Abstract
Tumor-induced osteomalacia (TIO) is a rare skeletal disease caused by hypersecretion of fibroblast growth factor 23 (FGF-23) from neoplasms of mesenchymal origin; patients with TIO present with insufficiency fractures, progressive bone pain, and delayed fracture unions. Herein, we report the case of a 48-year-old man with an insufficiency fracture in his left femoral neck associated with TIO. The causative tumor located in the patient's maxillary sinus had been resected; however, complete resection was impossible due to the location of the tumor. Therefore, the patient's osteomalacia persisted, and he experienced a left femoral neck fracture in the absence of severe trauma. Because delayed fracture union was anticipated in this patient, we performed an internal fixation using an implant with a lateral plate for angular stability and multiple screws for rotational stability. Although fracture union took 15 months, the patient's postoperative course was uneventful, and he could walk without any symptoms or assistance at his most recent follow-up 30 months after surgery. In TIO, hypersecretion of FGF-23 leads to increased renal excretion of phosphorus, increased bone resorption of calcium and phosphorus, decreased osteoblastic bone mineralization, and decreased gastrointestinal absorption of calcium and phosphorus, leading to insufficiency fractures and delayed fracture unions. Diagnosis of TIO is often delayed due to its rarity and vague symptoms. Total resection of the causative tumor is the optimal treatment; however, in cases wherein complete tumor resection is impossible, drug therapy may be insufficient, and the underlying TIO pathology, including bone fragility, may persist. Early diagnosis of TIO is important for preventing insufficiency fractures; however, when fractures are unavoidable, the surgical treatment of femoral neck fractures in patients with osteomalacia should account for a longer time frame for complete fracture union and therefore utilize implants with sufficient stability.
Highlights
Tumor-induced osteomalacia (TIO) is a skeletal disease induced by the inhibition of phosphorus reabsorption in the proximal renal tubules due to the action of fibroblast growth factor 23 (FGF-23) produced by a tumor [1, 2]
TIO is a rare disease in which hypersecretion of FGF-23 produced by a tumor leads to the inhibition of phosphorus reabsorption in the proximal tubules, increased bone resorption of calcium and phosphorus, suppressed osteoblastic bone mineralization, and decreased gastrointestinal absorption of calcium and phosphorus, resulting in bone fragility [1, 2]
The combined effect of these pathologic mechanisms induces a state of osteomalacia, with symptoms presenting in the form of gradual progressive bone pain, myopathies, fractures, and generalized muscle weakness [3]
Summary
Yu Inoue , Tomoaki Fukui, Keisuke Oe, Shinya Hayashi, Teruya Kawamoto, Ryosuke Kuroda, and Takahiro Niikura. Tumor-induced osteomalacia (TIO) is a rare skeletal disease caused by hypersecretion of fibroblast growth factor 23 (FGF-23) from neoplasms of mesenchymal origin; patients with TIO present with insufficiency fractures, progressive bone pain, and delayed fracture unions. The patient’s osteomalacia persisted, and he experienced a left femoral neck fracture in the absence of severe trauma. Total resection of the causative tumor is the optimal treatment; in cases wherein complete tumor resection is impossible, drug therapy may be insufficient, and the underlying TIO pathology, including bone fragility, may persist. Diagnosis of TIO is important for preventing insufficiency fractures; when fractures are unavoidable, the surgical treatment of femoral neck fractures in patients with osteomalacia should account for a longer time frame for complete fracture union and utilize implants with sufficient stability
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