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. 2009 Sep 1;4(5):435-442.
doi: 10.1586/eem.09.27.

Tumor-induced osteomalacia

Emily G Farrow  1 , Kenneth E White
Affiliations

Tumor-induced osteomalacia

Emily G Farrow et al. Expert Rev Endocrinol Metab. .

Abstract

Tumor-induced osteomalacia (TIO) is an acquired disorder of isolated renal phosphate wasting associated with tumors, typically of mesenchymal origin. Patients with TIO share similar biochemical and skeletal phenotypes with patients who have autosomal dominant hypophosphatemic rickets (ADHR) and X-linked hypophosphatemia. The study of TIO introduced the idea of the existence of circulating factors, referred to as 'phosphatonins', produced by the tumor, which act upon the kidney to reduce phosphate reabsorption. Although several factors have been identified, the phosphatonin FGF-23, also identified as the causative factor in ADHR, is currently the best characterized of these factors relative to phosphate handling. This review describes the importance of TIO in understanding phosphate homeostasis in the context of new endocrine interactions between the skeleton and the kidney.

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Figures

Figure 1
Figure 1. FGF-23 actions on phosphate metabolism
FGF-23 is normally produced by bone cells and secreted into the circulation, potentially in response to increased phosphate and/or 1,25(OH) 2 vitamin D. In TIO, a tumor produces excess FGF-23. FGF-23 may initially act in the renal DCT, subsequently leading to a decrease in Npt2a and Npt2c expression and a decrease in 1,25(OH)2 vitamin D production in the PT. Ultimately, continuously elevated serum FGF-23 results in renal phosphate wasting and hypophosphatemia, followed by osteomalacia and fractures. FGF-23 reduces PTH mRNA and protein, however the role of this action of FGF-23 in TIO remains to be determined. DCT: Distal convoluted tubule; Npt2: Type II sodium phosphate cotransporter; PT: Proximal tubule; PTH: Parathyroid hormone; TIO: Tumor-induced osteomalacia.
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