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Absence of vitamin D deficiency in young Nigerian children
M A Pfitzner1, T D Thacher, J M Pettifor
1Department of Pediatrics, University of Utah, Salt Lake City, Utah, USA.
Insights
Vitamin D deficiency was not observed in young Nigerian children despite a high prevalence of rickets. This suggests calcium deficiency, not vitamin D deficiency, may cause rickets in this population.
Area of Science:
- Nutritional science
- Pediatric health
- Public health in developing nations
Background:
- Nutritional rickets is prevalent in young Nigerian children.
- The role of vitamin D deficiency in this rickets prevalence is unclear.
Purpose of the Study:
- To determine the prevalence of vitamin D deficiency in young Nigerian children.
- To investigate the relationship between vitamin D levels and clinical rickets.
Main Methods:
- A randomized cluster sample of 218 children aged 6 to 35 months in Jos, Nigeria.
- Measured 25-hydroxyvitamin D (25-OHD) concentrations and assessed clinical signs of rickets.
- Analyzed serum calcium levels and breastfeeding status.
Main Results:
- No children had 25-OHD concentrations below 10 ng/mL, indicating no vitamin D deficiency.
- 9.2% of children presented with clinical signs of rickets.
- Children with rickets had lower serum calcium and were less likely to be breastfed, but 25-OHD levels were similar to those without rickets.
Conclusions:
- Vitamin D deficiency is not the cause of rickets in this Nigerian child population.
- Dietary calcium insufficiency is hypothesized to be the primary cause of clinical rickets.
- Findings challenge the traditional understanding of rickets etiology in this region.
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.