DIURNAL SALIVARY CORTISOL PATTERNS DURING PREGNANCY AND AFTER DELIVERY - RELATIONSHIP TO PLASMA CORTICOTROPIN-RELEASING-HORMONE
DIURNAL SALIVARY CORTISOL PATTERNS DURING PREGNANCY AND AFTER DELIVERY - RELATIONSHIP TO PLASMA CORTICOTROPIN-RELEASING-HORMONE
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DOI：
10.1111/j.1365-2265.1990.tb00492.x
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发表时间：
1990-08-01
影响因子：
3.2
通讯作者：
SCHULTE, HM
中科院分区：
文献类型：
--
作者：
ALLOLIO, B;HOFFMANN, J;SCHULTE, HM
本文对10名健康妇女在整个妊娠期每四周测定一次唾液皮质醇的昼夜节律。此外，还对12例妊娠晚期及产后3-5天的妇女进行了唾液皮质醇、血清皮质醇、血浆ACTH、血浆CRH和血清孕酮的昼夜变化分析。唾液皮质醇曲线在妊娠期间表现出明显的昼夜节律，平均唾液皮质醇从第25周至第28周开始增加，妊娠晚期达到非妊娠对照组浓度的两倍以上，分娩后迅速恢复正常浓度。唾液皮质醇曲线的变异系数在妊娠晚期由于皮质醇浓度的平行上移而降低（40.2 ± 0.01）。3.4%对77.6 .+-。产后6.6%，P < 0.01）。血浆ACTH和血清皮质醇在分娩前后均呈昼夜变化，产后浓度明显降低（P < 0.01）。在妊娠晚期，孕激素浓度在晚上显著较高（930 . ±. 85 nmol/l vs 813 . ±. 74 nmol/l，P < 0.01），但产后无昼夜变化。妊娠晚期血浆CRH水平显著升高（1.22 ± 0.01）。0.23 0900时为1.0 μ g/l），但没有表现出昼夜变化（1.30 ± 0.05 μ g/l）。0.28μ g/l，1900小时）。此外，尽管CRH水平的范围很广（0.13-3.60 μ g/l），但未注意到妊娠晚期游离皮质醇增加与血浆CRH之间的相关性。妊娠晚期血清孕酮水平与唾液皮质醇水平呈显著正相关（r = 0.70，P < 0.05）。这些发现表明，胎盘CRH不是母亲ACTH和皮质醇释放的唯一调节因子。相反，我们的研究表明，胎盘CRH对妊娠期母体肾上腺皮质功能的影响很小。妊娠期唾液皮质醇水平升高可能是由于高浓度孕酮的抗糖皮质激素作用导致糖皮质激素抵抗。
The circadian rhythm of salivary cortisol was studied in 10 healthy women every 4 weeks throughout pregnancy. In addition, in 12 women the diurnal patterns of salivary cortisol, serum cortisol, plamsa ACTH, plasma CRH and serum progesterone were analysed in late third trimester pregnancy and again 3-5 days after delivery. Salivary cortisol profiles exhibited a clear circadian rhythm during pregnancy with an increase in mean salivary cortisol from the 25th to 28th week onwards reaching concentrations in late pregnancy more than twice as high as in non-pregnant controls, rapidly returning to normal concentrations after delivery. The coefficient of variation of salivary cortisol profiles decreased in third trimester pregnancy due to a parallel upward shift of cortisol concentrations (40.2 .+-. 3.4% vs 77.6 .+-. 6.6% after delivery, P < 0.01). A diurnal pattern was also found for plasma ACTH and serum cortisol before and after delivery with lower concentrations post-partum (P < 0.01). In late pregnancy, progesterone concentrations were significantly higher in the evening (930 .+-. 85 nmol/l vs 813 .+-. 74 nmol/l at 0900 h, P < 0.01) but showed no diurnal variation post-partum. Plasma CRH was significantly elevated in late third trimester pregnancy (1.22 .+-. 0.23 .mu.g/l at 0900 h) but showed no diurnal change (1.30 .+-. 0.28 .mu.g/l at 1900 h). Moreover, no correlation between the free cortisol increase in late pregnancy and plasma CRH was noted despite a wide range of CRH levels (0.13-3.60 .mu.g/l). In contrast, a significant correlation was observed between the serum progesterone increase and the salivary cortisol increase in late pregnancy (r = 0.70, P < 0.05). These findings demonstrate that placental CRH is not the only regulator of maternal ACTH and cortisol release. Instead, our study suggests that placental CRH has little influence on baseline maternal adrenocortical function in pregnancy. The elevated salivary cortisol levels in pregnancy may be explained by glucocorticoid resistance owing to the antiglucocorticoid action of high progesterone concentrations.