Prevention and treatment of infant and childhood vitamin D deficiency in Australia and New Zealand: a consensus statement

Craig Munns, Margaret R Zacharin, Christine P Rodda, Jennifer A Batch, Ruth Morley, Noel E Cranswick, Maria E Craig, Wayne S Cutfield, Paul L Hofman, Barry J Taylor, Sonia R Grover, Julie A Pasco, David Burgner and Christopher T Cowell
Med J Aust 2006; 185 (5): 268-272. || doi: 10.5694/j.1326-5377.2006.tb00558.x
Published online: 4 September 2006

Vitamin D deficiency and nutritional rickets are again emerging as major paediatric health issues in Australia and New Zealand.1-5 The major cause is reduced synthesis of vitamin D3, with dark-skinned individuals or those who remain covered when outdoors for cultural reasons being most at risk. In this consensus statement, we review vitamin D metabolism and the risk factors for, and features of, vitamin D deficiency in infants, children and adolescents, and provide recommendations for treatment and subsequent prophylaxis.

Vitamin D sources in Australia and New Zealand

The major source of vitamin D (more than 80%) in Australia and New Zealand is skin exposure to sunlight (UVB radiation).7 Sun exposure also causes 99% of non-melanoma skin cancers and 95% of melanoma in Australia.8 Thus, a balance needs to be struck between sufficient sun exposure to maintain adequate vitamin D3 production and minimising the risk of skin cancer. No Australian or New Zealand paediatric data are available on the duration of UVB radiation exposure required to maintain adequate levels of vitamin D. Despite this, a recent Australian position statement on the risks and benefits of sun exposure advised that babies would receive enough UVB to maintain healthy vitamin D concentrations, even using sun protection, if small amounts of skin were exposed to sunlight for very brief periods before 10:00 and after 16:00 hours.9 Adult data on the duration of sun exposure to hands, arms and face and vitamin D3 production have recently been published.10 Given the different body proportions of children and the reduced capacity to synthesise vitamin D with ageing,11 children would likely require less sun exposure to produce an equivalent amount of vitamin D3 to that of adults. Further, those at greatest risk of vitamin D deficiency in our community — individuals with increased skin pigment — may require up to six times the sun exposure to achieve the same increase in vitamin D concentrations as individuals with light-coloured skin.12 Glass and sunscreen absorb UVB radiation, which decreases vitamin D3 production,13 and may increase the likelihood of vitamin D deficiency,14 especially in individuals with pigmented skin.


An infant’s vitamin D concentration reflects that of the mother.15 If a mother is vitamin D replete, her infant has an 8–12 week store of vitamin D.15 Human milk from vitamin D replete women has a vitamin D concentration of only 25 IU (< 1 μg) per litre.16,17 Most commercial baby formulas in Australia and New Zealand contain 400 IU (10 μg) of vitamin D3 per litre. An intake of 500 mL of baby formula per day therefore provides 200 IU (5 μg) of vitamin D, which is the amount recommended by the American Academy of Pediatrics as an adequate intake for healthy infants and children.18 Milk supplemented with vitamin D3 (up to 200 IU per 250 mL) has recently become available. However, the average daily intake of vitamin D by Australian adults from sources such as oily fish, eggs, and butter or margarine remains at only 50–100 IU (1.2–2.6 μg).7 So, without adequate sun exposure, consumption of vitamin D-fortified milk or vitamin D supplementation, it is difficult for pregnant and lactating mothers, breastfed babies, or children to obtain an adequate daily vitamin D intake from diet alone.

Infants and children at risk of vitamin D deficiency

Current Australian and New Zealand Paediatric Surveillance Unit (APSU and NZPSU) surveys examining the incidence of and risk factors for vitamin D-deficiency rickets will improve our understanding of paediatric vitamin D deficiency. From the current data, risk factors associated with vitamin D deficiency in infants and children can be broken down into three broad areas (Box 1).1-3,5,10,21,25,26 It is likely that multiple factors apply in a single affected individual. For example, recent migrants with a refugee background from Africa and the Middle East are at risk of vitamin D deficiency because of their dark skin, poor nutrition, reduced sunlight exposure and the prolonged breastfeeding of infants.

