FGF23‐related hypophosphatemic rickets preceding the onset of systemic lupus erythematosus: A juvenile case

Abstract

Key Clinical MessageThis case report describes the clinical course of a juvenile female with FGF23‐related hypophosphatemic rickets preceding the onset of SLE. Our study demonstrates the possibility of hypophosphatemic rickets as an early symptom of SLE.AbstractFibroblast growth factor 23 (FGF23)‐related hypophosphatemic rickets is observed in both genetic and acquired disorders. Various reports describe FGF23‐related hypophosphatemia with systemic lupus erythematosus (SLE), although FGF23‐related hypophosphatemia preceding the onset of SLE has never been described. Here, we report the case of a 9‐year‐old female with FGF23‐related hypophosphatemic rickets preceding the onset of SLE. The patient presented to us with arthralgia in the lower extremities and abnormality of gait lasting for 8 months. She was diagnosed with FGF23 hypophosphatemic rickets due to the presence of hypophosphatemic rickets symptoms and high serum levels of FGF23. Additional examination excluded hereditary diseases and tumor‐induced osteomalacia. Three months after diagnosis of FGF23‐related hypophosphatemic rickets, she developed nephritis and was diagnosed with SLE. She was treated with prednisolone, hemodialysis, and disease‐modifying drugs, as well as oral sodium phosphate to improve hypophosphatemia. Serum anti‐double‐stranded DNA antibody (dsDNAab) and plasma tumor necrosis factor‐α (TNF‐α) were elevated at FGF23‐related hypophosphatemic rickets diagnosis. During the clinical course, serum FGF23 correlated with dsDNAab and TNF‐α serum levels, which are involved in SLE disease activity. In this case, FGF23‐related hypophosphatemic rickets without hereditary diseases or tumor‐induced osteomalacia occurred before the appearance of juvenile SLE symptoms, and serum FGF23 represented disease activity in SLE.