Abstract
Background:FGF23 controls serum l,25(OH)2D3 levels and phosphate homeostasis. This study evaluates the effects of Ferritin on intact PTH, FGF23 and l,25(OH)2D3 in patients with major thalassemia. It evaluates FGF23 changes in patients with hypoparathyroidism to clarify the interaction between FGF23 and PTH in the absence of proper PTH function in human.
Methods:In this case-control study,25 patients with major-beta thalassemia with hypoparathyroidism and their age- and gender-matched patients with major-beta thalassemia having normal parathyroid function were enrolled. Biochemical studies assessed serum calcium, albumin phosphorus, alkaline phosphatase, PTH, FGF23, 25(OH)D, 1,25(OH)2D3, Ferritin and Fractional excretion of phosphorous.
Results:FGF23 was higher in the patients with hypoparathyroidism compared to controls(p=0.002). Fractional excretion of phosphorous was lower in patients with hypoparathyroidism, despite of high FGF23(p=0.001). There was a correlation between serum1,25(OH)2D3 and FGF23 with ferritin in the controls(P=<0.001and P=<0.001,respectively).
Conclusions: The present study suggested that rise in FGF23 in patients with thalassemia, may be due to either stimulating effect of PTH and 1,25(OH)2D3 on FGF23 production, or might be direct stimulating effect of ferritin. It seems that in hypoparathyroid patients with insufficient PTH action, the FGF23 is not able to exert its full function in reducing serum phosphorus level by its phosphaturic action.