypercalcemia is a common metabolic disorder in hospitalised patients. The common causes of inpatient hypercalcaemia are primary hyperparathyroidism and malignancy. Immobilisation hypercalcaemia is among the rare causes but its diagnosis requires an exhaustive evaluation to rule out common causes first. Prolong immobilisation stimulates osteoclastic bone resorption, osteopenia, osteoporosis and bone remodelling disorders. This induces resorptive hypercalciuria and suppression of the parathyroid 1,25-vitamin D axis. If untreated, patients may develop dehydration, personality changes, calcium oxalate nephrolithiasis and renal failure. Treatment is aimed at early mobilisation, hydration, and restoration of the balance between calcium excretion and resorption with a gradual bone metabolism reduction. Bisphosphonates and denosumab are also beneficial. Our patient was a difficult case as she developed severe hypercalcaemia and no obvious cause was identified. It was only when other causes of hypercalcaemia were ruled out and further investigations confirmed unexplained hypercalcaemia. Timely treatment of hypercalcaemia is a critical step for rapidly control of symptoms.