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• W3154339318 abstract "Abstract FGF23 measurements have entered clinical medicine several years ago, and FGF23 has become a treatment target in endocrinology with the introduction of burosumab in 2018. A detailed understanding of FGF23 is needed to properly differentiate various causes of hypophosphatemia with renal phosphorus losses. A variety of different genetic disorders that directly or indirectly affect FGF23 regulation cause inherited phosphate wasting, among which X-linked hypophosphatemia (XLH)—caused by a loss of function of the cell surface–bound protein-cleavage enzyme PHEX (phosphate-regulating neutral endopeptidase)—is by far the most frequent disease. Acquired causes of renal phosphorus wasting with high plasma FGF23 comprise hypophosphatemia after certain iron compounds for intravenous iron repletion and tumor-induced osteomalacia (“oncogenic osteomalacia”), in which so-called “phosphaturic mesenchymal tumors” excessively produce FGF23. Standard of care patients with XLH has been revolutionized when regulatory authorities both in the United States and Europe have approved burosumab, which is a fully human monoclonal antibody that neutralizes FGF23 and thus ameliorates hypophosphatemia. Beyond the field of phosphorus regulation, clinical implications of elevated FGF23 are less certain. Even though experimental and epidemiologic work suggests FGF23 to induce left ventricular hypertrophy and to affect cardiovascular outcome, it is premature to consider plasma FGF23 a clinical target for cardiovascular prevention in today's clinical practice." @default.
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• W3154339318 date "2021-01-01" @default.
• W3154339318 modified "2023-10-16" @default.
• W3154339318 title "FGF23—resolved issues, remaining controversies, and future questions—a clinician's perspective" @default.
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• W3154339318 doi "https://doi.org/10.1016/b978-0-12-818036-5.00005-7" @default.
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