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Review|Articles in Press, 103672

Fibroblastic growth factor 23 linking iron and bone metabolism. Hypothesis on how FGF23 is effected by blood donation

Published:February 24, 2023DOI:https://doi.org/10.1016/j.transci.2023.103672
      Fibroblastic growth factor 23 (FGF23) is a circulating hormone mainly secreted by the osteocytes in the bone. Around 2000, after decades of research, FGF23 was discovered as being the “circulating factor phosphatonin” that causes the symptoms in patients with autosomal dominant hypophosphatemic rickets (ADHR). This disease is characterized by hypophosphatemia and hypophosphaturia resulting in growth retardation, bone deformities and rickets. Patients with ADHR develop flares of hypophosphatemia that coincidence with the development of iron deficiency and thus microcytic anemia [
      • Farrow E.G.
      • Yu X.
      • Summers L.J.
      • Davis S.I.
      • Fleet J.C.
      • Allen M.R.
      • et al.
      Iron deficiency drives an autosomal dominant hypophosphatemic rickets and healthy humans.
      ,
      • Imel E.A.
      • Peacock M.
      • Gray A.K.
      • Padgett L.R.
      • Hui S.L.
      • Econs M.J.
      Iron modifies plasma FGF23 differently in autosomal dominant hypophosphatemic rickets and healthy humans.
      ]. This finding has led to studies that elucidated the role of FGF23 in the calcium phosphate balance and subsequential research that untangled the interactions between iron balance, erythropoiesis and FGF23. There is a remarkable similarity between the systemic effects of blood donation on the calcium phosphate balance and iron state on the one side and the stimuli that have been found to induce an increase in FGF23 levels on the other.
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