Features of vitamin D deficiency

Vitamin D deficiency has both osseous and non-osseous sequelae (Box 2). The most recognised are the osseous complications of rickets and osteomalacia. Rickets results from poor osteoid mineralisation adjacent to the growth plate, and osteomalacia from inadequate osteoid mineralisation at sites of bone modelling and remodelling.27 While rickets is only seen during growth, with a peak incidence during the periods of rapid growth in early infancy and early puberty,27 osteomalacia is common to both children and adults.

Non-osseous features of vitamin D deficiency include dilated cardiomegaly28 and marrow fibrosis with pancytopenia or microcytic hypochromic anaemia. Note the co-existence of vitamin D deficiency and iron deficiency.3 Other possible associations include disregulation of immune function and cellular differentiation and proliferation, and type 1 diabetes.23,24,29

Biochemical features of vitamin D deficiency

Vitamin D deficiency results in hypocalcaemia, secondary hyperparathyroidism, hypophosphataemia and elevated alkaline phosphatase titres.3 Many variations on this pattern may be observed, with elevated alkaline phosphatase titres being seen most commonly. Not infrequently, infants with profound hypocalcaemia and secondary hyperparathyroidism have normal or elevated serum phosphate levels, which may represent parathyroid hormone resistance at both the bone and renal level from prolonged vitamin D deficiency.3,30 This can lead to confusion with hypoparathyroidism or pseudohypoparathyroidism, as serum calcium and phosphate concentration results are frequently available before those for vitamin D and parathyroid hormone (PTH).3 Concentrations of calcitriol (1,25-[OH]2D) may be low, normal or high at the time of diagnosis, and are of no value in making the diagnosis.

Recommendations for treating moderate to severe vitamin D deficiency

Both ergocalciferol (25-OHD2) and cholecalciferol (25-OHD3) are effective therapy for vitamin D deficiency, with ergocalciferol being the most widely available preparation (Box 3). Replenishment of vitamin D stores requires a total vitamin D dose of 100 000–500 000 IU, depending on age (Box 3).32 Treatment with calcitriol (1,25-[OH]2D) is only indicated for hypocalcaemia (see below). Calcium supplementation is recommended if dietary intake is poor (Box 4). It should be noted that dietary calcium deficiency is a major risk factor for the development of rickets in Africa, and should be considered in the migrant population.31 If vitamin D deficiency or rickets does not resolve after adequate treatment, the child should be investigated for a malabsorption disorder (eg, coeliac disease) or a genetic rachitic disorder (eg, X-linked hypophosphataemic rickets).

The most serious consequence of vitamin D deficiency is hypocalcaemic seizure. While most common in infants aged less than 6 months, seizures can occur at any age. Bolus intravenous calcium is indicated to treat seizures and carpopedal spasm. A calcium infusion may be required if control is not achieved with 1 to 2 bolus doses (Box 3). Care must be taken when administering calcium intravenously, as extravasation results in severe chemical burns to the skin and subcutaneous tissues. Although it may be argued that 1,25-(OH)2D production after administration of 25-OHD would be sufficient to reverse hypocalcaemia, it is our opinion that either calcitriol or 1α-hydroxyvitamin D3 be coadministered until the serum calcium concentration is within normal limits. Children should be kept under close observation until the serum calcium concentration is over 1.8 mmol/L.

While vitamin D deficiency is the most common cause of hypocalcaemia after the first 4 days of life, other causes include dietary phosphate load, hypomagnesaemia, transient hypoparathyroidism, transient PTH resistance and congenital hypoparathyroidism.34 Levels of PTH and magnesium should therefore be assessed during the initial investigation of paediatric hypocalcaemia.

Stoss therapy

High-dose vitamin D therapy (stoss therapy) is an effective method for treating established or recalcitrant vitamin D deficiency.31,35 It involves oral or intramuscular administration of the total treatment dose of vitamin D (cholecalciferol or ergocalciferol), 300 000 IU (7500 μg) to 500 000 IU (12 500 μg), as a single dose, or two to four divided doses.36 The interval between doses can vary from days to several weeks depending on the protocol followed. There are many stoss therapy regimens, and further study is required to finalise the most effective regimen and ensure safety. After stoss therapy, the biochemical follow-up recommended is similar to that for daily dosing.

In Australia, concentrated vitamin D is not commercially available, limiting stoss therapy. In New Zealand, Calciferol Strong (50 000 IU cholecalciferol; PSM Healthcare, Auckland, NZ) — an oral preparation — is available.10 High-dose vitamin D for intramuscular injection effectively treats vitamin D deficiency secondary to malabsorption,35 but is not available in Australia or New Zealand. To facilitate the use of stoss therapy, a wider variety of vitamin D preparations are required in Australia and New Zealand.

