解决方案并不简单;在康恩综合征中使用-葡萄糖共运输体-2 抑制剂
1University of Health Sciences, Tepecik Training and Research Hospital, Department of Endocrinology and Metabolism, Turkey.
Blood pressure monitoring
|March 11, 2024
概括
-葡萄糖携带载体-2 抑制剂 (SGLT2-i) 增加了原发性高阿尔多斯顿症患者的血雷宁活性 (PRA). 这表明SGLT2-i可能会增强矿物质皮质类受体对抗剂的有效性或具有直接影响.
科学领域:
- 内分泌学 在内分泌学.
- 药理学 药理学是指药理学的学科.
背景情况:
- 原发性高阿尔多斯特隆症 (PA) 需要对血内活性 (PRA) 进行监测,以评估治疗的疗效.
- 矿物甲基皮质类受体对抗剂 (MRA) 增加PRA,表明足够的阿尔多激素对抗作用.
- -葡萄糖携带载体-2 抑制剂 (SGLT2-i) 具有心脏保护和保护作用,并可能影响PRA.
研究的目的:
- 为了研究SGLT2-i对原发性阿尔多多斯特症 (PA) 患者的PRA抑制的PRA,尽管高剂量螺旋龙治疗SGLT2-i对PRA的影响.
- 评估SGLT2-i是否可以克服PA中对螺旋中毒素的不充分PRA反应.
主要方法:
- 七名糖尿病PA患者的前性评估,尽管每天服用100毫克螺旋,但仍在接受甲福明和抑制PRA (<1 ng/ml/h) 的治疗.
- 甲胺被用empagliflozin取代,并在六个月后重新评估PRA水平.
主要成果:
- 在6个月的empagliflozin治疗后,PRA平均水平从0.464 ± 0.189 ng/ml/h显著增加到3.257 ± 1.881 ng/ml/h (P=0.008).
- 在七名患者中,六名患者的PRA水平超过1ng/ml/h.
- 一名患者没有达到PRA>1 ng/ml/h.
结论:
- 恩帕格利弗洛辛治疗导致PA患者的PRA显著增加,PA患者在螺旋中抑制了PRA.
- 需要进一步的研究来确定这种PRA增加是否反映了药物干扰,增强的螺旋拉克疗效,或直接的阿尔多素受体对抗由empagliflozin.
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