Endocrinology and Metabolism

Original Article

Clinical Study
Effects of Single Vitamin D₃ Injection (200,000 Units) on Serum Fibroblast Growth Factor 23 and Sclerostin Levels in Subjects with Vitamin D Deficiency: Dongdong Zhang, Da Hea Seo, Han Seok Choi, Hye-Sun Park, Yoon-Sok Chung, Sung-Kil Lim; Endocrinol Metab. 2017;32(4):451-459. Published online December 14, 2017; DOI: https://doi.org/10.3803/EnM.2017.32.4.451

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Background

Vitamin D deficiency remains common in all age groups and affects skeletal and non-skeletal health. Fibroblast growth factor 23 is a bone-derived hormone that regulates phosphate and 1,25-dihydroxyvitamin D homeostasis as a counter regulatory factor. 1,25-Dihydroxyvitamin D stimulates fibroblast growth factor 23 synthesis in bone, while fibroblast growth factor 23 suppresses 1,25-dihydroxyvitamin D production in the kidney. The aim of this study was to evaluate the effects of vitamin D₃ intramuscular injection therapy on serum fibroblast growth factor 23 concentrations, and several other parameters associated with bone metabolism such as sclerostin, dickkopf-1, and parathyroid hormone.

Methods

A total of 34 subjects with vitamin D deficiency (defined by serum 25-hydroxyvitamin D levels below 20 ng/mL) were randomly assigned to either the vitamin D injection group (200,000 units) or placebo treatment group. Serum calcium, phosphate, urine calcium/creatinine, serum 25-hydroxyvitamin D, fibroblast growth factor 23, sclerostin, parathyroid hormone, and dickkopf-1 levels were serially measured after treatment.

Results

Comparing the vitamin D injection group with the placebo group, no significant changes were observed in serum fibroblast growth factor 23, parathyroid hormone, or dickkopf-1 levels. Serum sclerostin concentrations transiently increased at week 4 in the vitamin D group. However, these elevated levels declined later and there were no statistically significant differences as compared with baseline levels.

Conclusion

Serum fibroblast factor 23, sclerostin, parathyroid hormone, and dickkopf-1 levels were not affected significantly by single intramuscular injection of vitamin D₃.

Citations

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Effect of vitamin D supplementation on circulating fibroblast growth factor-23 concentration in adults with prediabetes
Lisa Ceglia, Anastassios G. Pittas, Bess Dawson-Hughes
Aging Clinical and Experimental Research.2023; 35(3): 525. CrossRef
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Athena Myrou, Theodoros Aslanidis, Keli Makedou, Athanasios Mitsianis, Aikaterini Thisiadou, Paraskevi Karalazou, Georgios Chatzopoulos, Anastasios Papadopoulos, Antonios Kalis, Dimitrios Giagkoulis, Fotios Lezgidis, Christos Savopoulos
Cureus.2023;[Epub] CrossRef
The effect of vitamin D supplementation on serum levels of fibroblast growth factor- 23: A systematic review and meta-analysis of randomized controlled trials
Fatemeh Meshkini, Sepideh Soltani, Cain C.T. Clark, Vivian Tam, David Meyre, Omid Toupchian, Sahar Saraf-Bank, Shima Abdollahi
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Case Report

Bone Metabolism
A Novel PHEX Gene Mutation in a Patient with Sporadic Hypophosphatemic Rickets: Yea Eun Kang, Jun Hwa Hong, Jimin Kim, Kyong Hye Joung, Hyun Jin Kim, Bon Jeong Ku, Koon Soon Kim; Endocrinol Metab. 2014;29(2):195-201. Published online June 26, 2014; DOI: https://doi.org/10.3803/EnM.2014.29.2.195

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Abstract PDF PubReader

Phosphate regulating gene with homologies to endopeptidases on the X-chromosome (PHEX) is a common cause of X-linked hypophosphatemic (XLH) rickets. Diverse PHEX gene mutations have been reported; however, gene mutations in sporadic rickets are less common than in XLH rickets. Herein, we describe a 50-year-old female patient with sporadic hypophosphatemic rickets harboring a novel splicing-site mutation in the PHEX gene (c.663+1G>A) at the exon 5-intron 5 boundary. The patient had recently suffered from right thigh pain and an aggravated waddling gait. She also presented with very short stature, generalized bone pain, and muscle weakness. Despite low serum phosphate levels, her phosphate reabsorption rate was lower than normal. Additionally, her 1,25-dihydroxyvitamin D₃ concentration was lower than normal, although FGF23 level was normal. After treatment with alfacalcidol and elemental phosphate, her rachitic symptoms subsided, and callus formation was observed in the fracture site on the right femur.

Citations

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A pathogenic PHEX variant (c.1483-1G>C) in a Korean patient with X-linked hypophosphatemic rickets
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A novel de novo mosaic mutation in PHEX in a Korean patient with hypophosphatemic rickets
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Review Article

Bone Metabolism
Diagnostic Modalities for FGF23-Producing Tumors in Patients with Tumor-Induced Osteomalacia: Seiji Fukumoto; Endocrinol Metab. 2014;29(2):136-143. Published online June 26, 2014; DOI: https://doi.org/10.3803/EnM.2014.29.2.136

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Abstract PDF PubReader

Fibroblast growth factor 23 (FGF23) is a hormone that is produced by osteocytes and regulates phosphate and vitamin D metabolism through binding to the Klotho-FGF receptor complex. Excessive actions of FGF23 cause several kinds of hypophosphatemic rickets/osteomalacia. Tumor-induced rickets/osteomalacia (TIO) is a paraneoplastic syndrome caused by overproduction of FGF23 from the responsible tumors. Because TIO is cured by complete resection of the causative tumors, it is of great clinical importance to locate these tumors. Several imaging methods including skeletal survey by magnetic resonance imaging and octreotide scintigraphy have been used to identify the tumors that cause TIO. However, none of these imaging studies indicate that the detected tumors are actually producing FGF23. Recently, systemic venous sampling was conducted for locating FGF23-producing tumor in suspected patients with TIO and demonstrated that this test might be beneficial to a subset of patient. Further studies with more patients are necessary to establish the clinical utility of venous sampling in patients with TIO.

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