| Iron modifies plasma FGF23 differently in autosomal dominant hypophosphatemic rickets and healthy humans. | |
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MedLine Citation:
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PMID: 21880793 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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CONTEXT: In autosomal dominant hypophosphatemic rickets (ADHR), fibroblast growth factor 23 (FGF23) resists cleavage, causing increased plasma FGF23 levels. The clinical phenotype includes variable onset during childhood or adulthood and waxing/waning of hypophosphatemia. Delayed onset after puberty in females suggests iron status may be important. OBJECTIVE: Studies were performed to test the hypothesis that plasma C-terminal and intact FGF23 concentrations are related to serum iron concentrations in ADHR. DESIGN AND SETTING: Cross-sectional and longitudinal studies of ADHR and a cross-sectional study in healthy subjects were conducted at an academic medical center. PARTICIPANTS: Participants included 37 subjects with ADHR mutations from four kindreds and 158 healthy adult controls. MAIN OUTCOME MEASURE: The relationships of serum iron concentrations with plasma C-terminal and intact FGF23 concentrations were evaluated. RESULTS: Serum phosphate and 1,25-dihydroxyvitamin D correlated negatively with C-terminal FGF23 and intact FGF23 in ADHR but not in controls. Serum iron was negatively correlated to both C-terminal FGF23 (r = -0.386; P < 0.05) and intact FGF23 (r = -0.602; P < 0.0001) in ADHR. However, control subjects also demonstrated a negative relationship of serum iron with C-terminal FGF23 (r = -0.276; P < 0.001) but no relationship with intact FGF23. Longitudinally in ADHR subjects, C-terminal FGF23 and intact FGF23 concentrations changed negatively with iron concentrations (P < 0.001 and P = 0.055, respectively), serum phosphate changed negatively with C-terminal FGF23 and intact FGF23 (P < 0.001), and there was a positive relationship between serum iron and phosphate (P < 0.001). CONCLUSIONS: Low serum iron is associated with elevated FGF23 in ADHR. However, in controls, low serum iron was also associated with elevated C-terminal FGF23, but not intact FGF23, suggesting cleavage maintains homeostasis despite increased FGF23 expression. |
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Authors:
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Erik A Imel; Munro Peacock; Amie K Gray; Leah R Padgett; Siu L Hui; Michael J Econs |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2011-08-31 |
Journal Detail:
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Title: The Journal of clinical endocrinology and metabolism Volume: 96 ISSN: 1945-7197 ISO Abbreviation: J. Clin. Endocrinol. Metab. Publication Date: 2011 Nov |
Date Detail:
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Created Date: 2011-11-07 Completed Date: 2011-12-23 Revised Date: 2013-02-19 |
Medline Journal Info:
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Nlm Unique ID: 0375362 Medline TA: J Clin Endocrinol Metab Country: United States |
Other Details:
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Languages: eng Pagination: 3541-9 Citation Subset: AIM; IM |
Affiliation:
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Department of Medicine, Indiana University School of Medicine, 541 North Clinical Drive, CL 459, Indianapolis, Indiana 46202, USA. eimel@iupui.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adult Cross-Sectional Studies Female Fibroblast Growth Factors / blood*, genetics Humans Hypophosphatemia / genetics, metabolism* Iron / blood* Male Middle Aged Mutation Rickets / genetics, metabolism* Vitamin D / analogs & derivatives, blood |
| Grant Support | |
ID/Acronym/Agency:
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K23 AR057096/AR/NIAMS NIH HHS; K23AR057096/AR/NIAMS NIH HHS; L40 AR056526/AR/NIAMS NIH HHS; P01 AG18397/AG/NIA NIH HHS; R01 AR042228/AR/NIAMS NIH HHS; R01AR42228/AR/NIAMS NIH HHS; R21 AR061078-02/AR/NIAMS NIH HHS; UL1RR025761/RR/NCRR NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/fibroblast growth factor 23; 1406-16-2/Vitamin D; 62031-54-3/Fibroblast Growth Factors; 66772-14-3/1,25-dihydroxyvitamin D; 7439-89-6/Iron |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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