Background: Consultations for infantile hypercalcaemia have increased at Sydney Childrens Hospital since guidelines for vitamin D3 supplementation during pregnancy were introduced in 2006. Recent nationwide shortages of low-calcium formula (LCF) suggest this problem may be widespread.
Aim: To determine if infantile hypercalcaemia is occurring more commonly, identify potential aetiologies and clinical significance.
Methods: De-identified, first-measured serum calcium from all infants <6 months (n=5796) measured in our laboratory, were grouped by years 20052007 (n=1516), 20082010 (n=1945), and 20112013 (n=2335). We analysed 13 infants treated by our department for idiopathic infantile hypercalcaemia (IIH) from 2011 to 2013.
Results: Rates of hypercalcaemia (>2.75 mmol/l) increased from 2011 (1.1 vs 1.3 vs 8.7%, χ2 P<0.001). Rates of hypocalcaemia (<2.25 mmol/l) fell steadily (42.4 vs 32.3 vs 24.8%, χ2 P<0.001). Twelve mothers of our 13 infants with IIH received antenatal vitamin D3 supplementation. One infant also received 400 units/day Vitamin D3 postnatally. At diagnosis, median age was 13 days (range 450), 77% were breast-fed, 54% were symptomatic, and 25% had nephrocalcinosis. Median initial calcium was 3.00 mmol/l (range 2.844.03) and phosphate 2.04 mmol/l (1.13.33). PTH was not elevated (median 1.0 pmol/l (<0.33.1)), urinary calcium:creatinine ratio not suppressed (median 2.3, (0.49)), 25OHVitD lownormal (median 44 nmol/l (17218)) and 1,25(OH)2VitD elevated (median 232 pmol/l (64720)). In 7/10 infants with data available, treated with LCF for median 95 days (range 25310), median PTH rose to 17.1 pmol/l ((8.249.3), P=0.02) with a trend to lower 25OHVit D (median 23 nmol/l (<10108), P=0.09) despite continued high-normal calcium levels (median 2.66 mmol/l (2.112.75)).
Conclusion: IIH was associated with significant morbidity. Concurrent changes in rates of hyper and hypo-calcaemia suggest antenatal vitamin D3 supplementation as an aetiological factor. Our patients biochemistry raises variations in vitamin D metabolism or calcium set-point as potential associated factors. Monitoring treatment with LCF should not be based on calcaemia alone.
20 - 22 Sep 2014
European Society for Paediatric Endocrinology