Absence of vitamin D deficiency in young Nigerian children

Abstract

Objective: To determine the prevalence of vitamin D deficiency in young Nigerian children residing in an area where nutritional rickets is common.

Study design: A randomized cluster sample of children aged 6 to 35 months in Jos, Nigeria.

Results: Of 218 children evaluated, no child in the study had a 25-hydroxyvitamin D (25-OHD) concentration <10 ng/mL (the generally held definition of vitamin D deficiency). Children spent an average of 8.3 hours per day outside of the home. Twenty children (9.2%) had clinical findings of rickets. Children with clinical signs of rickets were more likely to be not currently breast fed and have significantly lower serum calcium concentrations than those without signs of rickets (9.1 vs 9.4 mg/dL, respectively, P =.01). Yet, 25-OHD levels were not significantly different between those children with clinical signs of rickets and those without such clinical signs.

Conclusion: Vitamin D deficiency was not found in this population of young children in whom clinical rickets is common. This is consistent with the hypothesis that dietary calcium insufficiency, without preexisting vitamin D deficiency, accounts for the development of clinical rickets in Nigerian children.

PIP: Deficiencies of either calcium or vitamin D can cause nutritional rickets. Findings are reported from a study conducted to assess the prevalence of vitamin D deficiency in young Nigerian children living in an area where nutritional rickets is common. A random sample of 218 children aged 6-35 months in Jos, Nigeria, was evaluated. The children were of mean age 22 months. No child had a 25-hydroxyvitamin D (25-OHD) concentration of less than 10 ng/ml, the generally held definition of vitamin D deficiency. Children spent an average of 8.3 hours/day outside of the home, and 20 children (9.2%) had clinical findings of rickets. Children with clinical signs of rickets were more likely to be not currently breast-fed and have significantly lower serum calcium concentrations than those with no signs of rickets. 25-OHD levels were not significantly different between children with clinical signs of rickets and those without such clinical signs. The failure to find vitamin D deficiency in this population of young children in whom clinical rickets is common is consistent with the hypothesis that dietary calcium insufficiency, without preexisting vitamin D deficiency, accounts for the development of rickets in Nigerian children.