ECE2023 Oral Communications Oral Communications 3: Pituitary and Neuroendocrinology 1 (6 abstracts)
Diagnosing Vasopressin Deficiency (Central Diabetes Insipidus) using Copeptin following Hypertonic Saline and Arginine Stimulation
Julie Refardt 1 , Cihan Atila 1 , Irina Chifu 2 , Emanuele Ferrante 3 , Zoran Erlic 4 , Juliana Drummond 5 , Beatrice Mantovani 6 , Roos Drexhage 7 , Sailer Clara Odilia 1 , Andrea Widmer 1 , Susan Felder 1 , Andrew Powlson 8 , Nina Hutter 1 , Deborah Vogt 1 , Mark Gurnell 8 , Beatriz Santana Soares 5 , Hans Hofland 7 , Felix Beuschlein 4 , Martin Fassnacht 2 , Bettina Winzeler 1 & Mirjam Christ-Crain 1
1University Hospital Basel, Endocrinology, Basel, Switzerland; 2University Hospital and University of Wuerzburg, Germany; 3Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Milano, Italy; 4University Hospital Zurich, Zurich, Switzerland; 5Medical School of the Federal University of Minas Gerais, Belo Horizonte, Brazil; 6University of Milan, Milano, Italy; 7Erasmus MC , Rotterdam, Netherlands; 8University of Cambridge & Addenbrooke’s Hospital, Cambridge, United Kingdom
Background: The main challenge in the diagnosis of arginine vasopressin deficiency (AVP-deficiency, formerly known as central diabetes insipidus), is its distinction against primary polydipsia. Hypertonic saline stimulated copeptin showed a high diagnostic accuracy of 97% in distinguishing between AVP-deficiency and primary polydipsia (Fenske W, Refardt J, NEJM 2018), but comprises discomfort for patients and requires close sodium monitoring. Arginine stimulated copeptin showed a similar diagnostic accuracy of 93% (Winzeler B, Lancet 2019) with the test being generally well tolerated. A head-to-head comparison is needed to find the best diagnostic test. We hypothesize that the arginine stimulation test is non-inferior to the hypertonic saline stimulation test (non-inferiority margin 10%) for the diagnosis of AVP-deficiency with an easier test protocol and better tolerability.
Methods: Between 2018 and 2022, 164 patients with hypotonic polyuria from seven tertiary medical centers underwent hypertonic saline and arginine stimulation in randomized order for diagnostic evaluation. Serum copeptin levels were measured at sodium-level of>149 mmol/l after hypertonic saline and 60 minutes after arginine infusion, respectively. The final diagnosis was made after treatment response at three-month follow-up blinded to copeptin levels. The main outcome measure was the overall diagnostic accuracy using the pre-defined copeptin cut-off of 4.9 pmol/l for the hypertonic saline and 3.8 pmol/l for the arginine stimulation.
Results: Of the 157 evaluable patients, 69 (44%) were diagnosed with AVP-deficiency and 88 (56%) with primary polydipsia. Of the 69 AVP-deficiency patients, 41 (59%) were judged to have a complete and 28 (41%) to have a partial defect. Copeptin samples are currently being measured in batch analysis and the diagnostic accuracy and tolerability results of both tests will be presented at the Endocrine Society meeting.
Conclusion: This prospective multicentre study will determine which test should be used for the differentiation between AVP-deficiency and primary polydipsia.
Volume 90
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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