Iron deficiency is a newly discovered stimulus of FGF23 production. High rates of iron deficiency and high FGF23 levels of unclear cause are both common in the neonatal period. In the setting of increased FGF23 production due to iron deficiency, we hypothesize that premature infants develop elevated biologically active FGF23 levels, essentially mimicking the molecular pathophysiology of genetic rickets. This novel hypothesis would help to explain metabolic bone disease of prematurity and suggest new treatment strategies. If iron deficiency is associated with excess FGF23, as we aim to determine in this study, interventional trials of iron may successfully reduce bone disease in these fragile infants.
|Effective start/end date||9/1/15 → 8/31/17|
- Northwestern Memorial Hospital (Exhibit B.26//NMH #6-FY2016)
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