0
Grand Rounds | Clinician's Corner

Tumor-Induced Osteomalacia

Suzanne M. Jan de Beur, MD
JAMA. 2005;294(10):1260-1267. doi:10.1001/jama.294.10.1260.
Text Size: A A A
Published online

Tumor-induced osteomalacia (TIO) is a rare paraneoplastic form of renal phosphate wasting that results in severe hypophosphatemia, a defect in vitamin D metabolism, and osteomalacia. This debilitating disorder is illustrated by the clinical presentation of a 55-year-old woman with progressive fatigue, weakness, and muscle and bone pain with fractures. After a protracted clinical course and extensive laboratory evaluation, tumor-induced osteomalacia was identified as the basis of her clinical presentation. In this article, the distinctive clinical characteristics of this syndrome, the advances in diagnosis of TIO, and new insights into the pathophysiology of this disorder are discussed.

Figures in this Article

Sign In to Access Full Content

Don't have Access?

Register and get free email Table of Contents alerts, saved searches, PowerPoint downloads, CME quizzes, and more

Subscribe for full-text access to content from 1998 forward and a host of useful features

Activate your current subscription (AMA members and current subscribers)

Purchase Online Access to this article for 24 hours

Figures

Figure 2. Radiographic and Histologic Features of Tumor-Induced Osteomalacia
Graphic Jump Location

A, Octreotide scan demonstrating small mesenchymal tumor in the head of the humerus (arrowhead). B, Hemangiopericytoma with numerous pericytes and vascular channels (hematoxylin and eosin stain). Original magnification ×100. C, Bone biopsy with Goldner stain. Excessive osteoid or unmineralized bone matrix composed mainly of collagen stains pink. Mineralized bone stains blue. Normal bone usually has a very thin, barely visible layer of osteoid. The presence of excessive osteoid is indicative of osteomalacia. This bone biopsy demonstrates severe osteomalacia. Original magnification ×20.

Figure 3. Mechanisms of FGF-23 Excess in Renal Phosphate-Wasting Syndromes
Graphic Jump Location

In tumor-induced osteomalacia, fibroblast growth factor 23 (FGF-23) and other phosphatonins ectopically produced by a mesenchymal tumor lead to excess circulating FGF-23 levels. In autosomal dominant hypophosphatemic rickets, FGF-23 excess results from mutations in the FGF-23 gene that render the protein resistant to cleavage and inactivation. In X-linked hypophosphatemia, the mechanism of FGF-23 excess is more speculative; mutations in the PHEX endopeptidase (presumably located on osteoblasts or osteocytes), are thought to either directly or indirectly result in FGF-23 excess by interfering with processing and inactivation of FGF-23.

Tables

References

CME


You need to register in order to view this quiz.
NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Multimedia

Some tools below are only available to our subscribers or users with an online account.

Web of Science® Times Cited: 47

Sign In to Access Full Content

Related Content

Customize your page view by dragging & repositioning the boxes below.

Articles Related By Topic
Related Topics
PubMed Articles
Pseudo-(tumor-induced) rickets. J Bone Miner Res 2001;16(8):1564-71.
Jobs
brightcove.createExperiences();