Effects of iron deficiency anemia and its treatment on fibroblast growth factor 23 and phosphate homeostasis in women.
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TLDR
It is proposed that intravenous iron lowers cF GF23 in humans by reducing fgf23 transcription as it does in mice, whereas carbohydrate moieties in certain iron preparations may simultaneously inhibit FGF23 degradation in osteocytes leading to transient increases in iFGF23 and reduced serum phosphate.Abstract:
Fibroblast growth factor 23 (FGF23) is an osteocyte-derived hormone that regulates phosphate and vitamin D homeostasis. Through unknown mechanisms, certain intravenous iron preparations induce acute, reversible increases in circulating FGF23 levels that lower serum phosphate in association with inappropriately low levels of calcitriol, similar to genetic diseases of primary FGF23 excess. In contrast, studies in wild-type mice suggest that iron deficiency stimulates fgf23 transcription but does not result in hypophosphatemia because FGF23 is cleaved within osteocytes by an unknown catabolic system. We tested the association of iron deficiency anemia with C-terminal FGF23 (cFGF23) and intact FGF23 (iFGF23) levels in 55 women with a history of heavy uterine bleeding, and assessed the longitudinal biochemical response over 35 days to equivalent doses of randomly-assigned, intravenous elemental iron in the form of ferric carboxymaltose (FCM) or iron dextran. Iron deficiency was associated with markedly elevated cFGF23 (807.8 ± 123.9 relative units [RU]/mL) but normal iFGF23 (28.5 ± 1.1 pg/mL) levels at baseline. Within 24 hours of iron administration, cFGF23 levels fell by approximately 80% in both groups. In contrast, iFGF23 transiently increased in the FCM group alone, and was followed by a transient, asymptomatic reduction in serum phosphate <2.0 mg/dL in 10 women in the FCM group compared to none in the iron dextran group. Reduced serum phosphate was accompanied by increased urinary fractional excretion of phosphate, decreased calcitriol levels, and increased parathyroid hormone levels. These findings suggest that iron deficiency increases cFGF23 levels, and that certain iron preparations temporarily increase iFGF23 levels. We propose that intravenous iron lowers cFGF23 in humans by reducing fgf23 transcription as it does in mice, whereas carbohydrate moieties in certain iron preparations may simultaneously inhibit FGF23 degradation in osteocytes leading to transient increases in iFGF23 and reduced serum phosphate.read more
Citations
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Journal ArticleDOI
Hypophosphataemia after ferric carboxymaltose is unrelated to symptoms, intestinal inflammation or vitamin D status.
Wendy Fang,Rachel Kenny,Qurat-ul-Ain Rizvi,Lawrence P. McMahon,Lawrence P. McMahon,Mayur Garg,Mayur Garg,Mayur Garg +7 more
TL;DR: Hypophosphataemia following FCM is common, unrelated to symptomatic adverse events, baseline intestinal or systemic inflammation, or vitamin D status, and no differences between patients with and without IBD were seen.
Journal ArticleDOI
Hypophosphatemia: A Practical Guide to Evaluation and Management.
TL;DR: In this paper , a review discusses normal phosphate homeostasis, clinical manifestations and causes of hypophosphatemia, and an approach to establish a diagnosis and appropriate management, as well as an approach for appropriate management.
Journal ArticleDOI
Hypophosphataemic Rickets Due to Parenteral Ferrous Carboxymaltose ina Young Man with Crohn Disease and Iron Deficiency: A Case Report andReview of Literature
Michael Reyes,Terrence Diamond +1 more
TL;DR: The case of recurrent fractures and hypophosphataemic rickets that occurred in a young man who received parenteral ferrous carboxymaltose for chronic iron deficiency associated with Crohn disease is presented.
Journal ArticleDOI
Letter: inconsistency in reporting of hypophosphatemia after intravenous iron
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Induction of FGF23-related hypophosphatemic osteomalacia by alcohol consumption
Naoko Hidaka,Hajime Kato,Minae Koga,Masaki Katsura,Yuko Oyama,Yuka Kinoshita,Seiji Fukumoto,Noriko Makita,Masaomi Nangaku,Nobuaki Ito +9 more
TL;DR: This condition is similar to iron infusion-induced FGF23-related hypophosphatemia in terms of the dysregulation of FGF 23 due to exogenous factors and is critical to obtain better patient outcomes and save medical resources.
References
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Journal ArticleDOI
Fibroblast growth factor 23 and mortality among patients undergoing hemodialysis.
Orlando M. Gutiérrez,Michael Mannstadt,Tamara Isakova,Jose Alejandro Rauh-Hain,Hector Tamez,Anand Shah,Kelsey Smith,Hang Lee,Ravi Thadhani,Harald Jüppner,Myles Wolf,Myles Wolf +11 more
TL;DR: Increased FGF-23 levels appear to be independently associated with mortality among patients who are beginning hemodialysis treatment, and a potential biomarker that can be used to guide strategies for the management of phosphorus balance in patients with chronic kidney disease is investigated.
Journal ArticleDOI
Cloning and characterization of FGF23 as a causative factor of tumor-induced osteomalacia
Takashi Shimada,Satoru Mizutani,Takanori Muto,Takashi Yoneya,Rieko Hino,Shu Takeda,Yasuhiro Takeuchi,Toshiro Fujita,Seiji Fukumoto,Takeyoshi Yamashita +9 more
TL;DR: It is concluded that overproduction of F GF23 causes TIO, whereas mutations in the FGF23 gene result in autosomal dominant hypophosphatemic rickets possibly by preventing proteolytic cleavage and enhancing biological activity of FGF 23.
Journal ArticleDOI
Circulating concentration of FGF-23 increases as renal function declines in patients with chronic kidney disease, but does not change in response to variation in phosphate intake in healthy volunteers.
TL;DR: Circulating FGF-23 was significantly elevated in patients with CKD and its concentration correlated with renal creatinine clearance, and in healthy volunteers, F GF-23 levels did not change after phosphate deprivation or phosphate loading.
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