This child has subcutaneous fat necrosis of the cheeks. Subcutaneous fat necrosis leads to endogenous production of 1,25 dihydroxy Vitamin D which may lead to increased calcium absorption from the intestine and hypercalcemia. Hypercalcemia can lead to failure to thrive, vomiting, polyuria, and polydipsia. Subcutaneous fat necrosis can occur commonly following birth asphyxia. The increased 1,25 (OH) Vitamin D3 levels lead to secondary hypoparathyroidism (hypercalcemia suppresses the parathyroid hormone). The treatment, in this case, would be to increase calcium excretion in the urine by hydration and furosemide; decrease calcium absorption from intestines by giving steroids (steroids are useful in only hypercalcemia due to Vitamin D overdose or excess production) and bisphosphonate therapy (IV Pamidronate).
Calcitonin may be tried in severe acute hypercalcemia to decrease the level of active calcium in the blood. In this child 25 hydroxy Vitamin D levels were normal, parathyroid hormone levels were low and 1, 25 dihydroxy Vitamin D3 levels were elevated suggestive of endogenous Vitamin D production.
