ArticleThe Journal of clinical endocrinology and metabolism2024
Serum Phosphorus as a Driver of Skeletal Morbidity in Fibrous Dysplasia.
Article in The Journal of clinical endocrinology and metabolism, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 9 citations in OpenAlex.
- A phase 2 trial of burosumab for treatment of fibroblast growth factor-23-mediated hypophosphatemia in children and adults with fibrous dysplasia.Bone research · 2026Trial
- Article
- When X Does Not Mark the Spot: Autosomal Dominant and Recessive Forms of Renal Hypophosphatemic Rickets and Osteomalacia.Current osteoporosis reports · 2026Review
- Burosumab use in fibroblast growth factor-23-mediated hypophosphatemia in McCune-Albright syndrome/fibrous dysplasia.JCEM case reports · 2026Article
- Low bone mineral density and pain impact in adults with sickle cell disease.Blood advances · 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
- Association between phosphorus intake and wrist fracture: the mediating role of bone mineral density.Food & nutrition research · 2026Article
- Burosumab treatment for FGF23-related hypophosphatemia in a two-year-old girl with McCune-Albright syndrome.Clinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology · 2026Article
- A phase 2 trial of burosumab for treatment of fibroblast growth factor-23 mediated hypophosphatemia in children and adults with fibrous dysplasia.medRxiv : the preprint server for health sciences · 2025Article
- Article
- Burosumab treatment of a child with McCune-Albright syndrome/polyostotic fibrous dysplasia: challenges and benefits.JBMR plus · 2025Article
- Use of burosumab in McCune Albright syndrome: case report and review of literature in mosaic disorders with FGF23 overproduction.Frontiers in endocrinology · 2025Review
- Update on the medical management of fibrous dysplasia of the bone.Therapeutic advances in endocrinology and metabolism · 2025Review
- Acquired Forms of Fibroblast Growth Factor 23-Related Hypophosphatemic Osteomalacia.Endocrinology and metabolism (Seoul, Korea) · 2024Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
contextFibrous dysplasia (FD) results in fractures, pain, and deformities. Abnormal osteoprogenitor cells overproduce FGF23, leading to hyperphosphaturia in most patients and frank hypophosphatemia in a subset. Studies suggest hypophosphatemia is associated with increased FD-related morbidity. However, the relationship between phosphorus and skeletal complications has not been investigated, and the optimal therapeutic target has not been determined.
objectiveCharacterize the impact of serum phosphorus on FD-related morbidity and identify levels associated with increased skeletal complications.
methodsNatural history study with 240 subjects at a clinical research center who had ≥1 fasting phosphorus level, determined as age- and sex-adjusted Z-scores. Subjects were categorized based on frank hypophosphatemia (Z-score ≤ -2; n = 48); low-normophosphatemia (> -2 to ≤ -1; n = 66); and high-normophosphatemia (> -1 to ≤ 2; n = 125). Main outcomes were fractures, orthopedic surgeries, and scoliosis.
resultsSubjects with frank and low-normophosphatemia had increased fracture and surgery rates vs high-normophosphatemia. The prevalence of moderate to severe scoliosis was similarly higher in the frank and low-normophosphatemia groups. In a subanalysis of patients matched for Skeletal Burden Score ≥35, fracture and surgery rates remained higher in the frank hypophosphatemia group, suggesting association between phosphorus and skeletal complications is not explained by differences in FD burden alone.
conclusionBoth frank hypophosphatemia and low-normophosphatemia are associated with increased FD-related complications. This supports FGF23-mediated hypophosphatemia as a driver of skeletal morbidity, which may impact a larger proportion of the FD/McCune-Albright syndrome population than previously recognized. These findings enable clinicians to identify at-risk patients and will inform development of prospective studies to determine optimal therapeutic targets.
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