to the editor: The article in the August 15, 2006, issue of American Family Physician¹ draws attention to the global resurgence of rickets, which has been reported in at least 59 countries in the past 20 years.² However, the article did not emphasize the role of inadequate calcium intake in nutritional rickets. Vitamin D deficiency often is assumed to be the cause of rickets, but calcium deficiency also may be a cause. Calcium deficiency is increasingly recognized as a cause of rickets in the United States, and is prevalent in parts of Africa and Asia where the intake of dairy products by children is negligible.

Whereas children with rickets related to vitamin D deficiency typically present in the first 18 months of life, children with rickets related to calcium deficiency usually present after 18 months of age. In the illustrative case described in the article, no value is provided for the child's calcidiol (25[OH]D₃) level to assess the vitamin D status, although it is described as being decreased. Children with calcium-deficiency rickets have reduced or normal calcidiol values, but they do not have the extremely low calcidiol values (less than 10 ng per mL) characteristic of vitamin D–deficiency rickets. Without measurement of serum calcidiol, it is difficult to distinguish rickets caused by calcium deficiency from rickets caused by vitamin D deficiency on clinical grounds alone. As many as 50 percent of American children with rickets have calcidiol values greater than 20 ng per mL, consistent with calcium deficiency.³ In children with calcium deficiency, the 1,25-hydroxyvitamin D concentration is markedly elevated. Children with rickets from calcium deficiency respond better to treatment with calcium than vitamin D.⁴ Nutritional rickets may more often result from combined calcium and vitamin D deficiencies interacting than from either cause alone. Inadequate calcium intake induces degradation of calcidiol,⁵ and inadequate vitamin D results in poor intestinal calcium absorption. Thus, each deficiency exacerbates the other. High intake of dietary inhibitors of calcium absorption (e.g., phytates in grains), limited sun exposure, and genetic variation of vitamin D enzymes and receptors also contribute to individual susceptibility to nutritional rickets.

Supplementation of vitamin D and calcium is prudent for children with nutritional rickets. Generally, 1,000 mg of elemental calcium daily in divided doses is safe and effective; chewable, flavored tablets of calcium carbonate are accepted by children. Children with calcium deficiency avidly absorb calcium because their 1,25-hydroxyvitamin D concentrations are elevated.⁶

Prolonged breastfeeding has been implicated as a predisposing cause of rickets. Although the calcium in breast milk is more bioavailable than that in cow's milk, the concentration of calcium in breast milk (260 to 330 mg per L) declines with increasing duration of lactation and is only about one fourth the concentration of calcium in cow's milk (1,200 mg per L). Introduction of vitamin D–fortified dairy products after one year of age can help prevent calcium deficiency by contributing toward the adequate intake of 500 mg of calcium in this age group.