The pathophysiology of hypophosphatemia.
Best Pract Res Clin Endocrinol Metab
; 38(2): 101851, 2024 Mar.
Article
em En
| MEDLINE
| ID: mdl-38087658
ABSTRACT
After identification of fibroblast growth factor (FGF) 23 as the pivotal regulator of chronic serum inorganic phosphate (Pi) levels, the etiology of disorders causing hypophosphatemic rickets/osteomalacia has been clarified, and measurement of intact FGF23 serves as a potent tool for differential diagnosis of chronic hypophosphatemia. Additionally, measurement of bone-specific alkaline phosphatase (BAP) is recommended to differentiate acute and subacute hypophosphatemia from chronic hypophosphatemia. This article divides the etiology of chronic hypophosphatemia into 4 groups A. FGF23 related, B. primary tubular dysfunction, C. disturbance of vitamin D metabolism, and D. parathyroid hormone 1 receptor (PTH1R) mediated. Each group is further divided into its inherited form and acquired form. Topics for each group are described, including "ectopic FGF23 syndrome," "alcohol consumption-induced FGF23-related hypophosphatemia," "anti-mitochondrial antibody associated hypophosphatemia," and "vitamin D-dependent rickets type 3." Finally, a flowchart for differential diagnosis of chronic hypophosphatemia is introduced.
Palavras-chave
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Osteomalacia
/
Hipofosfatemia
/
Raquitismo Hipofosfatêmico Familiar
Limite:
Humans
Idioma:
En
Ano de publicação:
2024
Tipo de documento:
Article