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托法西替尼治疗对类风湿性关节炎中血管酶转化酶活性的影响
Dorottya Kacsándi1, Miklós Fagyas2, Ágnes Horváth1
1Department of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Frontiers in medicine
|October 25, 2023
概括
用托法西提尼布抑制简氏激酶 (JAK) 会增加血管激素转化酶 (ACE) 和类风湿性关节炎 (RA) 患者的ACE/ACE2比率. 这种对氨酸 - 氨基氨酸 - 阿尔多斯特系统 (RAAS) 的调节可能解释了在RA中使用JAK抑制剂观察到的心血管影响.
科学领域:
- 类风湿病学 类风湿病学
- 心血管科学 心血管科学
- 药理学 药理学是指药理学的学科.
背景情况:
- 氨-阿尔多素系统 (RAAS) 对于心血管调节至关重要,并且与类风湿性关节炎 (RA) 有关.
- 关于Janus激酶 (JAK) 抑制对 RAAS 在 RA 患者的影响的数据有限.
研究的目的:
- 研究12个月托法西替尼治疗对RAAS生物标记物的影响,特别是血管酶转化酶 (ACE) 和ACE2.
- 评估托法西提尼布对ACE/ACE2比率的影响及其与RA疾病标志物和心血管参数的相关性.
主要方法:
- 一项前性研究涉及30名RA患者,他们接受了托法西提尼布治疗12个月.
- 血清ACE和ACE2水平,ACE/ACE2比率和心血管标志物 (ccIMT,口,cfPWV) 在基线,6个月和12个月测量.
- 还评估了炎症标志物 (CRP,ESR),类风湿因子 (RF) 和抗素蛋白自身抗体 (ACPA).
主要成果:
- 托法西替尼治疗导致ACE水平升高,6个月后ACE2活性暂时增加.
- 在治疗1年后,ACE/ACE2比率显著增加.
- 在ACE/ACE2比率和RA疾病标志物 (RF,ACPA,ESR,疾病持续时间) 之间发现了相关性.
结论:
- 在RA患者中,用托法西提尼布抑制JAK可通过增加血清ACE和ACE/ACE2比率来调节RAAS.
- 在JAK抑制期间,RAAS疾病活性和自身抗体状态影响RAAS调节.
- 这些RAAS变化为RA中JAK抑制相关的心血管影响提供了潜在的机制.
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