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Pediatric vitamin D and calcium nutrition in developing countries

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Abstract

Over one billion humans have insufficient circulating levels of vitamin D, and dietary insufficiency of calcium is common in developing countries. Worldwide, nutritional rickets is considered to be the most common non-communicable disease of children. Rickets can be due either to primary deficiencies of vitamin D or calcium or to combined deficiencies of both elements. Vitamin D deficiency is also increasingly linked to non-skeletal complications. Even without laboratory and radiologic resources, the diagnosis of rickets is considered clinically when a child presents with limb deformities and has beaded ribs and widened wrists and ankles. Prevention is possible through increased sun exposure and dietary enhancement. Treatment of nutritional rickets involves provision of adequate vitamin D and calcium. Further research is needed to elucidate the precise epidemiology of vitamin D and calcium deficiencies in developing countries, to determine the roles of additional pathologic factors contributing to the development and morbidity of rickets, to improve affordable and feasible means of diagnosing rickets in resource-limited areas, to better target at-risk populations for preventive interventions, to identify accurate dosing and delivery of therapeutic interventions, and to evaluate the long-term consequences of vitamin D and calcium deficiencies in childhood.

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Authors and Affiliations

  1. Department of Pediatric and Adolescent Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN, 55905, USA

    Philip R. Fischer

  2. Department of Family Medicine, Mayo Clinic, Rochester, MN, USA

    Tom D. Thacher

  3. Department of Paediatrics, Chris Hani Baragwanath Hospital, University of Witwatersrand, Johannesburg, South Africa

    John M. Pettifor

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  1. Philip R. Fischer
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  2. Tom D. Thacher
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Correspondence to Philip R. Fischer.

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Fischer, P.R., Thacher, T.D. & Pettifor, J.M. Pediatric vitamin D and calcium nutrition in developing countries. Rev Endocr Metab Disord 9, 181–192 (2008). https://doi.org/10.1007/s11154-008-9085-1

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