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Related Concept Videos

Bone Disorders01:29

Bone Disorders

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Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...
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A Normal FGF23 Does Not Preclude Tumor-Induced Osteomalacia.

Neeharika Nandam1, Sadia Ejaz1, William Ahrens2

  • 1Department of Medicine, Division of Endocrinology and Metabolism University of North Carolina at Chapel Hill Chapel Hill NC USA.

JBMR Plus
|February 22, 2021
PubMed
Summary

Tumor-induced osteomalacia (TIO) is a rare disorder causing bone loss due to excess fibroblast growth factor 23 (FGF23). Early diagnosis and surgical removal of the phosphaturic tumor are crucial for recovery.

Keywords:
DISORDERS OF CALCIUM/PHOSPHATE METABOLISMORTHOPEDIC INJURY/FRACTURE HEALINGOSTEOMALACIA AND RICKETSPTH/Vit D/FGF23TUMOR‐INDUCED BONE DISEASE

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Area of Science:

  • Endocrinology
  • Bone Metabolism
  • Oncology

Background:

  • Tumor-induced osteomalacia (TIO) is a rare paraneoplastic condition characterized by impaired bone mineralization.
  • It is primarily caused by excessive secretion of fibroblast growth factor 23 (FGF23) from mesenchymal tumors.
  • Patients often present with profound hypophosphatemia and bone pain, leading to fragility fractures.

Purpose of the Study:

  • To present a case of TIO in a middle-aged man with multiple fragility fractures.
  • To highlight the diagnostic challenges and pitfalls in interpreting laboratory findings for TIO.
  • To emphasize the importance of timely diagnosis and surgical intervention for TIO management.

Main Methods:

  • A case report of a 45-year-old male with multiple fragility fractures and hypophosphatemia.
  • Diagnostic workup included biochemical tests, genetic analysis for bone disorders, and imaging (PET/CT).
  • Tumor resection followed by assessment of clinical and biochemical response.

Main Results:

  • The patient experienced progressive functional deterioration due to multiple fragility fractures.
  • Initial FGF23 levels were not significantly elevated, complicating the diagnosis.
  • PET/CT identified a suprapatellar lesion, confirmed as a phosphaturic mesenchymal tumor upon biopsy.
  • Post-resection, the patient showed marked improvement in physical function, pain, and resolution of hypophosphatemia.

Conclusions:

  • TIO diagnosis requires careful exclusion of other causes of bone loss and meticulous interpretation of FGF23 levels.
  • Prompt surgical resection of the causative tumor is the definitive treatment for TIO.
  • This case underscores the importance of a high index of suspicion for TIO in patients with unexplained hypophosphatemia and fractures.