Prevention of vitamin D deficiency
Infants (< 12 months)

The most important factor for the development of vitamin D deficiency in infants is maternal vitamin D status.26,27 All pregnant women, especially those who are veiled or dark-skinned, should have their serum 25-OHD concentration evaluated during the first trimester of pregnancy. If they are moderately to severely vitamin D deficient, pregnant women should be treated with 3000–5000 IU daily until the serum 25-OHD concentration is over 50 nmol/L.10 These preparations should not contain vitamin A, which may lead to fetal toxicity. After this serum concentration is achieved, they should receive 400 IU daily, as should women with a mild deficiency.10,37 Routine vitamin D supplementation of all pregnant women is a controversial subject,37,38 and until local data are available on the incidence of vitamin D deficiency, this cannot be recommended.

We endorse breastfeeding for all infants. However, breast milk is a poor source of vitamin D.16,17 The American Academy of Pediatrics recommends supplementing all breastfed infants with vitamin D until they are weaned to 500 mL per day of vitamin D-fortified formula.18 While similar recommendations cannot be made in Australia and New Zealand until data are available on the vitamin D status of “low-risk” infants,26 breastfed infants of veiled or dark-skinned mothers should be supplemented with 400 IU vitamin D daily (eg, 0.45 mL Pentavite; Roche Consumer Health, Sydney, NSW) until at least 12 months of age.31 Other vitamin D preparations may be available at hospital pharmacies.

Toddlers and adolescents

While most healthy children in Australia and New Zealand receive enough sunlight exposure to maintain adequate vitamin D levels, a significant number living in the more temperate zones develop mild vitamin D deficiency during winter.21 In Tasmania, 8% of 8-year-old and 68% of 16-year-old children have serum 25-OHD concentrations less than 50 nmol/L.21,22 New Zealand data are comparable, with 50% of all children in all age groups with serum 25-OHD concentrations less than 50 nmol/L. If children can be encouraged to participate in regular outdoor activities, blanket vitamin D supplementation for children and adolescents is not warranted.

Children who are dark-skinned, veiled, exposed to reduced sunlight or who have an underlying medical condition, should receive 400 IU vitamin D daily (eg, be given a multivitamin) to prevent vitamin D deficiency.18 Siblings of a child diagnosed with vitamin D deficiency should be screened.3 The help of local community and cultural groups will be of major importance in ensuring the dissemination of these prevention strategies.

3 Management of vitamin D deficiency


Vitamin D deficiency



No seizure




< 1 month

10% calcium gluconate: 0.5 mL/kg (max 20 mL) intravenously over 30–60 minutes.

Calcium: 40–80 mg/kg/day (1–2 mmol/kg/day) orally in 4–6 doses, and Calcitriol: 50–100 ng/kg/day orally in 2–3 doses until serum calcium level is > 2.1 mmol/L.

Vitamin D: 1000 IU (25 μg) daily for 3 months.

Vitamin D: 400 IU (10 μg) daily or 150 000 IU (3750 μg) at the start of autumn.

1 month: Serum calcium and alkaline phosphatase.

3 months: Serum calcium, magnesium, phosphate, alkaline phosphatase, calcidiol, parathyroid hormone. Wrist x-ray to assess healing of rickets.

Annual: Calcidiol.

1–12 months

Vitamin D: 3000 IU (75 μg) daily for 3 months, or 300 000 IU (7500 μg) over 1–7 days.

> 12 months

Vitamin D: 5000 IU (125 μg) daily for 3 months, or 500 000 IU (15 000 μg) over 1–7 days.

* Aim of therapy is to stop seizure activity, not to normalise serum calcium.27 If seizures persist, a repeat bolus should be given and a calcium infusion of up to 4 mmol/kg/day may be required to maintain normocalcaemia. Calcium may be used intravenously to treat hypocalcaemia in the absence of seizures, but the risk of calcium burns and scarring must be considered. 1α-hydroxyvitamin D3 is an alternative to calcitriol at 60–120 ng/kg/day. Ergocalciferol (vitamin D2) or cholecalciferol (vitamin D3). This is high-dose vitamin D therapy (stoss therapy), and hypercalcaemia and nephrocalcinosis have been reported with such therapy in well nourished children.31

Calcitriol = 1,25-dihydroxyvitamin D. Calcidiol = 25-hydroxyvitamin D.

