Endocrine Abstracts

Background: Immobility can be associated with severe hypercalcaemia, especially when compounded by other risk factors such as concurrent hyperthyroidism and high dietary calcium/milk intake and associated complications such as renal stones and fractures.

Clinical case: 59y female presented acutely with confusion, vomiting, constipation and muscle weakness. She had history of obesity, stable Crohn’s disease with no recent increase in colonostomy output. Her calcium was high at 4 mmol/l (n-2.2-2.6 mmol/l), PTH low, but not suppressed at 2 pmol/l (n- 1.8-6.8 pmol/l), ALP- 138 U/l (n- 30-130 U/l), bicarbonate- 27.3 mmol/l, pH- 7.375. Screen for myeloma, sarcoid and cancer was negative. FT4 raised at 19 pmol/l (n- 7.7-15.1 pmol/l) and TSH 0.01 mu/l (n- 0.34-5.6 mu/l). CT scan excluded cancer and identified stones in kidneys and bladder and healed pubic ramus fractures suggesting a more insidious onset. She had moderate goitre. No history of lithium, calcium supplements, antacids use. Three months prior to presentation had cCa- 2.78 mmol/l, but not investigated. Dietary enquiry revealed consumption of minimum of 2-3 pints (1.1-1.7l) of semi-skimmed milk per day alongside at least two yogurts and cheddar cheese. This intake was calculated to be at least 1910-1614 mg/daily of calcium [2-3 x 704 mgs of calcium (milk) + 2 x 140 mg (yoghurts) + 222 mg (30g of cheddar cheese)]. Social enquiry revealed she has been completely bedbound for eight months due to severe knee osteoarthritis and malunion ulna fracture and chronic elbow dislocation impacting her ability to use walking aids. Patient responded to IV hydration and pamidronate infusion. Treatment with carbimazole was commenced and reduced calcium intake was advised. She was referred for urgent ulna reunion surgery followed by knee surgery. Her calcium reduced to 2.86 mmol/l and subsequently to 2.68 mmol/l during follow up. Her thyroid function normalised.

Conclusion: Our patient had hypercalcaemia of immobility, hyperthyroidism and milk alkali syndrome. It is important to be aware of these rarer causes (even in patients not obviously suffering paralysis from a spinal cord injury or a stroke) when alternative diagnoses have been excluded and explore them in detail at presentation. Immobilisation affects balance between bone formation and resorption by increased sclerostin secretion by osteocytes, which diminishes the bone formation stimuli by blocking the Wnt-Runx2 pathway in the osteoblast. This was paired with increased bone turn over from hyperthyroidism, oral calcium load and diminished renal calcium excretion from milk alkali syndrome.