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Departments of Pediatrics (Endocrinology) (M.C.D., T.O.C.) and Internal Medicine (Endocrinology) (M.E.M.), Yale University School of Medicine, New Haven, Connecticut 06520-8064
Address all correspondence and requests for reprints to: Thomas O. Carpenter, M.D., Yale University School of Medicine, 333 Cedar Street, 3103 LMP, P.O. Box 208064, New Haven, Connecticut 06520-8064. E-mail: thomas.carpenter{at}yale.edu.
The incidence of nutritional rickets appears to be increasing in North American infants and toddlers; it is widely assumed that this is due to vitamin D deficiency. Thus, records of 43 children with nutritional rickets from greater New Haven, Connecticut, from 1986–2002 were identified. The mean age of presentation was 20 months; 86% were of African-American, Hispanic, or Middle Eastern descent. More than 93% of children had been breastfed; however, 15% had received vitamin D supplementation. Eighty-six percent of those with food histories available were weaned to diets with minimal dairy content after nursing. Serum 25-hydroxyvitamin D was 20.9 ± 11.5 ng/ml and was less than 15 ng/ml in only 22% of patients. Three representative case histories suggest that dietary calcium intake may play a contributory role in the development of disease; 1 case documents radiographic and biochemical resolution of rachitic abnormalities after calcium treatment, but no vitamin D therapy. Clinicians should be aware that low dietary calcium intake after weaning may result in the development of nutritional rickets, and that attention to calcium intake as well as that of vitamin D is important in the establishment of optimal dietary practices for North American infants and children.
Abbreviations: 25-OHD, 25-Hydroxyvitamin D; 1,25-OH2D, 1,25-dihydroxyvitamin D; VDR, vitamin D receptor.
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