Tumor-induced osteomalacia
Tumor-induced osteomalacia (oncogenic osteomalacia) is an acquired renal phosphate-wasting disorder caused by a phosphaturic mesenchymal tumor that secretes fibroblast growth factor 23, producing bone pain, muscle weakness, and pseudofractures from impaired mineralization. First-line management is oral phosphate and calcitriol supplementation to restore mineralization while the causative tumor is identified.
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What this article covers
- Overview
Definition: tumor-induced osteomalacia, also called oncogenic osteomalacia, is an acquired disorder of inadequate bone mineralization caused by a mesenchymal tumor that produces an acquired renal tubular phosphate leak.
- Epidemiology
An acquired cause of osteomalacia: phosphate deficiency severe enough to impair mineralization can also result from malnutrition or increased renal losses, and mesenchymal tumors are a recognized…
- Risk factors
Presence of a mesenchymal tumor: an acquired tubular phosphate leak can occur with mesenchymal tumors, the mechanism underlying oncogenic osteomalacia.
- Pathophysiology
The phosphaturic hormone is fibroblast growth factor 23 (FGF23): it is the kidney's main phosphaturic hormone, driving renal phosphate excretion.
- Clinical features
Diffuse bone pain and tenderness to palpation: typical symptoms of osteomalacia, often at the tibial plateau and sternum in the general osteomalacia population.
- Differential diagnosis
X-linked hypophosphatemia: the same FGF23-mediated phosphate-wasting mechanism, but inherited and typically presenting in childhood with a family history, unlike the acquired adult-onset presentation here.
- Diagnosis
The diagnostic basis is biochemical and radiographic evidence of impaired mineralization from a phosphate leak, with a progressive rise in total alkaline phosphatase as an early clue that…
- Management
First, correct the mineralization defect with oral phosphate salts plus calcitriol while diagnostic localization of the causative tumor proceeds, because this treatment usually requires calcium…
- Complications
Pathologic fractures: chronic undermineralization from ongoing phosphate wasting predisposes to fractures of the ribs, pelvis, and feet.
- Prognosis
Improves with correction of the mineralization defect: clinical, biochemical, and bone mineral density improvement occur with treatment of the underlying phosphate and vitamin D deficiency.
- Prevention
Monitor serum and urinary calcium closely during phosphate/calcitriol therapy, keeping 24-hour urinary calcium below 300 mg, to avoid hypercalcemia, hypercalciuria, and nephrocalcinosis, since overcorrection is a recognized treatment risk.
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Related articles
- X-linked hypophosphatemia
X-linked hypophosphatemia is an inherited disorder of excess FGF23 activity that causes renal phosphate wasting at the proximal tubule, producing rachitic bone disease in children and osteomalacia in adults despite normal serum calcium and vitamin D. First-line treatment is oral phosphate salts with calcitriol, or burosumab, an anti-FGF23 monoclonal antibody, given alone and never combined with oral phosphate or active vitamin D.
- Vitamin D deficiency rickets
Vitamin D deficiency rickets is defective mineralization of the growing cartilaginous growth plate from inadequate vitamin D, most often in a breastfed infant without supplementation, presenting with bowing of the legs, a rachitic rosary, and delayed motor development around 15 months of age. Diagnosis rests on a low 25-hydroxyvitamin D with elevated parathyroid hormone and characteristic metaphyseal cupping and fraying on long-bone radiographs, and first-line treatment is ergocalciferol 2,000 IU PO once daily for 6 weeks with calcium supplementation.
- Osteoporosis
Osteoporosis is low bone strength that raises fragility fracture risk, diagnosed by a hip or spine T-score of -2.5 or less or by a fragility fracture itself. First-line treatment is an oral bisphosphonate, alendronate or risedronate, alongside adequate calcium and vitamin D intake.