Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2011) 25 P22


Immobility: a rare cause of hypercalcaemia

Rebecca Lim1, Emma Lewis2, Shirley Bowles2, Niru Goenka1, Frank Joseph1 & David Ewins1


1Diabetes and Endocrinology Unit, Countess of Chester Hospital NHS Foundation Trust, Chester, UK; 2Department of Blood Sciences, Countess of Chester Hospital NHS Foundation Trust, Chester, UK.

A 57-year-old man with a history of alcohol excess was admitted following a road traffic accident. He suffered multiple trauma with fractures to his left femur, tibia and fibula, his right pubic ramus and several ribs. In addition severe abdominal trauma necessitated nephrectomy and splenectomy. Routine biochemistry and bone profile on admission was within normal limits.

He had a prolonged stay in the Intensive Therapy Unit (ITU) with acute kidney injury and type 2 respiratory failure complicating hospital acquired pneumonia. Two months (64 days) into admission he was noted to have an elevated adjusted calcium of 3.35 mmol/l (2.1–2.7 mmol/l), a low serum phosphate of 0.03 mmol/l (0.8–1.4 mmol/l), alkaline phosphatase of 91 IU/l (40–129 IU/l), albumin 35 g/l (30–49 g/l), and mild renal impairment.

The adjusted calcium levels had progressively increased since admission and PTH was suppressed at 0.5 pmol/l (1.5–6.9) excluding hyperparathyroidism. His thyroid function tests, serum electrophoresis, urine Bence-Jones protein and PTHrP were all normal.

A diagnosis of immobility hypercalcaemia was made and excessive bone resorption confirmed by the presence of increased urinary excretion of pyridinium crosslinks – urine pyridinoline/creatinine ratio 386 nmol/mmol (NR 5–21.8). Following treatment with intravenous fluids and intravenous pamidronate (90 mg) the hypercalcaemia returned to normal within one week and normocalcaemia (and normophosphataemia) was maintained when mobilisation commenced over the next few weeks.

On reviewing the timeline and exclusion of other causes, it would appear the elevated level of hypercalcaemia was related to severe trauma and prolonged immobility. Immobilisation hypercalcaemia was first described by Albright et al. in 1941 and is thought to be due to increased bone resorption. It is an under-recognised cause of hypercalcaemia especially in hospitalised patients with prolonged inactivity. Patients with pre-existent renal dysfunction are at increased risk and it has been associated, as in our patient, with the presence of sepsis.

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