  • Craig Munns1
  • Margaret R Zacharin2
  • Christine P Rodda3
  • Jennifer A Batch4
  • Ruth Morley2
  • Noel E Cranswick2
  • Maria E Craig1,5,6
  • Wayne S Cutfield7
  • Paul L Hofman7
  • Barry J Taylor8
  • Sonia R Grover9
  • Julie A Pasco10
  • David Burgner11
  • Christopher T Cowell1,5

  • 1 The Children's Hospital at Westmead, Sydney, NSW.
  • 2 The Royal Children's Hospital, Melbourne, VIC.
  • 3 Monash Medical Centre, Melbourne, VIC.
  • 4 The Royal Children's Hospital, Brisbane, QLD.
  • 5 Department of Paediatrics and Child Health, University of Sydney, Sydney, NSW.
  • 6 School of Women's and Children's Health, University of New South Wales, Sydney, NSW.
  • 7 Department of Endocrinology and Diabetes, Starship Hospital, Auckland, New Zealand.
  • 8 Dunedin School of Medicine, Paediatrics and Child Health, University of Otago, Dunedin, New Zealand.
  • 9 Mercy Hospital for Women, Melbourne, VIC.
  • 10 Barwon Health, University of Melbourne, Geelong, VIC.
  • 11 School of Paediatrics and Child Health, University of Western Australia, Perth, WA.


Competing interests:

None identified.

