ArticleBone2014
Iron and fibroblast growth factor 23 in X-linked hypophosphatemia.
Article in Bone, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 38 citations in OpenAlex.
- Oral Iron Replacement Normalizes Fibroblast Growth Factor 23 in Iron-Deficient Patients With Autosomal Dominant Hypophosphatemic Rickets.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020Trial
- Article
- Current Practices in Monitoring Children and Adults With X-linked Hypophosphatemia: A Global Survey of Expert Experience.The Journal of clinical endocrinology and metabolism · 2025Article
- Interdisciplinary management of FGF23-related phosphate wasting syndromes: a Consensus Statement on the evaluation, diagnosis and care of patients with X-linked hypophosphataemia.Nature reviews. Endocrinology · 2022Review
- Iron deficiency plays essential roles in the trigger, treatment, and prognosis of autosomal dominant hypophosphatemic rickets.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2021Article
- Congenital Conditions of Hypophosphatemia in Children.Calcified tissue international · 2021Review
- Consensus Recommendations for the Diagnosis and Management of X-Linked Hypophosphatemia in Belgium.Frontiers in endocrinology · 2021Review
- FGF23 and Associated Disorders of Phosphate Wasting.Pediatric endocrinology reviews : PER · 2019Review
- Clinical practice recommendations for the diagnosis and management of X-linked hypophosphataemia.Nature reviews. Nephrology · 2019Article
- Pharmacological management of X-linked hypophosphataemia.British journal of clinical pharmacology · 2019Review
- Physiological regulation of phosphate by vitamin D, parathyroid hormone (PTH) and phosphate (Pi).Pflugers Archiv : European journal of physiology · 2019Review
- Review
- The metabolic bone disease associated with theBone reports · 2017Article
- Dental management of patients with X-linked hypophosphatemia.Restorative dentistry & endodontics · 2017Article
- Serum fibroblast growth factor 23, serum iron and bone mineral density in premenopausal women.Bone · 2016Article
- Systemic Control of Bone Homeostasis by FGF23 Signaling.Current molecular biology reports · 2016Article
- Fibroblast growth factor 23 and acute kidney injury.Pediatric nephrology (Berlin, Germany) · 2015Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundExcess fibroblast growth factor 23 (FGF23) causes hypophosphatemia in autosomal dominant hypophosphatemic rickets (ADHR) and X-linked hypophosphatemia (XLH). Iron status influences C-terminal FGF23 (incorporating fragments plus intact FGF23) in ADHR and healthy subjects, and intact FGF23 in ADHR. We hypothesized that in XLH serum iron would inversely correlate to C-terminal FGF23, but not to intact FGF23, mirroring the relationships in normal controls.
methodsSubjects included 25 untreated outpatients with XLH at a tertiary medical center and 158 healthy adult controls. Serum iron and plasma intact FGF23 and C-terminal FGF23 were measured in stored samples.
resultsIntact FGF23 was greater than the control mean in 100% of XLH patients, and >2SD above the control mean in 88%, compared to 71% and 21% respectively for C-terminal FGF23. In XLH, iron correlated negatively to log-C-terminal FGF23 (r=-0.523, p<0.01), with a steeper slope than in controls (p<0.001). Iron was not related to log-intact FGF23 in either group. The log-ratio of intact FGF23 to C-terminal FGF23 was higher in XLH (0.00±0.44) than controls (-0.28±0.21, p<0.01), and correlated positively to serum iron (controls r=0.276, p<0.001; XLH r=0.428, p<0.05), with a steeper slope in XLH (p<0.01).
conclusionLike controls, serum iron in XLH is inversely related to C-terminal FGF23 but not intact FGF23. XLH patients are more likely to have elevated intact FGF23 than C-terminal FGF23. The relationships of iron to FGF23 in XLH suggest that altered regulation of FGF23 cleaving may contribute to maintaining hypophosphatemia around an abnormal set-point.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.