Serum FGF-23 and Vitamin D Deficiency

2014-08-27 03:14:38 | BioPortfolio


We aimed to determine the effect of vitamin D replacement therapy on serum FGF-23 concentrations in vitamin D deficient women and to compare the FGF-23 concentrations of vitamin D deficient patients with healthy subjects and patients with genetically-determined hypophosphatemic rickets.


Study group was composed of vitamin D deficient females (n =18, mean age 29.1±9.9 yrs), vitamin D sufficient healthy females (control group; n = 19, mean age 28.5±5.2 yrs) and patients with genetically-determined hypophosphatemic rickets (n=13, mean age 26.5±15.1 yrs). Groups were compared for serum FGF-23, 1,25 dihydroxy vitamin D3, calcium, phosphate, bone turnover markers, intact parathyroid hormone and urinary excretion of calcium and phosphate. Vitamin D deficient group was re-evaluated after a standard treatment regimen.

Study Design

Observational Model: Case Control, Time Perspective: Prospective




Istanbul University, Istanbul Faculty of Medicine, Department of Internal Medicine, Division of Endocrinology and Metabolism




Istanbul University

Results (where available)

View Results


Published on BioPortfolio: 2014-08-27T03:14:38-0400

Clinical Trials [10 Associated Clinical Trials listed on BioPortfolio]

A Study of KRN23 in Pediatric Patients With X-linked Hypophosphatemic Rickets/Osteomalacia

The purpose of the study is to assess the efficacy and safety of KRN23 administered subcutaneously once every 2 weeks in children with X-linked hypophosphatemic rickets/osteomalacia(XLH)

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The researchers are trying to evaluate a newer imaging technique (Ga-DOTATATE PET/CT) to see if it is more sensitive to localize the source of the hormone, which has caused the low phospha...

A Study of KRN23 in Subjects With Tumor-Induced Osteomalacia or Epidermal Nevus Syndrome

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Open Label Study of KRN23 on Osteomalacia in Adults With X-linked Hypophosphatemia (XLH)

UX023-CL304 is a Phase 3 open-label, single-arm, multicenter study to establish the effects of KRN23 on bone quality and osteomalacia associated with XLH. Approximately 10 adult subjects w...

Study of KRN23 in Adult Subjects With Tumor-Induced Osteomalacia (TIO) or Epidermal Nevus Syndrome (ENS)

UX023T-CL201 is an, open-label, Phase 2 study. The study will be conducted in adults aged 18 years or older with TIO or ENS whose tumor/skin lesion is inoperable to assess the efficacy and...

PubMed Articles [28 Associated PubMed Articles listed on BioPortfolio]

Rickets/Osteomalacia. FGF23-related hypophosphatemic rickets/osteomalacia.

FGF23 is a hormone that reduces blood phosphate level. Excessive actions of FGF23 result in several kinds of hypophosphatemic rickets/osteomalacia such as X-linked hypophosphatemic rickets and tumor-i...

Osteomalacia-Clinical aspects, diagnostics and treatment.

Osteomalacia is a bone disease caused by impaired skeletal mineralization. Vitamin D dependent types have to be distinguished from hypophosphatemic forms. Typical signs and symptoms include diffuse ...

Rickets/Osteomalacia. Anti-FGF23 antibody therapy in patients with FGF23-related hypophosphatemic rickets and osteomalacia.

Fibroblast growth factor 23(FGF23)is a phosphaturic hormone, and its excess causes several kinds of congenital and acquired hypophosphatemic diseases. A combination of oral active vitamin D3 and phosp...

Rickets/Osteomalacia. Diagnosis of tumor-induced osteomalacia.

Tumor-induced osteomalacia is a fibroblast growth factor 23(FGF23)-related hypophosphatemic disorder caused by FGF23 producing tumor. TIO represents bone pain, fracture/pseudofracture, muscle weakness...

Severe hypophosphatemia induced by denosumab in a patient with osteomalacia and tenofovir disoproxil fumarate-related acquired Fanconi syndrome.

Denosumab, a novel agent that inhibits osteoclasts, reduces the risk of fracture in patients with osteoporosis. However, worsening of hypophosphatemia and other symptoms may be induced by denosumab in...

Medical and Biotech [MESH] Definitions

A disorder characterized by HYPOPHOSPHATEMIA; RICKETS; OSTEOMALACIA; resulting from lack of phosphate reabsorption by the kidneys and possible defects in vitamin D metabolism.

A condition marked by softening of the bones (due to impaired mineralization, with excess accumulation of osteoid), with pain, tenderness, muscular weakness, anorexia, and loss of weight, resulting from deficiency of vitamin D and calcium. (Dorland, 27th ed)

A hereditary disorder characterized by HYPOPHOSPHATEMIA; RICKETS; OSTEOMALACIA; renal defects in phosphate reabsorption and vitamin D metabolism; and growth retardation. Autosomal and X-linked dominant and recessive variants have been reported.

A condition of an abnormally low level of PHOSPHATES in the blood. Severe hypophosphatemia (below 1 mg/liter) can affect every organ in the body leading to HEMOLYSIS; LASSITUDE; SEIZURES; and COMA. Chronic hypophosphatemia can lead to MUSCLE WEAKNESS; and bone diseases, such as RICKETS and OSTEOMALACIA.

The major circulating metabolite of VITAMIN D3. It is produced in the LIVER and is the best indicator of the body's vitamin D stores. It is effective in the treatment of RICKETS and OSTEOMALACIA, both in azotemic and non-azotemic patients. Calcifediol also has mineralizing properties.

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