Stephanie Kehler1, Mary Kay Rayens1,2, Kristin Ashford3. 1. 1 College of Nursing, University of Kentucky, Lexington, KY, USA. 2. 2 College of Public Health, University of Kentucky, Lexington, KY, USA. 3. 3 Undergraduate Faculty & Interprofessional Education Affairs, College of Nursing, University of Kentucky, Lexington, KY, USA.
Abstract
BACKGROUND: 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. OBJECTIVES: The purpose of this analysis was to evaluate the relationships of hypertensive status and stress with inflammatory biomarkers throughout pregnancy. METHOD: 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. RESULTS: 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. CONCLUSIONS: 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.
BACKGROUND: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. OBJECTIVES: The purpose of this analysis was to evaluate the relationships of hypertensive status and stress with inflammatory biomarkers throughout pregnancy. METHOD: 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. RESULTS: 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. CONCLUSIONS: The associations of stress and hypertensive status with inflammatory biomarkers are complex. Stress and hypertension were associated with changes in inflammatory response. Hypertensivewomen with high stress experienced a heightened anti-inflammatory response, potentially a compensatory mechanism. To better understand this relationship, further longitudinal studies are warranted.
Authors: Jeffrey S Gilbert; Michael J Ryan; Babbette B LaMarca; Mona Sedeek; Sydney R Murphy; Joey P Granger Journal: Am J Physiol Heart Circ Physiol Date: 2007-11-30 Impact factor: 4.733
Authors: Camilla S Kronborg; Jakob Gjedsted; Erik Vittinghus; Troels K Hansen; Jim Allen; Ulla B Knudsen Journal: Acta Obstet Gynecol Scand Date: 2011-05-20 Impact factor: 3.636