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Editorial

Indian Pediatr 2014;51: 259-260

How Should We Manage Vitamin D Deficiency Rickets?


John M Pettifor

MRC/University Developmental Pathways for Health Research Unit, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa.
Email: [email protected]

 


Despite considerable concern being expressed by health professionals about the almost global distribution and high prevalence of vitamin D deficiency among communities [1,2], there are few trials that have evaluated the efficacy of various treatment regimens against one another for the prevention or management of vitamin D deficiency rickets in children. In this issue, Gupta and his colleagues [3] have assessed the efficacy of two different levels of Stoss therapy, to not only treat vitamin D rickets but also to correct the vitamin D status, of young children. They concluded that both 300,000 IU and 600,000 IU vitamin D
3 as single day doses were equally effective in treating children between 6 months and 5 years of age with vitamin D deficiency rickets, but that neither dose was able to normalize the vitamin D status of the children – 3 months after the administered dose. Although no adverse clinical events were detected during the course of the study, a small number of children had asymptomatic hypercalcemia at 4 weeks or 3 months.

Although the management, both of vitamin D deficiency rickets, and of maintaining an adequate vitamin D status, is theoretically straight forward, as all that is required is a daily dose of vitamin D – which will vary in size depending on whether one is correcting vitamin D deficiency or maintaining vitamin D status – the realities are very different. A number of studies in both developed and developing countries have highlighted difficulties in ensuring patient treatment adherence, which is likely to be particularly problematic in the prevention strategies [4,5]. Thus in discussing possible options for management, it is appropriate to discuss the treatment of vitamin D deficiency separately from that used for the prevention of vitamin D deficiency.

Single dose treatment (Stoss therapy) for vitamin D deficiency rickets makes considerable sense as it ensures patient compliance and reduces the risk of incorrect dosage being administered by the caregiver; however, there is no consensus among health providers as to what is the most appropriate dose. A single day dose between 300,000 IU and 600,000 IU vitamin D2 or D3 given orally or intramuscularly has been recommended [6], but asymptomatic hypercalcemia and hypercalciuria have been reported by a number of researchers [3,7,8]. Lower doses of between 150,000 IU and 200,000 IU have also resulted in rapid healing of the biochemical and radiological abnormalities of rickets without the adverse effects [7,9,10]. Although further studies may be required to confirm the efficacy of 150,000 IU as a treatment dose, health professionals should in the meantime be cautious about using higher doses of vitamin D (such as 600,000 IU), especially in young children, in light of the reported adverse effects.

The prevention of vitamin D deficiency at a population level requires a concerted effort from public health specialists. Although the use of daily supplements is effective for individual subjects, who are at risk of vitamin D deficiency, it is unlikely to address the problem in communities or segments of communities at-risk (such as infants and young children, teenagers, and pregnant women). Intermittent vitamin D supplementation [11,12] or appropriate food fortification [13] should be considered. The possibility of combining intermittent vitamin D supplements with the immunization schedule would allow for targeting of young children, while providing supplements (100,000 IU) every three to four months at high school would target adolescents [14]. Although the use of intermittent therapy makes considerable practical sense at a public health level, Hollis and Wagner provide a cautionary note that the actual circulating concentrations of the parent compound itself (vitamin D) might play an important role in the vitamin D endocrine/autocrine system [15], and thus they suggest that daily treatment regimens may have different effects in comparison to those using intermittent regimens. As yet, empirical information is limited, but we should be aware of the possibility of different outcomes depending on the frequency of vitamin D supplementation.

With all the highly sophisticated technologies and advances that are available and have been made in clinical medicine, the failure to eradicate vitamin D deficiency and particularly rickets is an indictment on the health professionals’ and national governments’ commitment to address the problem. Perhaps now that research is suggesting that a poor vitamin D status might have consequences on the health of adults, our legislators might pay more attention to eradicating vitamin D deficiency.

Funding: None; Competing interests: None stated.

References

1. Hossein-nezhad A, Holick MF. Vitamin D for health: a global perspective. Mayo Clin Proc. 2013;88:720-55.

2. Harinarayan CV, Joshi SR. Vitamin D status in India – its implications and remedial measures. J Assoc Physicians India. 2009;57:40-48.

3. Mittal H, Rai S, Shah D, Madhu SV, Mehrotra G, Malhotra RK, et al. 300,000 IU or 600,000 IU of oral vitamin D3 for treatment of nutritional rickets: A randomized controlled trial. Indian Pediatr. 2014;51:265-72

4. Grant CC, Stewart AW, Scragg R, Milne T, Rowden J, Ekeroma A, et al. Vitamin D during pregnancy and infancy and infant serum 25-hydroxyvitamin D concentration. Pediatrics. 2014;133:e143-53.

5. Rodd C, Jean-Philippe S, Vanstone C, Weiler H. Comparison of 2 vitamin D supplementation modalities in newborns: adherence and preference. Appl Physiol Nutr Metab. 2011;36:414-8.

6. Shah BR, Finberg L. Single-day therapy for nutritional vitamin D-deficiency rickets: a preferred method. J Pediatr. 1994;125:487-90.

7. Cesur Y, Caksen H, Gundem A, Kirimi E, Odabas D. Comparison of low and high dose of vitamin D treatment in nutritional vitamin D deficiency rickets. J Pediatr Endocrinol Metab. 2003;16:1105-9.

8. Markestad T, Hesse V, Siebenhuner M, Jahreis G, Aksnes L, Plenert W, et al. Intermittent high-dose vitamin D prophylaxis during infancy: effect on vitamin D metabolites, calcium, and phosphorus. Am J Clin Nutr. 1987;46:652-8.

9. Billoo AG, Murtaza G, Memon MA, Khaskheli SA, Iqbal K, Rao MH. Comparison of oral versus injectable vitamin-D for the treatment of nutritional vitamin-D deficiency rickets. J Coll Physicians Surg Pak. 2009;19:428-31.

10. Emel T, Dođan DA, Erdem G, Faruk O. Therapy strategies in vitamin D deficiency with or without rickets: efficiency of low-dose stoss therapy. J Pediatr Endocrinol Metab. 2012;25:107-10.

11. Shaw NJ, Pal BR. Vitamin D deficiency in UK Asian families: activating a new concern. Arch Dis Child. 2002;86:147-9.

12. Oliveri B, Cassinelli H, Mautalen C, Ayala M. Vitamin D prophylaxis in children with a single dose of 150000 IU of vitamin D. Eur J Clin Nutr. 1996;50:807-10.

13. Ekbote VH, Khadilkar AV, Chiplonkar SA, Hanumante NM, Khadilkar VV, Mughal MZ. A pilot randomized controlled trial of oral calcium and vitamin D supplementation using fortified laddoos in underprivileged Indian toddlers. Eur J Clin Nutr. 2011;65:440-6.

14. Duhamel JF, Zeghoud F, Sempe M, Boudailliez B, Odievre M, Laurans M, et al. Prevention of vitamin D deficiency in adolescents and pre-adolescents. An interventional multicenter study on the biological effect of repeated doses of 100,000 IU of vitamin D3. Arch Pediatr. 2000;7:148-53.

15. Hollis BW, Wagner CL. The role of the parent compound vitamin D with respect to metabolism and function: why clinical dose intervals can affect clinical outcomes. J Clin Endocrinol Metab. 2013;98:4619-28.

 

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