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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 mg per deciliter [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 mg per deciliter [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.
Source Information
From the Departments of Family Medicine (T.D.T.), Paediatrics (J.O.L.), and Chemical Pathology (C.O.I.), Jos University Teaching Hospital, Jos, Nigeria; the Department of Pediatric and Adolescent Medicine, Mayo Clinic, Rochester, Minn. (P.R.F.); the Medical Research Council Mineral Metabolism Research Unit, Department of Paediatrics, University of the Witwatersrand and Chris HaniBaragwanath Hospital, Johannesburg, South Africa (J.M.P.); and the Departments of Family and Preventive Medicine (J.C.R.) and Pediatrics (G.M.C.), University of Utah Health Sciences Center, Salt Lake City. Presented in abstract form at the South African Nutrition Congress, Pilanesburg, South Africa, May 2529, 1998.
Address reprint requests to Dr. Fischer at the Department of Pediatric and Adolescent Medicine, Mayo Clinic, 200 First St., SW, Rochester, MN 55905, or at fischer.phil{at}mayo.edu.
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