Effects of parathyroid hormone rhPTH(1–84) on phosphate homeostasis and vitamin D metabolism in hypoparathyroidism: REPLACE phase 3 study

Clarke, B.L.; Vokes, Tamara; Bilezikian, John P.; Shoback, Dolores; Lagast, Hjalmar; Mannstadt, Michael

doi:10.1007/s12020-016-1141-0

Cited by 54 publications

(62 citation statements)

References 25 publications

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“…Animal studies also showed that PTH-null mice experienced high PO 4 in spite of high circulating FGF-23, resembling participants with hypoparathyroidism in the present study [54]. In another study on hypoparathyroid patients, treatment with rhPTH could reduce serum PO 4 level from the upper normal range to the normal values parallel with increased urinary PO 4 excretion [55][56][57]. These findings also support our hypothesis about the importance of PTH in phosphaturic action of FGF-23.…”

Section: Resultssupporting

confidence: 90%

Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

Saki

Kassaee

Salehifar

et al. 2019

Preprint

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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.

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Section: Resultssupporting

confidence: 90%

Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

Saki

Kassaee

Salehifar

et al. 2019

Preprint

View full text Add to dashboard Cite

show abstract

“…Animal studies also showed that PTH-null mice experienced high PO 4 in spite of high circulating FGF-23, resembling participants with hypoparathyroidism in the present study [55]. In another study on hypoparathyroid patients, treatment with rhPTH could reduce serum PO 4 level from the upper normal range to the normal values parallel with increased urinary PO 4 excretion [56][57][58]. These findings also support our hypothesis about the importance of PTH in phosphaturic action of FGF-23.…”

Section: Discussionsupporting

confidence: 90%

Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

2020

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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.

show abstract

“…Animal studies also showed that PTH-null mice experienced high 8 PO 4 in spite of high circulating FGF-23, resembling participants with hypoparathyroidism in the present study [55]. In another study on hypoparathyroid patients, treatment with rhPTH could reduce serum PO 4 level from the upper normal range to the normal values parallel with increased urinary PO 4 excretion [56][57][58]. These findings also support our hypothesis about the importance of PTH in phosphaturic action of FGF-23.…”

Section: Pth Also Increases Renal Po 4 Excretion At Proximal Tubule Osupporting

confidence: 90%

Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

Saki

Kassaee

Salehifar

et al. 2019

Preprint

View full text Add to dashboard Cite

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.

show abstract

Effects of parathyroid hormone rhPTH(1–84) on phosphate homeostasis and vitamin D metabolism in hypoparathyroidism: REPLACE phase 3 study

Cited by 54 publications

References 25 publications

Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

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