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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.
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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.

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

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