Antenatal iron supplementation, FGF23, and bone metabolism in Kenyan women and their offspring: secondary analysis of a randomized controlled trial
Publication: The American Journal of Clinical Nutrition
Braithwaite, V., Mwangi, M., Jones, K., Demir, A., Prentice, A., Prentice, A., Andang’o, P. and Verhoef, H.
1 March 2021
Fibroblast growth factor-23 (FGF23) regulates body phosphate homeostasis primarily by increasing phosphaturia. It also acts as a vitamin D-regulating hormone. Maternal iron deficiency is associated with perturbed expression and/or regulation of FGF23 and hence might be implicated in the pathogenesis of hypophosphatemia-driven rickets in their offspring.
Rural Kenyan women with singleton pregnancies and hemoglobin concentrations ≥ 90 g/L were randomly allocated to daily, supervised supplementation with 60 mg elemental iron as ferrous fumarate or placebo from 13–23 weeks of gestation until 1 month postpartum.
The researchers reanalyzed all available plasma samples collected in 433 mothers and 414 neonates at birth and confirmed that iron supplementation can reverse elevated FGF23 production caused by iron deficiency in iron-deficient mothers and their neonates.
Further investigations are warranted to assess to what extent iron supplementation can prevent FGF23-mediated hypophosphatemic rickets or osteomalacia.
