ECEESPE2025 Poster Presentations Pituitary, Neuroendocrinology and Puberty (162 abstracts)
Disrupted ACTH and cortisol response to osmotic and non-osmotic stress in patients with AVP-deficiency
Andi Nikaj 1 , Cihan Atila 1 , Irina Chifu 2 , Emanuele Ferrante 3 , Zoran Erlic 4 , Juliana Drummond 5 , Rita Indirli 3 , Roosmarijn Drexhage 6 , Andrew Powlson 7 , Mark Gurnell 7 , Beatriz Santana Soares Rocha 5 , Johannes Hofland 6 , Felix Beuschlein 4,8 , Martin Fassnacht 2 , Bettina Winzeler 9 , Julie Refardt 6,9 & Mirjam Christ-Crain 9
1University Hospital Basel, Department of Endocrinology, Diabetology and Metabolism, Basel, Switzerland; 2University Hospital of Wuerzburg, Division of Endocrinology and Diabetes, Wuerzburg, Germany; 3Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Milan, Italy; 4University Hospital of Zurich (USZ), Zurich, Switzerland; 5Medical School of the Federal University of Minas Gerais, Belo Horizonte, Brazil; 6Erasmus Medical Center Rotterdam, Rotterdam, Netherlands; 7Wellcome-MRC Institute of Metabolic Science, University of Cambridge & Addenbrooke’s Hospital, Cambridge, United Kingdom; 8Klinikum der Universität, Ludwig-Maximilians-Universität München, Munich, Germany; 9University Hospital Basel, Department of Internal Medicine, Basel, Switzerland
JOINT2074
Background: Arginine vasopressin is synthesized in the magnocellular neurons of the hypothalamic supraoptic (SON) and paraventricular nuclei (PVN) and stored in the posterior pituitary. It is released into the bloodstream in response to increased osmolality or non-osmotic stimuli such as hypovolemia or stress. During stress, specialized PVN neurons co-release corticotropin-releasing hormone (CRH) and AVP. AVP amplifies CRH-induced adrenocorticotropic hormone (ACTH) secretion. Elevated cortisol or AVP levels exert negative feedback on the hypothalamus and pituitary to regulate CRH and ACTH secretion. However, disruptions in the AVP system can impair this feedback mechanism, resulting in sustained cortisol elevations.
Methods: This is a secondary analysis of a prospective study conducted at seven tertiary medical centers in Europe and Brazil (2018 to 2022), that utilised the hypertonic saline and the arginine infusion for the diagnostic evaluation of patients presenting with polyuria-polydipsia syndrome. ACTH and cortisol were measured at baseline and expected peak for hypertonic saline and arginine stimulation in patients with AVP-Deficiency and primary polydipsia (i.e., clinical controls). The primary objective was to investigate the effect of hypertonic saline and arginine on the HPA axis response between both groups. The ACTH and cortisol differences were compared between groups using a linear mixed effects model and between the stimulation tests using linear regression model.
Findings: This analysis included 20 patients with AVP-Deficiency and 10 clinical controls. Upon arginine (non-osmotic stress), patients with AVP-Deficiency showed a greater increase in plasma ACTH (difference: -9.2 ng/l [95% CI -17 to -1.8]) and plasma cortisol (difference: -141 nmol/l [95% CI -242 to -40]) comparted to clinical controls. Upon hypertonic saline (osmotic stress), the change in plasma ACTH was similar between patients with AVP-Deficiency and clinical controls (difference: -0.31 ng/l [95% CI -11 to 10]), while the increase in plasma cortisol was greater in patients with AVP-Deficiency compared to clinical controls (difference: -78 nmol/l [95% CI -188 to 32]). Independent of the type of stimulation, patients with AVP deficiency exhibited a significantly greater increase in plasma ACTH (-7.0 ng/l [95% CI -13.3 to -0.8], P = 0.04) and plasma cortisol (-106 nmol/l [95% CI -188 to -24], P = 0.02) compared to clinical controls, with no significant effects between stimulation type and ACTH (P = 0.36) or cortisol response (P = 0.09).
Interpretation: This study demonstrates an altered sustained ACTH and cortisol response pattern to non-osmotic and osmotic stress in patients with AVP-Deficiency, indicating impaired regulation of the HPA axis.
Volume 110
Article tools
My recent searches
My recently viewed abstracts
Authors
Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
© Bioscientifica 2025 |
Privacy policy |
Cookie settings
BiosciAbstracts
Bioscientifica Abstracts is the gateway to a series of products that provide a permanent, citable record of abstracts for biomedical and life science conferences.
Find out more