ArticleJournal of the Endocrine Society2018
Fibroblast Growth Factor 23-Induced Hypophosphatemia in Acute Leukemia.
Article in Journal of the Endocrine Society, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Increased Cadmium Load, Vitamin D Deficiency, and Elevated FGF23 Levels as Pathophysiological Factors Potentially Linked to the Onset of Acute Lymphoblastic Leukemia: A Review.Journal of personalized medicine · 2024Review
- Exploration of the skeletal phenotype of theFrontiers in endocrinology · 2023Article
- Hypophosphatemia and FGF23 tumor-induced osteomalacia in two cases of metastatic breast cancer.Clinical nephrology · 2021Article
- Tumor-Induced Osteomalacia.Calcified tissue international · 2021Review
- Increased FGF-23 levels are linked to ineffective erythropoiesis and impaired bone mineralization in myelodysplastic syndromes.JCI insight · 2020Article
- The diagnostic challenges and clinical course of a myeloid/lymphoid neoplasm with eosinophilia andCold Spring Harbor molecular case studies · 2020Article
- Drug-Induced Hypophosphatemia: Current Insights.Drug safety · 2020Review
- Oncogenic osteomalacia and metastatic breast cancer: a case report and review of the literature.Journal of diabetes and metabolic disorders · 2019Article
- The Heart and Kidney: Abnormal Phosphate Homeostasis Is Associated With Atherosclerosis.Journal of the Endocrine Society · 2019Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Fibroblast growth factor 23 (FGF23)-induced hypophosphatemia is a rare paraneoplastic syndrome of phosphate wasting that, if unrecognized, may cause tumor-induced osteomalacia. It is classically associated with benign mesenchymal tumors but occasionally has been found in patients with other malignancies. Hypophosphatemia has been associated with acute leukemia but has not previously been reported to be due to inappropriate FGF23 secretion. Here, we describe FGF23-induced severe hypophosphatemia and renal phosphate wasting associated with a mixed-phenotype Philadelphia chromosome-like acute leukemia in a previously healthy 22-year-old man. He was found to have low serum 1,25-dihydroxyvitamin D and extremely high FGF23 levels, as well as inappropriate urinary phosphorus excretion. The hypophosphatemia improved with calcitriol and oral phosphate treatment but normalized only during chemotherapy-induced ablation of the blasts. FGF23 levels declined with a reduction in peripheral blast counts. Using real-time reverse transcription polymerase chain reaction, we found that the leukemia cells were the source of FGF23. To our knowledge, this is the first description of FGF23-induced hypophosphatemia associated with acute leukemia. We recommend that the FGF23 paraneoplastic syndrome be considered as a possible etiology of hypophosphatemia in patients with acute leukemia.
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