Kehler Stephanie, Rayens Mary Kay, Ashford Kristin
1 College of Nursing, University of Kentucky, Lexington, KY, USA.
2 College of Public Health, University of Kentucky, Lexington, KY, USA.
Biol Res Nurs. 2019 May;21(3):245-252. doi: 10.1177/1099800419828104. Epub 2019 Mar 11.
Hypertensive disorders are common pregnancy complications in the United States. Although the exact mechanism underlying hypertensive disorders in pregnancy is unknown, there is evidence of involvement of a maladaptive maternal inflammatory response. Psychological maternal stress experienced during pregnancy can increase the risk of a hypertensive disorder by altering the maternal inflammatory response.
The purpose of this analysis was to evaluate the relationships of hypertensive status and stress with inflammatory biomarkers throughout pregnancy.
A 1:2 case-control design was used to analyze secondary data longitudinally with repeated measures of a multicenter, culturally and ethnically diverse pregnant population. Demographic data, psychological stress, and serum inflammatory data were analyzed. The sample consisted of 30 pregnant women with hypertension and 61 normotensive women. Measurements were taken once in each trimester of pregnancy.
Trimester-specific levels of inflammatory biomarkers varied based on stress and hypertensive status. IL-6 was elevated in the hypertensive, high-stress group, while IL-8 was greater among those with high stress, regardless of hypertensive status or trimester. For IL-1α and IL-1β, there was a significant stress-by-trimester interaction, while IL-10 was associated with a significant three-way interaction among stress level, hypertension status, and trimester.
The associations of stress and hypertensive status with inflammatory biomarkers are complex. Stress and hypertension were associated with changes in inflammatory response. Hypertensive women with high stress experienced a heightened anti-inflammatory response, potentially a compensatory mechanism. To better understand this relationship, further longitudinal studies are warranted.
高血压疾病是美国常见的妊娠并发症。尽管妊娠高血压疾病的确切机制尚不清楚，但有证据表明母体炎症反应失调与之有关。孕期母亲经历的心理压力可通过改变母体炎症反应增加患高血压疾病的风险。
本分析的目的是评估整个孕期高血压状态和压力与炎症生物标志物之间的关系。
采用1:2病例对照设计，对一个多中心、文化和种族多样的孕妇群体的重复测量数据进行纵向分析。分析人口统计学数据、心理压力和血清炎症数据。样本包括30名患有高血压的孕妇和61名血压正常的孕妇。在孕期的每个阶段各进行一次测量。
炎症生物标志物的特定孕期水平因压力和高血压状态而异。在高血压、高压力组中，白细胞介素-6升高，而白细胞介素-8在高压力人群中更高，无论高血压状态或孕期如何。对于白细胞介素-1α和白细胞介素-1β，存在显著的压力与孕期交互作用，而白细胞介素-10与压力水平、高血压状态和孕期之间的显著三向交互作用有关。
压力和高血压状态与炎症生物标志物之间的关联很复杂。压力和高血压与炎症反应的变化有关。高压力的高血压女性经历了增强的抗炎反应，这可能是一种代偿机制。为了更好地理解这种关系，有必要进行进一步的纵向研究。
