ArticleJBMR plus2025
Excess fibroblast growth factor 23 in alcoholic osteomalacia is derived from the bone.
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 1 paper.
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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
1 citing paper in PubMed.
- Hypophosphatemia in Patients Receiving Intravenous Iron Supplementation for Iron-Deficiency Anemia: A Narrative Review.Journal of clinical medicine · 2026Review
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Authors and funding
22 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excess fibroblast growth factor 23 (FGF23), a mature osteocyte-derived phosphaturic hormone, causes chronic hypophosphatemic osteomalacia in adults. This rare condition was recently reported in 2 alcoholic patients, with marked improvement upon cessation of alcohol consumption, suggesting a link between alcohol and FGF23-related hypophosphatemia within the highly limited cases. This study aimed to investigate whether the source of excess FGF23 in alcohol-induced FGF23-related hypophosphatemic osteomalacia is the bone or the other organs. To achieve this goal, an immunohistochemical approach for the bone obtained from a patient was employed. Initial attempts at quantifying FGF23 in the bone using conventional immunohistochemistry (IHC) faced issues in quantifiability and sensitivity for low FGF23 expression levels. Therefore, next-generation IHC with phosphor-integrated dots (PIDs) was applied, which enabled the quantification of FGF23 expression in the bone across a broad range. Preliminary analyses using IHC with PIDs on normal bone samples (
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