Background: Nutritional rickets remains prevalent in many tropical countries despite the fact that such countries have ample sunlight. Some postulate that a deficiency of dietary calcium, rather than vitamin D, is often responsible for rickets after infancy.
Methods: We enrolled 123 Nigerian children (median age, 46 months) with rickets in a randomized, double-blind, controlled trial of 24 weeks of treatment with vitamin D (600,000 U intramuscularly at enrollment and at 12 weeks), calcium (1000 mg daily), or a combination of vitamin D and calcium. We compared the calcium intake of the children at enrollment with that of control children without rickets who were matched for sex, age, and weight. We measured serum calcium and alkaline phosphatase and used a 10-point radiographic score to assess the response to treatment at 24 weeks.
Results: The daily dietary calcium intake was low in the children with rickets and the control children (median, 203 mg and 196 mg, respectively; P=0.64). Treatment produced a smaller increase in the mean (+/-SD) serum calcium concentration in the vitamin D group (from 7.8+/-0.8 mg per deciliter [2.0+/-0.2 mmol per liter] at base line to 8.3+/-0.7 mg per deciliter [2.1+/-0.2 mmol per liter] at 24 weeks) than in the calcium group (from 7.5+/-0.8 [1.9+/-0.2 mmol per liter] to 9.0+/-0.6 mg per deciliter [2.2+/-0.2 mmol per liter], P<0.001) or the combination-therapy group (from 7.7+/-1.0 [1.9+/-0.25 mmol per liter] to 9.1+/-0.6 mg per deciliter [2.3+/-0.2 mmol per liter], P<0.001). A greater proportion of children in the calcium and combination-therapy groups than in the vitamin D group reached the combined end point of a serum alkaline phosphatase concentration of 350 U per liter or less and radiographic evidence of nearly complete healing of rickets (61 percent, 58 percent, and 19 percent, respectively; P<0.001).
Conclusions: Nigerian children with rickets have a low intake of calcium and have a better response to treatment with calcium alone or in combination with vitamin D than to treatment with vitamin D alone.
PIP: A randomized, double-blind, controlled trial was conducted to compare the efficacy of calcium, vitamin D, and a combination of both in the treatment of nutritional rickets among Nigerian children. Subjects included 123 Nigerian children with the deformity characteristics of rickets. For each child who was enrolled, a parent or guardian was asked to recruit a control child with the same sex, age, weight, and who had no clinical signs of rickets. Children with rickets were under treatment for 24 weeks with vitamin D (600,000 U intramuscularly at enrollment and at 12 weeks), calcium (1000 mg daily), or a combination of both. Then the serum calcium and alkaline phosphates were measured and a 10-point radiographic score was used to assess the response to the 24-week treatment. The results revealed a low dietary calcium intake in children with rickets and in control children. Children under vitamin D treatment appeared to have a small increase in the mean serum calcium concentration when compared to children under calcium treatment or a combination of both vitamin D and calcium. A greater proportion of children in the calcium and combination-therapy groups than in the vitamin D group reached the combined end point of a serum alkaline phosphates concentration of 350 U/liter or less and radiographic evidence of nearly complete healing of rickets. Overall, compliance ranged from 92% to 96% across the three groups. Since Nigerian children with rickets had low calcium intake, treatment should focus on dietary supplementation with calcium or a combination of calcium and vitamin D.