  • 1. Nozza JM, Rodda CP. Vitamin D deficiency in mothers of infants with rickets. Med J Aust 2001; 175: 253-255. <MJA full text>
  • 2. Pillow JJ, Forrest PJ, Rodda CP. Vitamin D deficiency in infants and young children born to migrant parents. J Paediatr Child Health 1995; 31: 180-184.
  • 3. Robinson PD, Hogler W, Craig ME, et al. The re-emerging burden of rickets: a decade of experience from Sydney. Arch Dis Child 2006; 91: 564-568.
  • 4. Blok BH, Grant CC, McNeil AR, Reid IR. Characteristics of children with florid vitamin D deficient rickets in the Auckland region in 1998. N Z Med J 2000; 113: 374-376.
  • 5. Greenway A, Zacharin M. Vitamin D status of chronically ill or disabled children in Victoria. J Paediatr Child Health 2003; 39: 543-547.
  • 6. DeLuca HF, Zierold C. Mechanisms and functions of vitamin D. Nutr Rev 1998; 56 (2 Pt 2): S4-S10; discussion S54-S75.
  • 7. Nowson CA, Margerison C. Vitamin D intake and vitamin D status of Australians. Med J Aust 2002; 177: 149-152. <MJA full text>
  • 8. Armstrong BK. How sun exposure causes skin cancer. In: Hill D, Elwood JM, English DR, editors. Prevention of skin cancer. Dordrecht: Kluwer Academic Publishers, 2004.
  • 9. Risks and benefits of sun exposure position statement. 2005. Approved by the Australian and New Zealand Bone and Mineral Society, Osteoporosis Australia, Australasian College of Dermatologists and the Cancer Council Australia. (accessed Jul 2006).
  • 10. Working Group of the Australian and New Zealand Bone and Mineral Society, Endocrine Society of Australia and Osteoporosis Australia. Vitamin D and adult bone health in Australia and New Zealand: a position statement. Med J Aust 2005; 182: 281-285. <MJA full text>
  • 11. Riggs BL. Role of the vitamin D-endocrine system in the pathophysiology of postmenopausal osteoporosis. J Cell Biochem 2003; 88: 209-215.
  • 12. Clemens TL, Adams JS, Henderson SL, Holick MF. Increased skin pigment reduces the capacity of skin to synthesise vitamin D3. Lancet 1982; 1: 74-76.
  • 13. Holick MF. Vitamin D: the underappreciated D-lightful hormone that is important for skeletal and cellular health. Curr Opin Endocrinol Diabetes 2002; 9: 87-98.
  • 14. Holick MF. McCollum Award Lecture, 1994: vitamin D — new horizons for the 21st century. Am J Clin Nutr 1994; 60: 619-630.
  • 15. Pettifor JM. Nutritional rickets: deficiency of vitamin D, calcium, or both? Am J Clin Nutr 2004; 80 (6 Suppl): 1725S-1729S.
  • 16. Reeve LE, Chesney RW, DeLuca HF. Vitamin D of human milk: identification of biologically active forms. Am J Clin Nutr 1982; 36: 122-126.
  • 17. Hollis BW, Roos BA, Draper HH, Lambert PW. Vitamin D and its metabolites in human and bovine milk. J Nutr 1981; 111: 1240-1248.
  • 18. Gartner LM, Greer FR. Prevention of rickets and vitamin D deficiency: new guidelines for vitamin D intake. Pediatrics 2003; 111: 908-910.
  • 19. Glendenning P. Issues of standardization and assay-specific clinical decision limits for the measurement of 25-hydroxyvitamin D. Am J Clin Nutr 2003; 77: 522-523.
  • 20. Docio S, Riancho JA, Perez A, et al. Seasonal deficiency of vitamin D in children: a potential target for osteoporosis-preventing strategies? J Bone Miner Res 1998; 13: 544-548.
  • 21. Jones G, Dwyer T, Hynes KL, et al. Vitamin D insufficiency in adolescent males in Southern Tasmania: prevalence, determinants, and relationship to bone turnover markers. Osteoporos Int 2005; 16: 636-641.
  • 22. Jones G, Blizzard C, Riley MD, et al. Vitamin D levels in prepubertal children in Southern Tasmania: prevalence and determinants. Eur J Clin Nutr 1999; 53: 824-829.
  • 23. Holick MF. Sunlight and vitamin D for bone health and prevention of autoimmune diseases, cancers, and cardiovascular disease. Am J Clin Nutr 2004; 80 (6 Suppl): 1678S-1688S.
  • 24. DeLuca HF. Overview of general physiologic features and functions of vitamin D. Am J Clin Nutr 2004; 80 (6 Suppl): 1689S-1696S.
  • 25. Mason RS, Diamond TH. Vitamin D deficiency and multicultural Australia. Med J Aust 2001; 175: 236-237. <MJA full text>
  • 26. Thomson K, Morley R, Grover SR, Zacharin MR. Postnatal evaluation of vitamin D and bone health in women who were vitamin D-deficient in pregnancy, and in their infants. Med J Aust 2004; 181: 486-488. <MJA full text>
  • 27. Wharton B, Bishop N. Rickets. Lancet 2003; 362: 1389-1400.
  • 28. Abdullah M, Bigras JL, McCrindle BW. Dilated cardiomyopathy as a first sign of nutritional vitamin D deficiency rickets in infancy. Can J Cardiol 1999; 15: 699-701.
  • 29. Mathieu C, Gysemans C, Giulietti A, Bouillon R. Vitamin D and diabetes. Diabetologia 2005; 48: 1247-1257.
  • 30. Ladhani S, Srinivasan L, Buchanan C, Allgrove J. Presentation of vitamin D deficiency. Arch Dis Child 2004; 89: 781-784.
  • 31. Hochberg Z, Bereket A, Davenport M, et al. Consensus development for the supplementation of vitamin D in childhood and adolescence. Horm Res 2002; 58: 39-51.
  • 32. Pettifor JM. Nutritional and drug-induced rickets and osteomalacia. In: Favus MJ, editor. Primer on the metabolic bone diseases and disorders of mineral metabolism. 5th ed. Washington, DC: American Society of Bone and Mineral Research, 2003: 399-407.
  • 33. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, Food and Nutrition Board, Institute of Medicine. Dietry reference intakes for calcium, phosphorus, magnesium, Vitamin D and fluoride. Washington, DC: National Academy Press, 1997.
  • 34. Hsu SC, Levine MA. Perinatal calcium metabolism: physiology and pathophysiology. Semin Neonatol 2004; 9: 23-36.
  • 35. Alyaarubi S, Rodd C. Treatment of malabsorption vitamin D deficiency myopathy with intramuscular vitamin D. J Pediatr Endocrinol Metab 2005; 18: 719-722.
  • 36. Shah BR, Finberg L. Single-day therapy for nutritional vitamin D-deficiency rickets: a preferred method. J Pediatr 1994; 125: 487-490.
  • 37. Moy R, Shaw N, Mather I. Vitamin D supplementation in pregnancy. Lancet 2004; 363: 574.
  • 38. Mahomed K, Gulmezoglu AM. Vitamin D supplementation in pregnancy. Cochrane Database Syst Rev 2000; (2): CD000228.


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