Adrenal Pathologies During Pregnancy and Postpartum

St-Jean, Matthieu; Bourdeau, Isabelle; Lacroix, André

doi:10.1016/b978-0-12-814823-5.00025-8

Cited by 3 publications

(2 citation statements)

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“…During pregnancy, dramatic changes in the functioning of the maternal hypothalamic-pituitary-adrenal (HPA) axis are observed because the placenta expresses the genes for human corticotropin-releasing hormone (hCRH) and the precursor for adrenocorticotropic hormone (ACTH) and beta-endorphin (proopiomelanocortin). Placental corticotropin-releasing hormone (pCRH) production increases dramatically over gestation, and pCRH plays a central role in the regulation of fetal maturation and the timing of parturition 4 .…”

Section: Introductionmentioning

confidence: 99%

“…Typically, in response to the cognitive appraisal of significant stressors, CRH is produced in the paraventricular nucleus of the hypothalamus and released into the pituitary gland. CRH then stimulates the release of ACTH in Maternal cortisol levels on fetal heart rate the anterior pituitary, which subsequently results in the adrenal cortex releasing several glucocorticoids, including cortisol, in humans 4,9 . Consequently, pCRH and cortisol in maternal plasma increase exponentially across pregnancy, and maternal levels can be 60 to 700 times higher than before pregnancy 10 .…”

Section: Introductionmentioning

confidence: 99%

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Effect of maternal cortisol levels on fetal heart rate patterns in primiparous pregnant women in the third trimester

Turan

Kaya

2023

Rev. Assoc. Med. Bras.

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SUMMARY OBJECTIVE: This study aimed to determine whether maternal cortisol levels affect fetal heart rate patterns in primiparous pregnant women in the third trimester. METHODS: This cross-sectional descriptive study included 400 primiparous pregnant women with uncomplicated pregnancies between November and December 2022. The study included primiparous pregnant women over 18 years old in the third trimester who had not exercised for at least 2 h before the fetal heart rate monitoring and had a healthy pregnancy without consuming any food or drink. Fetuses with decelerating heartbeats and pregnant women who showed uterine contraction and cervical dilation during the fetal heart rate monitoring were excluded from the study. Research data were collected with the data collection form. The fetal heart rate data were collected using a cardiotocograph. At least two accelerations during the 20-min nonstress test period were the basis for diagnosing a reactive nonstress test. About 5 mL of maternal saliva for cortisol measurements was collected before fetal heart rate monitoring. Research data were analyzed with IBM SPSS Statistics for Macintosh, Version 28.0. A p-value of <0.05 was considered significant. RESULTS: There were no significant differences in the comparison of the groups in terms of education and income status, family type, fetal gender, pregnancy planning status, BMI and age averages, or gestational week averages (p>0.05). The number of at least two accelerations required for the diagnosis of reactive NST was also higher in Group 1 (maternal salivary cortisol level ≤24.20). A moderately positive relationship between fetal heart rate and maternal salivary cortisol was observed (r=0.448, p=0.000). In total, 11.9% of the total change in fetal heart rate level is explained by maternal cortisol (R 2 =0.119). Maternal cortisol increases fetal heart rate level (ß=0.349). CONCLUSION: These findings suggest that stress in primiparous pregnant women with high cortisol levels may influence fetal heart rate patterns. It was revealed that the increase in cortisol level, considered a stress hormone, may be a harbinger of fetal tachycardia.

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Section: Introductionmentioning

confidence: 99%