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早产青少年的产前皮质类固醇与肾素-血管紧张素-醛固酮系统

Antenatal corticosteroids and the renin-angiotensin-aldosterone system in adolescents born preterm.

作者信息

South Andrew M, Nixon Patricia A, Chappell Mark C, Diz Debra I, Russell Gregory B, Snively Beverly M, Shaltout Hossam A, Rose James C, O'Shea T Michael, Washburn Lisa K

机构信息

Department of Pediatrics, Wake Forest School of Medicine, Winston Salem, North Carolina.

Hypertension and Vascular Research Center, Wake Forest School of Medicine, Winston Salem, North Carolina.

出版信息

Pediatr Res. 2017 Jan;81(1-1):88-93. doi: 10.1038/pr.2016.179. Epub 2016 Sep 16.

Abstract

BACKGROUND

Antenatal corticosteroid (ANCS) treatment hastens fetal lung maturity and improves survival of premature infants, but the long-term effects of ANCS are not well-described. Animal models suggest that ANCS increases the risk of cardiovascular disease through programmed changes in the renin-angiotensin (Ang)-aldosterone system (RAAS). We hypothesized that ANCS exposure alters the RAAS in adolescents born prematurely.

METHODS

A cohort of 173 adolescents born prematurely was evaluated, of whom 92 were exposed to ANCS. We measured plasma and urine Ang II and Ang-(1-7) and calculated Ang II/Ang-(1-7) ratios. We used general linear regression models to estimate the difference in the RAAS between the ANCS-exposed and unexposed groups, adjusting for confounding variables.

RESULTS

In unadjusted analyses, and after adjustment for sex, race, and maternal hypertension, ANCS exposure was associated with increased urinary Ang II/Ang-(1-7) (estimate 0.27 (95% CI 0.03, 0.5), P = 0.03), increased plasma Ang-(1-7) (0.66 (0.26, 1.07), P = 0.002), and decreased plasma Ang II/Ang-(1-7) (-0.48 (-0.91, -0.06), P = 0.03).

CONCLUSION

These alterations indicate an imbalance in the urinary RAAS, promoting the actions of Ang II at the expense of Ang-(1-7), which over time may increase the risk of renal inflammation and fibrosis and ultimately hypertension and renal disease.

摘要

背景

产前使用糖皮质激素(ANCS)可加速胎儿肺成熟并提高早产儿存活率,但ANCS的长期影响尚未得到充分描述。动物模型表明,ANCS通过肾素-血管紧张素(Ang)-醛固酮系统(RAAS)的程序性变化增加心血管疾病风险。我们假设,暴露于ANCS会改变早产出生青少年的RAAS。

方法

对173名早产出生的青少年进行队列研究,其中92人暴露于ANCS。我们测量了血浆和尿液中的Ang II和Ang-(1-7),并计算了Ang II/Ang-(1-7)比值。我们使用一般线性回归模型来估计暴露于ANCS组和未暴露组之间RAAS的差异,并对混杂变量进行了调整。

结果

在未调整分析中,以及在对性别、种族和母亲高血压进行调整后,暴露于ANCS与尿Ang II/Ang-(1-7)升高(估计值0.27(95%CI 0.03,0.5),P = 0.03)、血浆Ang-(1-7)升高(0.66(0.26,1.07),P = 0.002)和血浆Ang II/Ang-(1-7)降低(-0.48(-0.91,-0.06),P = 0.03)相关。

结论

这些改变表明尿RAAS失衡,以Ang-(1-7)为代价促进Ang II的作用,随着时间的推移,这可能会增加肾炎症和纤维化的风险,并最终导致高血压和肾脏疾病。

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