| [ Summary ] |
The role of fibroblast growth factor 23 (FGF23) in hypophosphatemia and abnormal vitamin D metabolism in McCune-Albright syndrome (MAS) was shown in this review article. FGF23 was also speculated to be produced in fibrous bone dysplasia tissues in MAS patients. For the mechanism of hypophosphatemia, clinical and laboratory evidence suggested the presence of a humoral factor, which inhibited intestinal phosphate transport in addition to FGF23. Also, the role of other phosphaturic factors, such as matrix extracellular phosphoglycoprotein (MEPE) and frizzled related protein-4 (FRP-4) have not been investigated in MAS until now. Thus, it is still possible that FGF23 is not the only factor, which is associated with the pathophysiology of hypophosphatemia in MAS. |