目的:原发性多饮的特征是摄入过多的液体,这可能会抑制加压素水平。据推测,由于加压素共同调节HPA轴,抑制的加压素水平会导致下丘脑-垂体-肾上腺(HPA)轴失调。然而,数据是矛盾的。这项研究的目的是研究与健康对照相比,原发性烦渴患者HPA轴的标志物。
方法:探索性分析,结合来自两个不同的前瞻性观察研究的数据。
方法:我们纳入了34例原发性多饮患者(68%为女性,中位年龄29.5岁(四分位距,IQR:26.0,38.8)和20个健康对照(55%女性,中位年龄24.0岁[IQR:22.0,27.2])。
方法:主要结果是使用昼夜节律血清和唾液皮质醇评估的HPA轴活性的差异,促肾上腺皮质激素(ACTH)刺激之前和之后的24小时尿游离皮质醇和皮质醇水平;使用Wilcoxon秩和检验评估原发性多饮患者和健康对照组之间的空腹和肽水平。
结果:昼夜节律血清皮质醇水平没有差异(p=.9),各组之间尿游离皮质醇水平(p=0.17)和血清皮质醇对ACTH刺激的反应(p=0.77)。与健康对照组相比,原发性多食患者的昼夜节律唾液皮质醇水平显着降低,估计差异为-3.7nmol/L(95%CI:-5.5,-1.8nmol/L,p<.001)。与健康志愿者相比,原发性多饮患者的空腹和肽素水平显着降低(p<0.01)。
结论:我们的结果表明,原发性多饮患者和健康对照组之间的HPA轴活性没有差异。观察到的唾液皮质醇水平的差异可能与唾液中的稀释效应有关,而不是考虑其他发现而改变的压力轴。
Primary polydipsia is characterized by excessive fluid intake which may suppress vasopressin levels. It is speculated that suppressed vasopressin levels lead to a dysregulated hypothalamic-pituitary-adrenal (HPA) axis as vasopressin co-modulates the HPA axis. However, data are contradictory. The aim of this study was to investigate markers of the HPA axis in patients with primary polydipsia compared to healthy controls.
Exploratory analysis combining data from two different prospective observational studies.
We included 34 patients with primary polydipsia (68% females, median aged 29.5 years (interquartile range, IQR: 26.0, 38.8) and 20 healthy controls (55% females, median age 24.0 years [IQR: 22.0, 27.2]).
The main outcome was difference in HPA axis activity assessed using circadian serum and salivary cortisol, 24-h urinary free cortisol and cortisol levels before and after adrenocorticotropic hormone (ACTH) stimulation; vasopressin suppression was assessed measuring fasting copeptin levels between patients with primary polydipsia and healthy controls using Wilcoxon rank-sum test.
No difference was seen in circadian serum cortisol levels (p = .9), urinary free cortisol levels (p = .17) and serum cortisol in response to ACTH stimulation (p = .77) between groups. Circadian salivary cortisol levels were significantly lower in patients with primary polydipsia compared to healthy controls with an estimated difference of -3.7 nmol/L (95% CI: -5.5, -1.8 nmol/L, p < .001). Fasting copeptin levels were significantly lower in patients with primary polydipsia compared to healthy volunteers (p < 0.01).
Our results suggest no difference in HPA axis activity between patients with primary polydipsia and healthy controls. The observed difference in salivary cortisol levels may be linked to a dilution effect in saliva rather than an altered stress axis considering the other findings.