Investigation and Management of Hypercalcaemia in Children
Investigation and Management of Hypercalcaemia in Children
There are many other causes of hypercalcaemia ( Box 2 and Box 3 ) that lead to elevated calcium levels by diverse mechanisms. High plasma T3 levels, observed in thyrotoxicosis, have a direct effect to increase osteoclast activity and cause hypercalcaemia. Hypercalcaemia may occur during acute adrenal insufficiency and is possibly secondary to altered vitamin D synthesis in the setting of glucocorticoid deficiency, and also from volume depletion from mineralocorticoid deficiency. Chronic maternal hypocalcaemia (from untreated or under treated hypoparathyroidism or pseudohypoparathyroidism) may cause secondary fetal hyperparathyroidism from reduced materno-fetal calcium transfer, and subsequent transient neonatal hypercalcaemia, which does not require surgical intervention.
Hypophosphataemia stimulates increased activity of the 1-α hydroxylase enzyme, which is probably mediated by reductions in circulating FGF23. The resultant increased 1,25-dihydroxyvitamin D3 levels cause enhanced calcium absorption from the intestine and hypercalcaemia. Phosphate depletion, from inadequate phosphate supplementation of preterm milk formula can cause hypercalcaemia and metabolic bone disease of prematurity. In older children phosphate depletion may result from insufficient phosphate supplementation in parenteral nutrition and secondary hypercalcaemia.
Miscellaneous Causes of Hypercalcaemia
There are many other causes of hypercalcaemia ( Box 2 and Box 3 ) that lead to elevated calcium levels by diverse mechanisms. High plasma T3 levels, observed in thyrotoxicosis, have a direct effect to increase osteoclast activity and cause hypercalcaemia. Hypercalcaemia may occur during acute adrenal insufficiency and is possibly secondary to altered vitamin D synthesis in the setting of glucocorticoid deficiency, and also from volume depletion from mineralocorticoid deficiency. Chronic maternal hypocalcaemia (from untreated or under treated hypoparathyroidism or pseudohypoparathyroidism) may cause secondary fetal hyperparathyroidism from reduced materno-fetal calcium transfer, and subsequent transient neonatal hypercalcaemia, which does not require surgical intervention.
Hypophosphataemia stimulates increased activity of the 1-α hydroxylase enzyme, which is probably mediated by reductions in circulating FGF23. The resultant increased 1,25-dihydroxyvitamin D3 levels cause enhanced calcium absorption from the intestine and hypercalcaemia. Phosphate depletion, from inadequate phosphate supplementation of preterm milk formula can cause hypercalcaemia and metabolic bone disease of prematurity. In older children phosphate depletion may result from insufficient phosphate supplementation in parenteral nutrition and secondary hypercalcaemia.
