ArticleJBMR plus2025
Approach to determining etiology of hypophosphatemia in a patient with coexisting phosphaturic mesenchymal tumor and fibrous dysplasia.
Article in JBMR plus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Osteomalacia Following Iron Infusion Therapy in a Patient With Rendu-Osler-Weber Syndrome: F-18-FDG PET/CT Discrimination of a Stress Fracture in the Setting of a Musculoskeletal Tumor Mimic.Clinical case reports · 2026Article
- Case Report: A case of x-linked hypophosphatemic rickets complicated with polyostotic fibrous dysplasia caused by PHEX gene mutation and literature review.Frontiers in endocrinology · 2026Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulated FGF23 production is a demonstrated cause of hypophosphatemia and osteomalacia. Diseases associated with these conditions include phosphaturic mesenchymal tumor (PMT) causing tumor induced osteomalacia, various forms of rickets, and fibrous dysplasia (FD). Coexistence of 2 conditions that can increase FGF23 concentrations is rare. We report a case of a 79-yr-old man who presented with rib and right flank pain. Imaging revealed bone lesions in the right iliac wing, left supra-acetabular area, and L4 vertebral body. Biopsies showed a right iliac PMT and left supra-acetabular FD. Cryoablation of both lesions resolved the phosphaturia with normalization of phosphorus level. Coexistence of PMT and FD in this patient with hypophosphatemia raised questions about the source of the FGF23, meaning of coexistence of PMT and FD in the same patient and, about the nature of the third lesion in the L4 vertebral body. Using FGF23 mRNA chromogenic in situ hybridization, we identified the PMT, rather than the FD, as the source of FGF23. Lack of
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