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Quoted phrase not found in phrase index: "Tumoral calcinosis, hyperphosphatemic, familial, 2"
Page 1
PTH and FGF23 Exert Interdependent Effects on Renal Phosphate Handling: Evidence From Patients With Hypoparathyroidism and Hyperphosphatemic Familial Tumoral Calcinosis Treated With Synthetic Human PTH 1-34.
Ovejero D, Hartley IR, de Castro Diaz LF, Theng E, Li X, Gafni RI, Collins MT. Ovejero D, et al. J Bone Miner Res. 2022 Feb;37(2):179-184. doi: 10.1002/jbmr.4429. Epub 2021 Sep 15. J Bone Miner Res. 2022. PMID: 34464000 Free article.
Parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) both influence blood phosphate levels by regulating urinary phosphate reabsorption. Clinical data suggest that adequate renal phosphate handling requires the presence of both FGF23 and PTH, but robust eviden …
Parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) both influence blood phosphate levels by regulating urinary phosphate reab …
Use of Teriparatide in Hyperphosphatemic Familial Tumor Calcinosis: Evaluating the Interaction Between FGF23 and PTH on the Phosphaturic Effect.
Pallone SG, Kunii IS, da Silva REC, Lazaretti-Castro M. Pallone SG, et al. Calcif Tissue Int. 2022 Jul;111(1):102-106. doi: 10.1007/s00223-022-00969-x. Epub 2022 Mar 25. Calcif Tissue Int. 2022. PMID: 35338393

Laboratory tests on admission were as follows: phosphate (P) 7.1 mg/dL (Normal range (NR) 2.5-4.5 mg/dL), FGF23 c-terminal 2050 RU/mL (NR < 150 RU/mL), and intact FGF23 (iFGF23) 18.93 pg/mL (NR 12.0-69.0 pg/mL). ...In an attempt to further decrease P, a 36-day cycle of

…
Laboratory tests on admission were as follows: phosphate (P) 7.1 mg/dL (Normal range (NR) 2.5-4.5 mg/dL), FGF23 c-terminal 2050 RU/mL …
Hyperphosphatemic tumoral calcinosis caused by FGF23 compound heterozygous mutations: what are the therapeutic options for a better control of phosphatemia?
Claramunt-Taberner D, Bertholet-Thomas A, Carlier MC, Dijoud F, Chotel F, Silve C, Bacchetta J. Claramunt-Taberner D, et al. Pediatr Nephrol. 2018 Jul;33(7):1263-1267. doi: 10.1007/s00467-018-3945-z. Epub 2018 Mar 28. Pediatr Nephrol. 2018. PMID: 29594503
CASE-DIAGNOSIS/TREATMENT: A 15-year-old girl was referred for a 1.2-kg-calcified mass of the thigh, with hyperphosphatemia (2.8 mmol/L); vascular impairment and soft tissue calcifications were already present. ...
CASE-DIAGNOSIS/TREATMENT: A 15-year-old girl was referred for a 1.2-kg-calcified mass of the thigh, with hyperphosphatemia (2. …
FGF23 contains two distinct high-affinity binding sites enabling bivalent interactions with α-Klotho.
Suzuki Y, Kuzina E, An SJ, Tome F, Mohanty J, Li W, Lee S, Liu Y, Lax I, Schlessinger J. Suzuki Y, et al. Proc Natl Acad Sci U S A. 2020 Dec 15;117(50):31800-31807. doi: 10.1073/pnas.2018554117. Epub 2020 Nov 30. Proc Natl Acad Sci U S A. 2020. PMID: 33257569 Free PMC article.
Here we report that the C-terminal tail of FGF23, a region responsible for KLA binding, contains two tandem repeats, repeat 1 (R1) and repeat 2 (R2) that function as two distinct ligands for KLA. FGF23 variants with a single KLA binding site, FGF23-R1, FGF23-R2, or FGF23-w …
Here we report that the C-terminal tail of FGF23, a region responsible for KLA binding, contains two tandem repeats, repeat 1 (R1) and repea …
Development and Validation of a Simple Diagnostic Method to Detect Gain and Loss of Function Defects in Fibroblast Growth Factor-23.
Ramadan AR, Shawar SM, Alghamdi MA. Ramadan AR, et al. Horm Res Paediatr. 2016;86(1):45-52. doi: 10.1159/000447113. Epub 2016 Jun 30. Horm Res Paediatr. 2016. PMID: 27355663 Clinical Trial.
None of the mutations could be identified using standard restriction fragment length polymorphism. The only technique currently available to confirm the clinical diagnosis is DNA sequencing. METHODS: Using a tri-primer ARMS-PCR, in vitro site-directed mutagenesis and DNA s …
None of the mutations could be identified using standard restriction fragment length polymorphism. The only technique currently available to …