Background: phosphate homeostasis is mediated through complex counter regulatory feedback balance between parathyroid hormone, FGF-23 and 1,25(OH)2D. Both parathyroid hormone and FGF-23 regulate proximal tubular phosphate excretion through signaling on sodium-phosphate cotransporters II a and II c. However, the interaction between these hormones on phosphate excretion is not clearly understood. We performed the present study to evaluate whether the existence of sufficient parathyroid hormone is necessary for full phosphaturic function of FGF-23 or not. Methods: In this case-control study, 19 patients with hypoparathyroidism and their age-and gender-matched normal population were enrolled. Serum calcium, phosphate, alkaline phosphatase,parathyroid hormone, FGF-23, 25(OH)D, 1,25(OH)2D and Fractional excretion of phosphorous were assessed and compared between the two groups, using SPSS software. Results: The mean serum calcium and parathyroid hormone level was significantly lower in hypoparathyroid patients in comparison with the control group (P < 0.001 and P < 0.001, respectively). We found high serum level of phosphate and FGF-23 in hypoparathyroid patients compared to the control group (P < 0.001 and P < 0.001, respectively). However, there was no significant difference in Fractional excretion of phosphorous or 1,25OH2D level between the two groups. There was a positive correlation between serum FGF-23 and Fractional excretion of phosphorous just in the normal individuals (P < 0.001, r = 0.79). Conclusions: Although the FGF-23 is a main regulator of urinary phosphate excretion but the existence of sufficient parathyroid hormone is necessary for the full phosphaturic effect of FGF-23.

Background phosphate homeostasis is mediated through complex counter regulatory feed-back balance between parathyroid hormone, FGF-23 and 1,25(OH)2D. Both parathyroid hormone and FGF-23 regulate proximal tubular phosphate excretion through signaling on sodium- phosphate cotransporters IIa and IIc. However, the interaction between these hormones on phosphate excretion is not clearly understood. We performed the present study to evaluate whether the existence of sufficient parathyroid hormone is necessary for full phosphaturic function of FGF-23 or not. Methods In this case-control study, 19 patients with hypoparathyroidism and their age- and gender-matched normal population were enrolled. Serum calcium, phosphate, alkaline phosphatase,parathyroid hormone, FGF-23, 25(OH)D, 1,25(OH)2D and Fractional excretion of phosphorous were assessed and compared between the two groups, using SPSS software. Results The mean serum calcium and parathyroid hormone level was significantly lower in hypoparathyroid patients in comparison with the control group(P<0.001 and P<0.001, respectively). We found high serum level of phosphate and FGF-23 in hypoparathyroid patients compared to the control group (P<0.001 and P<0.001,respectively). However, there was no significant difference in Fractional excretion of phosphorous or 1,25OH2D level between the two groups. There was a positive correlation between serum FGF-23 and Fractional excretion of phosphorous just in the normal control population(P <0.001, r = 0.79). Conclusions Although the FGF-23 is a main regulator of urinary phosphate excretion but the existence of sufficient parathyroid hormone is necessary for the full phosphaturic effect of FGF-23.

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.

PurposeTo report a case of Wolfram syndrome (WS) characterized by diabetes mellitus, diabetes insipidus, progressive optic atrophy, and deafness.Case reportA 19-year-old female patient, a known case of diabetes mellitus type I from six years before, presented with progressive vision loss since four years earlier. On fundoscopic examination, she had bilateral optic atrophy without diabetic retinopathy. The patient also had diabetes insipidus, neurosensory deafness, and neurogenic bladder.ConclusionWS should be considered a differential diagnosis in patients with diabetes mellitus who present with optic atrophy, and it is necessary to perform a hearing test as well as collecting 24-h urine output.

Triple-lumen central catheter insertion is a simple, noninvasive option in patients with recurrent MPE that can be performed the patient's bedside. Further research is needed to confirm the results and to assess the impact of central catheter insertion on the quality of life of these patients.

Background FGF23 controls serum l,25(OH) 2 D 3 levels and phosphate homeostasis. This study evaluates the effects of Ferritin on intact PTH, FGF23 and l,25(OH) 2 D 3 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 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 the 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 the controls (p=0.002). Fractional excretion of phosphorous was lower in patients with hypoparathyroidism, despite the high level of 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 showed a strong positive correlation between serum ferritin and FGF23 and 1,25(OH)2D3. We hypothesized that ferritin could have stimulatory effect on production of 1,25(OH)2D3. Also, rise in FGF23 in patients with thalassemia, might be associated with either stimulating effect of PTH and 1,25(OH)2D3, or might be related to direct stimulating effect of ferritin.

Background:phosphate homeostasis is mediated through complex counter regulatory feed-back balance between parathyroid hormone, FGF-23 and 1,25(OH)2D. Both parathyroid hormone and FGF-23 regulate proximal tubular phosphate excretion through signaling on sodium- phosphate cotransporters II a and II c . However, the interaction between these hormones on phosphate excretion is not clearly understood. We performed the present study to evaluate whether the existence of sufficient parathyroid hormone is necessary for full phosphaturic function of FGF-23 or not. Methods:In this case-control study, 19 patients with hypoparathyroidism and their age- and gender-matched normal population were enrolled. Serum calcium, phosphate, alkaline phosphatase,parathyroid hormone, FGF-23, 25(OH)D, 1,25(OH)2D and Fractional excretion of phosphorous were assessed and compared between the two groups, using SPSS software. Results:The mean serum calcium and parathyroid hormone level was significantly lower in hypoparathyroid patients in comparison with the control group(P<0.001 and P<0.001, respectively). We found high serum level of phosphate and FGF-23 in hypoparathyroid patients compared to the control group (P<0.001 and P<0.001,respectively). However, there was no significant difference in Fractional excretion of phosphorous or 1,25OH2D level between the two groups. There was a positive correlation between serum FGF-23 and Fractional excretion of phosphorous just in the normal individuals (P <0.001, r = 0.79). Conclusions:Although the FGF-23 is a main regulator of urinary phosphate excretion but the existence of sufficient parathyroid hormone is necessary for the full phosphaturic effect of FGF-23.

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.