Endocrine Abstracts

Primary hyperparathyroidism is a common cause of hypercalcaemia increasing in prevalence with age peaking in females at 70-90 years of age (492 cases/100,000 population) and in males above 80 years of age (264 cases/100,000 population). Immobilisation hypercalcaemia is regarded as an uncommon non-parathyroid hormone dependent cause of hypercalcaemia typically occurring in young patients with spinal cord injuries and neuromuscular disorders. It is of complex physical and molecular aetiology with increased osteoclast activity predominating over osteoblast activity resulting in bone loss and hypercalcaemia. When superimposed on primary hyperparathyroidism confusion as to the aetiology of the hypercalcaemia can occur.

Case studies: We describe the cases of two elderly females (92 years of age case 1 and 77 years of age case 2) with known ‘asymptomatic’ primary hyperparathyroidism. Both were independently living prior to hospitalisation with recent falls. Both had acute kidney injury and biochemical evidence of mild primary hyperparathyroidism. Following admission they were immobile due to the sustained soft tissue injuries and calcium levels significantly increased despite a fall in parathyroid hormone levels. Beta-cross laps were raised in both and case 1 had vitamin D deficiency. Both developed delirium prolonging their immobilisation. Case 1 was initially treated with cinacalcet which was ineffective. Treatment with intravenous pamidronate lowered calcium levels with a rise in PTH levels and resolution of delirium and acute kidney injury. Mobilisation maintained calcium at ‘asymptomatic’ pre-admission levels.

Discussion: Despite the high prevalence of the falls, immobilisation and hyperparathyroidism triad in the elderly there is a paucity of cases reporting hypercalcaemia. The commonest reported causes of hypercalcemia in the elderly being primary hyperparathyroidism and malignancy. Hypercalcaemia causes neurological, muscular and psychiatric symptoms in the elderly at a lower level than in younger patients which may contribute to falls. In the patients we describe it is possible that the hypercalcaemia contributed to the falls with consequent immobilisation and rapid rise in calcium resulting in delirium which delayed their rehabilitation.

Conclusion: 1) Immobilisation should be considered in the differential diagnosis of hypercalcaemia in elderly patients particularly those with primary hyperparathyroidism. 2) ‘Asymptomatic’ primary hyperparathyroidism may have subtle neuromuscular and psychiatric effects contributing to falls risk. 3) The threshold for treatment of hypercalcaemia in the elderly should possibly be lower than in younger patients.