尽管有生物化学控制,但FGF23的升高揭示了慢性甲状腺功能低下症中隐藏的矿物质失调
Matteo Malagrinò1,2, Anna Piazza1,2, Nicolò Bisceglia1,2
1Division of Endocrinology and Diabetes Prevention and Care, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna 40138, Italy.
Journal of the Endocrine Society
|February 2, 2026
概括
纤维细胞生长因子 (FGF23) 在慢性缺甲状腺症中经常升高,这表明酸盐代谢受损. 这种增加在促进酸盐分泌方面似乎无效,原因是性抵抗.
科学领域:
- 内分泌学 在内分泌学.
- 腎臟病學 (nephrology) 是一種醫學專業.
- 矿物质的新陈代谢.
背景情况:
- 纤维细胞生长因子 (FGF23) 是一种调节酸盐平衡的关键激素.
- 它在影响和酸盐水平的状况 - - 甲状腺功能低下症中的作用尚不清楚.
- 了解FGF23在缺甲状腺症中的作用,可能会揭示一些关于心脏和脏并发症的见解.
研究的目的:
- 为了确定患有慢性偏偏甲状腺症的患者中异常FGF23度的患病率.
- 研究FGF23水平与矿物代谢之间的关系.
- 在这个患者群体中探索FGF23与脏酸盐处理的关联.
主要方法:
- 一个横截面的,观察性研究设计.
- 包括48名患有慢性副甲状腺功能障碍症的患者.
- 分析了包括FGF23,,酸盐,PTH,1,25-二氧维生素D,eGFR和TmPO4/GFR在内的生物化学参数.
主要成果:
- 71%的患者表现出FGF23水平升高,即使有充分的生化控制.
- FGF23水平与较长的疾病持续时间,较低的eGFR,较低的PTH,降低的1,25(OH) 2D和较高的Ca × P产物相关.
- 尽管高FGF23,脏酸盐再吸收 (TmPO4 / GFR) 矛盾地增加,表明脏抵抗.
结论:
- FGF23的升高在慢性缺甲状腺症中很常见,表明酸盐代谢受损.
- 增加的FGF23在促进酸盐分泌方面似乎无效,可能是由于抵抗.
- 需要进一步的研究来澄清FGF23作为生物标志物,风险因素和治疗甲状腺功能低下的治疗标的作用.
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