更新于：2024-11-01

FGF23 positive Hypophosphatemia

FGF23阳性低磷血症

更新于：2024-11-01

基本信息

别名-

简介-

关联

项与 FGF23阳性低磷血症相关的药物

Burosumab-TWZA

布罗索尤单抗

靶点

FGF23

作用机制

FGF23拮抗剂

在研机构

Kyowa Kirin Australia Pty Ltd. [+4]

原研机构

Kyowa Kirin Co., Ltd.

在研适应症

FGF23阳性低磷血症 [+4]

非在研适应症

慢性疼痛 [+1]

最高研发阶段批准上市

首次获批国家/地区

欧盟 [+3]

首次获批日期2018-02-19

KLOT-1123

靶点

FGF23

作用机制

FGF23拮抗剂

在研机构

EPOK Therapeutics, Inc.

原研机构

EPOK Therapeutics, Inc.

在研适应症

慢性肾病 [+1]

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 FGF23阳性低磷血症相关的临床结果

登录后查看更多信息

100 项与 FGF23阳性低磷血症相关的转化医学

登录后查看更多信息

0 项与 FGF23阳性低磷血症相关的专利（医药）

登录后查看更多信息

项与 FGF23阳性低磷血症相关的文献（医药）

2024-10-01·Journal of the Formosan Medical Association

Effective bone healing after corrective osteotomy in a patient with FGF23-related hypophosphatemic disease using short-term burosumab treatment

Article

作者: Chiu, Hsin-Sung ; Tsai, Meng-Ju Melody ; Wang, Ting-Ming ; Lee, Ni-Chung ; Tung, Yi-Ching

Hypophosphatemic rickets is a rare metabolic bone disease caused by renal phosphate wasting, leading to impaired bone mineralization. We present a case of a boy with fibroblast growth factor 23 (FGF23)-related hypophosphatemic rickets who did not achieve callus consolidation after six months of conventional therapy with phosphate and active vitamin D following corrective osteotomy. After one month of therapy with an FGF23 antibody (burosumab), the patient demonstrated significant improvement and no longer required a walking aid. Following six months of burosumab therapy, the bone had nearly fully healed. This report is the first to address the short-term use of burosumab therapy to promote bone healing after orthopedic surgery. Our findings further emphasize the clinical advantages and short-term applications of burosumab in FGF23-related hypophosphatemic diseases, especially for patients undergoing orthopedic surgery.

2024-03-01·Best Practice & Research Clinical Endocrinology & Metabolism

The pathophysiology of hypophosphatemia

Review

作者: Kato, Hajime ; Hidaka, Naoko ; Ito, Nobuaki

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.

2024-01-01·Clinical Case Reports

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

作者: tabei, Yoko ; Hamajima, Emi ; Shimada, Masaharu ; Wada, Aya ; Ohtsu, Yoshiaki ; Takizawa, Takumi ; Osawa, Yoshimitsu

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.