Association of vitamin D and FGF23 with serum ferritin in hypoparathyroid thalassemia: a case control study
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RESEARCH ARTICLE
Open Access
Association of vitamin D and FGF23 with serum ferritin in hypoparathyroid thalassemia: a case control study Forough Saki, Azita Salehifar, Seyed Reza Kassaee and Gholamhossein Ranjbar Omrani*
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 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. Methods: In 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. Results: FGF23 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). Conclusions: The 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. Keywords: PTH, FGF23, Ferritin, L,25(oh)2D3, Hypoparathyroidism, Major beta-thalassemia
Background Thalassemia is an inheritable disease caused by abnormal hemoglobin production, resulting in ineffective erythropoiesis and increased peripheral hemolysis. The clinical outcomes of iron overload vary and reflect the key location of iron deposition. 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 * Correspondence: [email protected] Shiraz Endocrinology and Metabolism Research Cente, Shiraz University of Medical Sciences, Shiraz, Iran
intensive chelation therapy, make them prone to many endocrine complications, such as hypogonadotropic hypogonadism, diabetes mellitus, hypothyroidism, and hypoparathyroidism [2, 3]. PTH is a potent stimulator in producing l, 25(OH)2D3 by increasing 1-alfa-hydroxylase activity in the proximal renal tubules. Reduced PTH secretion results in hypocalcemia and hyperphosphatemia [4, 5]. 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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