Abstract |
An appropriate phosphate homeostasis is absolutely required for correct bone mineralization and remodeling, for diverse signaling pathways as well as cell membrane formation. Its disequilibrium results in serious complications like hypophosphatemia and excessively reduced fractional tubule phosphate reabsorption (TRP). A rare cause of such a disturbed phosphate balance is tumor-induced osteomalacia (TIO)--a phosphate wasting disorder sometimes associated with certain mesenchymal tumors. These primitive tumors secrete so-called phosphatonins--recently identified factors involved in the regulation of phosphate homeostasis such as the secreted frizzled related protein 4 (sFRP-4), the fibroblast growth factors 7 and 23 (FGF-7/-23), or the matrix extracellular phosphoglycoprotein (MEPE). Progressive muscular weakness and spontaneous bone fractures caused by inadequate osteoid mineralization are the characteristic clinical symptoms, which completely resolve after tumor resection. Here we report a new case of TIO caused by tumor secreted FGF-23 and review the literature to facilitate the correct diagnosis of this rare disorder.
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Authors | M Woznowski, I Quack, J Stegbauer, N Büchner, L C Rump, G Schieren |
Journal | Clinical nephrology
(Clin Nephrol)
Vol. 70
Issue 5
Pg. 431-8
(Nov 2008)
ISSN: 0301-0430 [Print] Germany |
PMID | 19000546
(Publication Type: Case Reports, Journal Article)
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Chemical References |
- FGF23 protein, human
- Phosphates
- Fibroblast Growth Factor-23
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Topics |
- Adult
- Biopsy
- Diagnosis, Differential
- Fibroblast Growth Factor-23
- Follow-Up Studies
- Humans
- Hypophosphatemia, Familial
(complications, diagnosis, urine)
- Magnetic Resonance Imaging
- Male
- Osteomalacia
(diagnosis, etiology, urine)
- Paraneoplastic Syndromes
(diagnosis, etiology)
- Phosphates
(urine)
- Tomography, X-Ray Computed
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