ESPE Abstracts (2014) 82 P-D-1-2-38

ESPE2014 Poster Presentations Bone (12 abstracts)

Increased Rates of Infantile Hypercalcaemia Following Guidelines for Antenatal Vitamin D3 Supplementation

Lisa A Amato a, , Kristen A Neville a, , Shihab Hameed a, , Wei Shern Quek b , Charles F Verge a, , Helen J Woodhead a, , Chris P White b, , Andrea Rita Horvath c & Jan L Walker a,

aSydney Children’s Hospital, Sydney, New South Wales, Australia; bUniversity of New South Wales, Sydney, New South Wales, Australia; cPrince of Wales Hospital, Randwick, New South Wales, Australia

Background: Consultations for infantile hypercalcaemia have increased at Sydney Children’s 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 2005–2007 (n=1516), 2008–2010 (n=1945), and 2011–2013 (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 4–50), 77% were breast-fed, 54% were symptomatic, and 25% had nephrocalcinosis. Median initial calcium was 3.00 mmol/l (range 2.84–4.03) and phosphate 2.04 mmol/l (1.1–3.33). PTH was not elevated (median 1.0 pmol/l (<0.3–3.1)), urinary calcium:creatinine ratio not suppressed (median 2.3, (0.4–9)), 25OHVitD low–normal (median 44 nmol/l (17–218)) and 1,25(OH)2VitD elevated (median 232 pmol/l (64–720)). In 7/10 infants with data available, treated with LCF for median 95 days (range 25–310), median PTH rose to 17.1 pmol/l ((8.2–49.3), P=0.02) with a trend to lower 25OHVit D (median 23 nmol/l (<10–108), P=0.09) despite continued high-normal calcium levels (median 2.66 mmol/l (2.11–2.75)).

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.

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