These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Fibroblast growth factor 23, parathyroid hormone, and 1alpha,25-dihydroxyvitamin D in surgically treated primary hyperparathyroidism.
    Author: Tebben PJ, Singh RJ, Clarke BL, Kumar R.
    Journal: Mayo Clin Proc; 2004 Dec; 79(12):1508-13. PubMed ID: 15595334.
    Abstract:
    OBJECTIVE: To determine whether fibroblast growth factor 23 (FGF23) contributes to the hypophosphatemia of primary hyperparathyroldism. PATIENTS AND METHODS: Thirteen adult patients with primary hyperparathyroidism had serum collected before and after parathyroidectomy for analysis of inorganic phosphorus, calcium, 1alpha,25-dihydroxyvitamin D (1alpha,25[OH]2D), parathyroid hormone (PTH), FGF23, creatinine, and bone-specific alkaline phosphatase (BSAP). Patients were recruited between July 24, 2003, and February 11, 2004. RESULTS: Before surgery, patients had elevated serum calcium and PTH concentrations. Serum phosphorus concentrations were in the low-normal range. The FGF23 concentrations were not elevated in patients with primary hyperparathyroidism compared with healthy controls. Within 24 hours of surgery, serum calcium, PTH, 1alpha,25(OH)2D, and BSAP concentrations were lower (P < .002 for all) and phosphorus concentrations were higher (P = .003) than in the preoperative state. The FGF23 concentrations were similar 1 day and 6 weeks after surgery. The FGF23 concentrations did not correlate with serum phosphorus, calcium, PTH, 1alpha,25(OH)2D, creatinine, or BSAP concentrations in the preoperative or postoperative state. CONCLUSION: Parathyroid hormone is the major regulator of serum phosphorus concentrations in patients with primary hyperparathyroidism. Fibroblast growth factor 23 does not appear to play a role in phosphorus homeostasis in patients with surgically treated primary hyperparathyroidism.
    [Abstract] [Full Text] [Related] [New Search]