Calcimimetics as an adjuvant treatment for familial hypophosphatemic rickets.

Calcimimetics as an adjuvant treatment for familial hypophosphatemic rickets. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Calcimimetics as an adjuvant treatment for familial hypophosphatemic rickets. Abstract Text:

BACKGROUND AND OBJECTIVES: The treatment for X-linked hypophosphatemia (XLH) with phosphate and calcitriol can be complicated by secondary hyperparathyroidism and nephrocalcinosis. Furthermore, vitamin D and phosphate stimulate FGF23 production, the pathogenic factor causing XLH. We investigated in XLH patients: 1) whether treatment with the calcimimetic agent, cinacalcet, will block the rise in parathyroid hormone (PTH) caused by phosphate administration; and 2) whether treatment with oral phosphate and calcitriol increases FGF23 levels. DESIGN, SETTING, PARTICIPANTS, AND MEASUREMENTS: Eight subjects with XLH were given a single oral dose of phosphate, followed the next day by combined treatment with phosphate and cinacalcet. Serum measurements of ionized calcium (Ca), phosphate, creatinine, intact PTH, 1,25(OH)(2)D, FGF23, and tubular threshold for phosphate/glomerular filtration rate (TP/GFR) were assessed in response to short-term treatment with phosphate and cinacalcet and compared with long-term administration of phosphate and calcitriol. RESULTS: Oral phosphate load increased serum phosphate, decreased ionized calcium, and increased PTH. Twenty-four hours later, FGF23 significantly increased and 1,25(OH)(2)D decreased. The concomitant administration of phosphate and cinacalcet resulted in further decrease in serum Ca(2+) but suppression of PTH and greater increase in serum phosphate and TP/GFR. Chronic treatment with phosphate and calcitriol resulted in a smaller increment in serum phosphate and high serum FGF23. CONCLUSIONS: Traditional therapy of XLH with phosphate and calcitriol elevates FGF23 and has the potential to stimulate PTH. Short-term treatment with cinacalcet suppresses PTH, leading to increase in TP/GFR and serum phosphate. Thus, long-term clinical studies are needed to investigate whether cinacalcet may be a useful adjuvant in the treatment of XLH, allowing the use of lower doses of phosphate and calcitriol.

Calcimimetics as an adjuvant treatment for familial hypophosphatemic rickets. Publishing Authors By Initials

For similar abstracts research abstracts see: abstracts research

PUBMED ID PMID:

MEDLINE DATE:

Calcimimetics as an adjuvant treatment for familial hypophosphatemic rickets. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Clinical journal of the American Society of Nephro

VOLUME: 3

Page Numbers: 658-64

Journal Abbreviation:

ISSN: 1555-905X

DAY: 6

MONTH: 02

YEAR: 2008

Calcimimetics as an adjuvant treatment for familial hypophosphatemic rickets. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 101271570

Calcimimetics as an adjuvant treatment for familial hypophosphatemic rickets. Keywords Mesh Terms:

KEYWORDS:

MESH TERMS:

Chemical & Substance for Abstract: Calcimimetics as an adjuvant treatment for familial hypophosphatemic rickets. Information

Substance Name:

Registry Number:

Grant and Affiliation Information for Calcimimetics as an adjuvant treatment for familial hypophosphatemic rickets.

AFFILIATION: Pediatric Nephrology, Bone and Mineral Disorders Clinic, Children's Mercy Hospital, University of Missouri, Kansas City, MO 64108, USA. ualon@cmh.edu

Country: United States

AGENCY: United States NIAMS

GRANT: R01-AR45955

ACRONYM: AR

MEDLINETA: Clin J Am Soc Nephrol

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Calcimimetics as an adjuvant treatment for familial hypophosphatemic rickets Related Publications

• Calcimimetics as an adjuvant treatment for familial hypophosphatemic rickets.
• Characterization of the upstream mouse Cbfa1/Runx2 promoter.
• Development and progression of secondary hyperparathyroidism in chronic kidney disease: lessons from molecular genetics.
• Distinct roles for intrinsic osteocyte abnormalities and systemic factors in regulation of FGF23 and bone mineralization in Hyp mice.
• Field trial and modeling of uptake rates of in situ lipid-free polyethylene membrane passive sampler.
• Health disparities and culturally specific treatment: Perspectives and expectancies of African American smokers.
• How fibroblast growth factor 23 works.
• Investigating habitat value to inform contaminant remediation options: Approach.
• Investigating habitat value to inform contaminant remediation options: Case study.
• Oral paricalcitol: a viewpoint by james B. Wetmore and L. Darryl quarles.
• Pathogenic role of Fgf23 in Dmp1-null mice.
• Phosphorylated acidic serine-aspartate-rich MEPE-associated motif peptide from matrix extracellular phosphoglycoprotein inhibits phosphate regulating gene with homologies to endopeptidases on the X-chromosome enzyme activity.
• Polycystin-1 Regulates Skeletogenesis through Stimulation of the Osteoblast-specific Transcription Factor RUNX2-II.
• Role of hyperphosphatemia and 1,25-dihydroxyvitamin D in vascular calcification and mortality in fibroblastic growth factor 23 null mice.