Abstract
BackgroundFGF23 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 also evaluates FGF23 changes in patients with hypoparathyroidism to clarify the interaction between FGF23 and PTH in the absence of proper PTH functioning in human.MethodsIn this case-control study, 25 major-beta thalassemia patients with hypoparathyroidism were age- and gender-matched with major-beta thalassemia patients having normal parathyroid function. Biochemical studies assessed the serum calcium, albumin, phosphorus, alkaline phosphatase, PTH, FGF23, 25(OH) D, 1,25(OH)2D3, ferritin, and the fractional excretion of phosphorous.ResultsFGF23 was higher in the patients with hypoparathyroidism than the controls (P = 0.002). The fractional excretion of phosphorous was lower in patients with hypoparathyroidism, despite the high level of FGF23 (P = 0.001). There was a correlation between serum 1,25(OH)2D3 and FGF23 with ferritin in the controls (P = < 0.001and P = < 0.001, respectively).ConclusionsThe present study showed a strong positive correlation between serum ferritin and levels of FGF23 and 1,25(OH)2D3. We hypothesized that ferritin could have a stimulatory effect on the production of 1,25(OH)2D3. Moreover, a rise in FGF23 in patients with thalassemia, might be either associated with the stimulating effect of PTH and 1,25(OH)2D3, or directly related to the stimulating effect of ferritin.
Highlights
fibroblast growth factor 23 (FGF23) controls serum l,25(OH)2D3 levels and phosphate homeostasis
In our previous case-control study, we evaluated FGF23 function in hypoparathyroid patients compared to a healthy population, and we find that the FGF23 is a main regulator of urinary phosphate excretion but the existence of sufficient parathyroid hormone is necessary for the full phosphaturic effect of FGF23 [28]
The mean serum calcium and parathyroid hormone (PTH) levels were lower in patients with hypoparathyroidism (8.7 ± 1.6 mg/dL, and 13.93 ± 4.6 pg/mL) than the control (10.1 ± 0.9 mg/dL, and 55.6 ± 15.7 pg/mL), (P = 0.001 and P < 0.001, respectively)
Summary
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 functioning in human. The concentration of ferritin in serum provides a quantitative measure for iron storage [1]. In patients with major thalassemia, frequent blood transfusion and iron overload, despite. PTH and fibroblast growth factor 23 (FGF23) are the primary hormones that regulate the phosphate and calcium homeostasis [6]. FGF23 is a member of FGF19 subfamily, produced by osteocytes in response to high levels of serum phosphate
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