In:
Clinical Endocrinology, Wiley
Abstract:
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. Design Exploratory analysis combining data from two different prospective observational studies. Patients 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]). Measurements 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. Results 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). Conclusion 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.
Type of Medium:
Online Resource
ISSN:
0300-0664
,
1365-2265
Language:
English
Publisher:
Wiley
Publication Date:
2022
detail.hit.zdb_id:
2004597-9
