Intracranial phosphaturic mesenchymal tumor mimicking meningioma and causing tumor-induced osteomalacia: a case report.
4 affiliations
- 1Department of Medicine, Division of Endocrinology, Hartford Hospital, Hartford, CT 06102, United States.
- 2Department of Radiology, Hartford Hospital, Hartford, CT 06102, United States.
- 3Department of Neurosurgery, Hartford Hospital, Hartford, CT 06102, United States.
- 4Department of Pathology, Hartford Hospital, Hartford, CT 06102, United States.
Abstract
A 32-yr-old woman presented with a 2-year history of progressive bone pain, proximal muscle weakness, worsening ambulation, and bilateral hip insufficiency fractures without preceding trauma. Laboratory evaluation revealed severe hypophosphatemia (1.1 mg/dL), elevated bone-specific alkaline phosphatase, progressive secondary hyperparathyroidism, and inappropriately elevated circulating FGF-23, with fasting paired serum and urine studies confirming renal phosphate wasting (tubular maximum phosphate reabsorption per glomerular filtration rate 1.88 mg/dL; fractional excretion of phosphate 14.6%), consistent with tumor-induced osteomalacia (TIO). Functional imaging with ⁶⁸Ga-DOTATATE PET/CT demonstrated intense tracer uptake in a small anterior cranial lesion. Brain MRI revealed a dural-based olfactory groove lesion interpreted radiographically as a meningioma. Selective venous sampling demonstrated a cranial-to-peripheral gradient in intact FGF-23 consistent with drainage from the anterior cranial fossa. Surgical resection produced postoperative normalization of FGF-23 and rapid correction of hypophosphatemia. Histology showed meningioma-like architecture with whorls and psammoma bodies, but expanded molecular testing did not identify canonical meningioma-associated alterations, and DNA methylation profiling classified the lesion as a mesenchymal neoplasm not elsewhere classified and fusion negative. FGF-23 in situ hybridization was positive, and the final surgical pathology diagnosis was mesenchymal tumor favoring phosphaturic mesenchymal tumor over meningioma. This case illustrates how a mesenchymal tumor arising in the meninges can mimic meningioma radiographically and histologically while producing the endocrine phenotype of TIO.
Related
- Case Report: Phosphaturic mesenchymal tumor arising from the jugular bulb without symptomatic osteomalacia.
- Burosumab-responsive micro tumor-induced osteomalacia caused by a 6-mm phosphaturic mesenchymal tumor of the femoral head: a case report with review of literature on small (≤10 mm) FGF23-producing tumors
- Intracranial Rosai–Dorfman Disease Presenting as a Posterior Fossa Dural-Based Mass Mimicking Meningioma: A Case Report
- Surgical hip dislocation for the phosphaturic mesenchymal tumor of the femoral head and neck: a clinical outcome analysis.
- Intraosseous sarcoidosis mimicking orbital apex meningioma: Report of a case
BibTeX
@article{rabiei2026intracranial,
title = {{Intracranial phosphaturic mesenchymal tumor mimicking meningioma and causing tumor-induced osteomalacia: a case report.}},
author = {Samaneh Rabiei and Daniel Collins and Paul Schwartz and Antonella Pallante and Xianyuan Song and Vitaly Kantorovich},
journal = {JBMR plus},
year = {2026},
month = sep,
doi = {10.1093/jbmrpl/ziag156},
url = {https://europepmc.org/article/MED/42936393},
note = {CC BY},
}
RIS
TY - JOUR
TI - Intracranial phosphaturic mesenchymal tumor mimicking meningioma and causing tumor-induced osteomalacia: a case report.
AU - Samaneh Rabiei
AU - Daniel Collins
AU - Paul Schwartz
AU - Antonella Pallante
AU - Xianyuan Song
AU - Vitaly Kantorovich
PY - 2026
DA - 2026/09/17
JO - JBMR plus
DO - 10.1093/jbmrpl/ziag156
UR - https://europepmc.org/article/MED/42936393
AB - A 32-yr-old woman presented with a 2-year history of progressive bone pain, proximal muscle weakness, worsening ambulation, and bilateral hip insufficiency fractures without preceding trauma. Laboratory evaluation revealed severe hypophosphatemia (1.1 mg/dL), elevated bone-specific alkaline phosphatase, progressive secondary hyperparathyroidism, and inappropriately elevated circulating FGF-23, with fasting paired serum and urine studies confirming renal phosphate wasting (tubular maximum phosphate reabsorption per glomerular filtration rate 1.88 mg/dL; fractional excretion of phosphate 14.6%), consistent with tumor-induced osteomalacia (TIO). Functional imaging with ⁶⁸Ga-DOTATATE PET/CT demonstrated intense tracer uptake in a small anterior cranial lesion. Brain MRI revealed a dural-based olfactory groove lesion interpreted radiographically as a meningioma. Selective venous sampling demonstrated a cranial-to-peripheral gradient in intact FGF-23 consistent with drainage from the anterior cranial fossa. Surgical resection produced postoperative normalization of FGF-23 and rapid correction of hypophosphatemia. Histology showed meningioma-like architecture with whorls and psammoma bodies, but expanded molecular testing did not identify canonical meningioma-associated alterations, and DNA methylation profiling classified the lesion as a mesenchymal neoplasm not elsewhere classified and fusion negative. FGF-23 in situ hybridization was positive, and the final surgical pathology diagnosis was mesenchymal tumor favoring phosphaturic mesenchymal tumor over meningioma. This case illustrates how a mesenchymal tumor arising in the meninges can mimic meningioma radiographically and histologically while producing the endocrine phenotype of TIO.
SN - 2473-4039
ER -