Evaluation of Serum Level of FGF23 and 1,25(OH) 2 D 3  in Primary Hyperparathyroidism Patients Before and After Parathyroidectomy

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Abstract

Purpose

Parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) play critical roles in phosphate homeostasis. To the best of our knowledge, there are limited data on the impact of FGF23 and PTH on serum calcium, 1,25(OH) ₂D ₃, and phosphate in patients with primary hyperparathyroidism (PHPT). We examined these parameters and their correlations in PHPT patients before and after parathyroidectomy (PTX).

Patients and Methods

In this prospective cohort study, 29 PHPT patients who met the inclusion criteria were selected. The patient’s blood samples were taken three times: before the operation, 24 h after the operation, and 1 week after the operation. The concentrations of serum calcium, FGF23, 1,25(OH) ₂D ₃, phosphate, PTH, and alkaline phosphatase were measured in a referral laboratory at each of the three steps. Moreover, 25(OH)D was primarily measured just before the surgery.

Results

Of 29 patients included in this study with a mean age of 52.37±12.3 years, majority were females (75.8%). Serum FGF23 and 1,25(OH) ₂D ₃ levels were high before PTX and decreased after the operation; however, the difference was not statistically significant. FGF23 levels were significantly correlated with 1,25(OH) ₂D ₃ at each of the three steps (r=0.964, P <0.01; r=0.985, P <0.0; and r=0.976, P <0.05). The variations in calcium, phosphate, creatinine, and PTH were preoperatively and postoperatively significant.

Conclusion

Although 1,25(OH) ₂D ₃ and FGF23 levels were preoperatively higher in PHPT, their variations were not meaningful. There was a statistically direct significant relationship between 1,25(OH) ₂D ₃ and FGF23 preoperatively and postoperatively; however, the correlations between FGF23 and calcium, phosphate, and PTH were not significant.

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Most cited references 18

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Primary hyperparathyroidism: review and recommendations on evaluation, diagnosis, and management. A Canadian and international consensus

A Khan, D A Hanley, R Rizzoli … (2016)

The purpose of this review is to assess the most recent evidence in the management of primary hyperparathyroidism (PHPT) and provide updated recommendations for its evaluation, diagnosis and treatment. A Medline search of "Hyperparathyroidism. Primary" was conducted and the literature with the highest levels of evidence were reviewed and used to formulate recommendations. PHPT is a common endocrine disorder usually discovered by routine biochemical screening. PHPT is defined as hypercalcemia with increased or inappropriately normal plasma parathyroid hormone (PTH). It is most commonly seen after the age of 50 years, with women predominating by three to fourfold. In countries with routine multichannel screening, PHPT is identified earlier and may be asymptomatic. Where biochemical testing is not routine, PHPT is more likely to present with skeletal complications, or nephrolithiasis. Parathyroidectomy (PTx) is indicated for those with symptomatic disease. For asymptomatic patients, recent guidelines have recommended criteria for surgery, however PTx can also be considered in those who do not meet criteria, and prefer surgery. Non-surgical therapies are available when surgery is not appropriate. This review presents the current state of the art in the diagnosis and management of PHPT and updates the Canadian Position paper on PHPT. An overview of the impact of PHPT on the skeleton and other target organs is presented with international consensus. Differences in the international presentation of this condition are also summarized.

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Parathyroid hormone regulates fibroblast growth factor-23 in a mouse model of primary hyperparathyroidism.

Takehisa Kawata, Yasuo Imanishi, Keisuke Kobayashi … (2007)

The importance of fibroblast growth factor 23 (FGF-23) in the pathogenesis of phosphate wasting disorders has been established, but controversy remains about how parathyroid hormone (PTH), which also stimulates urinary phosphate excretion, regulates the circulating level of FGF-23. We found that the serum FGF-23 concentration was higher in PTH-cyclin D1 transgenic mice, a model of primary hyperparathyroidism, than in wild-type mice. The serum FGF-23 concentration was significantly and directly correlated with serum PTH and calcium, and inversely correlated with phosphate levels in 90- to 118-week-old mice (all P < 0.005). Quantitative real-time reverse-transcriptase PCR revealed abundant expression of fgf23 in bone, especially in calvaria. The fgf23 expression in calvaria was significantly higher in the transgenic mice compared to the wild-type mice, and correlated well with serum FGF-23 levels. There was a direct correlation between the expression of fgf23 and the expression of osteocalcin and ALP, suggesting that activation of osteoblasts is important in the regulation of FGF-23. Serum FGF-23 levels decreased in the transgenic mice after parathyroidectomy. In conclusion, PTH plays a major role in the regulation of serum FGF-23 level in primary hyperparathyroidism, likely via activation of osteoblasts in bone.

