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

被引:30
作者
South, Andrew M. [1 ,2 ]
Nixon, Patricia A. [1 ,3 ]
Chappell, Mark C. [2 ,4 ]
Diz, Debra I. [2 ,4 ]
Russell, Gregory B. [5 ]
Snively, Beverly M. [5 ]
Shaltout, Hossam A. [2 ,6 ]
Rose, James C. [6 ]
O'Shea, T. Michael [2 ,7 ]
Washburn, Lisa K. [1 ,2 ]
机构
[1] Wake Forest Sch Med, Dept Pediat, Winston Salem, NC 27101 USA
[2] Wake Forest Sch Med, Hypertens & Vasc Res Ctr, Winston Salem, NC 27101 USA
[3] Wake Forest Univ, Dept Hlth & Exercise Sci, Winston Salem, NC 27109 USA
[4] Wake Forest Sch Med, Dept Surg, Winston Salem, NC USA
[5] Wake Forest Sch Med, Dept Biostat Sci, Winston Salem, NC USA
[6] Wake Forest Sch Med, Dept Obstet & Gynecol, Winston Salem, NC USA
[7] Univ N Carolina, Dept Pediat, Sch Med, Chapel Hill, NC USA
关键词
RESPIRATORY-DISTRESS-SYNDROME; BLOOD-PRESSURE; GLUCOCORTICOID EXPOSURE; CONVERTING ENZYME; HYPERTENSIVE-RATS; CONTROLLED-TRIAL; FOLLOW-UP; BETAMETHASONE; PREVENTION; WEIGHT;
D O I
10.1038/pr.2016.179
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
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.
引用
收藏
页码:88 / 93
页数:6
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