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Physiological Actions of Fibroblast Growth Factor-23

Reinhold Erben (2018)

Fibroblast growth factor-23 (FGF23) is a bone-derived hormone suppressing phosphate reabsorption and vitamin D hormone synthesis in the kidney. At physiological concentrations of the hormone, the endocrine actions of FGF23 in the kidney are αKlotho-dependent, because high-affinity binding of FGF23 to FGF receptors requires the presence of the co-receptor αKlotho on target cells. It is well established that excessive concentrations of intact FGF23 in the blood lead to phosphate wasting in patients with normal kidney function. Based on the importance of diseases associated with gain of FGF23 function such as phosphate-wasting diseases and chronic kidney disease, a large body of literature has focused on the pathophysiological consequences of FGF23 excess. Less emphasis has been put on the role of FGF23 in normal physiology. Nevertheless, during recent years, lessons we have learned from loss-of-function models have shown that besides the paramount physiological roles of FGF23 in the control of 1α-hydroxylase expression and of apical membrane expression of sodium-phosphate co-transporters in proximal renal tubules, FGF23 also is an important stimulator of calcium and sodium reabsorption in distal renal tubules. In addition, there is an emerging role of FGF23 as an auto-/paracrine regulator of alkaline phosphatase expression and mineralization in bone. In contrast to the renal actions of FGF23, the FGF23-mediated suppression of alkaline phosphatase in bone is αKlotho-independent. Moreover, FGF23 may be a physiological suppressor of differentiation of hematopoietic stem cells into the erythroid lineage in the bone microenvironment. At present, there is little evidence for a physiological role of FGF23 in organs other than kidney and bone. The purpose of this mini-review is to highlight the current knowledge about the complex physiological functions of FGF23.

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Author and article information

Journal

Journal ID (nlm-ta): Int J Gen Med

Journal ID (iso-abbrev): Int J Gen Med

Journal ID (publisher-id): IJGM

Journal ID (pmc): ijgm

Title: International Journal of General Medicine

Publisher: Dove

ISSN (Electronic): 1178-7074

Publication date (Electronic): 11 June 2020

Publication date Collection: 2020

Volume: 13

Pages: 289-295

Affiliations

[1 ]Metabolic Syndrome Research Center, Mashhad University of Medical Sciences , Mashhad, Iran

[2 ]Student Research Committee, Mashhad University of Medical Sciences , Mashhad, Iran

[3 ]Clinical Research Development Unit, Imam Reza Hospital, Mashhad University of Medical Sciences , Mashhad, Iran

[4 ]Cancer Research Center, Mashhad University of Medical Sciences , Mashhad, Iran

Author notes

Correspondence: Masoud Mohebbi Emam Reza Hospital , Mashhad9137913316, IranTel +98-9155123712Fax +98-5138022370 Email mohebbim@mums.ac.ir

Author information

Mozhgan Afkhamizadeh http://orcid.org/0000-0002-0998-3694

Ali Teimouri http://orcid.org/0000-0001-5900-4493

Mona Najaf Najafi http://orcid.org/0000-0002-2646-7720

Leila Vazifeh Mostaan http://orcid.org/0000-0001-8322-906X

Masoud Mohebbi http://orcid.org/0000-0002-2285-6809

Article

Publisher ID: 253246

DOI: 10.2147/IJGM.S253246

PMC ID: 7295333

SO-VID: faa69310-b9bc-44a2-96fe-9d9d84e67977

License:

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

History

Date received : 10 March 2020

Date accepted : 28 May 2020

Page count

Figures: 3, Tables: 3, References: 20, Pages: 7

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