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  • Author: Mirjam Christ-Crain x
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Cihan Atila Department of Endocrinology, Diabetology and Metabolism, University Hospital Basel, Basel, Switzerland
Department of Clinical Research, University of Basel, Basel, Switzerland

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Sophie Monnerat Department of Endocrinology, Diabetology and Metabolism, University Hospital Basel, Basel, Switzerland
Department of Clinical Research, University of Basel, Basel, Switzerland

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Roland Bingisser Emergency Department, University Hospital Basel, Basel, Switzerland

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Martin Siegemund Department of Intensive Care, University Hospital Basel, Basel, Switzerland

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Maurin Lampart Department of Cardiology and Cardiovascular Research Institute Basel (CRIB), University Hospital Basel, University of Basel, Basel, Switzerland

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Marco Rueegg Emergency Department, University Hospital Basel, Basel, Switzerland

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Núria Zellweger Department of Intensive Care, University Hospital Basel, Basel, Switzerland

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Stefan Osswald Department of Cardiology and Cardiovascular Research Institute Basel (CRIB), University Hospital Basel, University of Basel, Basel, Switzerland

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Katharina Rentsch Department of Laboratory Medicine, University Hospital Basel, Basel, Switzerland

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Mirjam Christ-Crain Department of Endocrinology, Diabetology and Metabolism, University Hospital Basel, Basel, Switzerland
Department of Clinical Research, University of Basel, Basel, Switzerland

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Raphael Twerenbold Department of Cardiology and Cardiovascular Research Institute Basel (CRIB), University Hospital Basel, University of Basel, Basel, Switzerland
University Center of Cardiovascular Science & Department of Cardiology, University Heart and Vascular Center Hamburg, University Medical Center Hamburg-Eppendorf, Hamburg, Germany
German Center for Cardiovascular Research (DZHK), Partner Site Hamburg–Kiel–Lübeck, Hamburg, Germany

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Objective

Hyponatremia in COVID-19 is often due to the syndrome of inadequate antidiuresis (SIAD), possibly mediated by interleukin-6 (IL-6)-induced non-osmotic arginine vasopressin (AVP) secretion. We hypothesized an inverse association between IL-6 and plasma sodium concentration, stronger in COVID-19 compared to other respiratory infections.

Design

Secondary analysis of a prospective cohort study including patients with COVID-19 suspicion admitted to the Emergency Department, University Hospital of Basel, Switzerland, between March and July 2020.

Methods

We included patients with PCR-confirmed COVID-19 and patients with similar symptoms, further subclassified into bacterial and other viral respiratory infections. The primary objective was to investigate the association between plasma sodium and IL-6 levels.

Results

A total of 500 patients were included, 184 (37%) with COVID-19, 92 (18%) with bacterial respiratory infections, and 224 (45%) with other viral respiratory infections. In all groups, median (IQR) IL-6 levels were significantly higher in hyponatremic compared to normonatremic patients (COVID-19: 43.4 (28.4, 59.8) vs 9.2 (2.8, 32.7) pg/mL, P < 0.001; bacterial: 122.1 (63.0, 282.0) vs 67.1 (24.9, 252.0) pg/mL, P < 0.05; viral: 14.1 (6.9, 84.7) vs 4.3 (2.1, 14.4) pg/mL, P < 0.05). IL-6 levels were negatively correlated with plasma sodium levels in COVID-19, whereas the correlation in bacterial and other viral infections was weaker (COVID-19: R = −0.48, P < 0.001; bacterial: R = −0.25, P = 0.05, viral: R = −0.27, P < 0.001).

Conclusions

IL-6 levels were inversely correlated with plasma sodium levels, with a stronger correlation in COVID-19 compared to bacterial and other viral infections. IL-6 might stimulate AVP secretion and lead to higher rates of hyponatremia due to the SIAD in these patients.

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The Working Group for Renaming Diabetes Insipidus
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Hiroshi Arima Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan
Japan Endocrine Society

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Timothy Cheetham Department of Paediatric Endocrinology, Newcastle University Faculty of Medical Sciences, Great North Children’s Hospital, Royal Victoria Infirmary, Newcastle upon Tyne, UK
European Society for Pediatric Endocrinology

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Mirjam Christ-Crain Department of Endocrinology, Diabetes and Metabolism, University Hospital Basel, University of Basel, Switzerland
European Society of Endocrinology

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Deborah Cooper Department of Endocrinology, Diabetes and Metabolism, University Hospital Basel, University of Basel, Switzerland

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Mark Gurnell European Society of Endocrinology
Wellcome-MRC Institute of Metabolic Science, University of Cambridge & Addenbrooke’s Hospital, Cambridge Biomedical Campus, Cambridge, UK

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Juliana B Drummond Faculdade de Medicina da UFMG, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil
Brazilian Society of Endocrinology and Metabolism

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Miles Levy Endocrinology, University Hospitals of Leicester, Leicester, UK
Society for Endocrinology

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Ann I McCormack Hormones and Cancer Group, Garvan Institute of Medical Research, Sydney, New South Wales, Australia
Endocrine Society of Australia

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Joseph Verbalis Endocrinology and Metabolism, Georgetown University Medical Center, Washington DC, District of Columbia, USA
Endocrine Society

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John Newell-Price Endocrine Society
Department of Oncology and Metabolism, The Medical School, University of Sheffield, Sheffield, UK

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John A H Wass Department of Endocrinology, Oxford Centre for Diabetes Endocrinology & Metabolism – Endocrinology, Oxford, UK
Pituitary Society

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What’s in a name? That which we call a rose/By any other name would smell as sweet’ (Juliet, from Romeo and Juliet by William Shakespeare). Shakespeare’s implication is that a name is nothing but a word, and it therefore represents a convention with no intrinsic meaning. While this may be relevant to romantic literature, disease names do have real meanings, and consequences, in medicine. Hence, there must be a very good rationale for changing the name of a disease that has a centuries-old historical context. A working group of representatives from national and international endocrinology, and pediatric endocrine societies now proposes changing the name of ‘diabetes insipidus’ to ‘arginine vasopressin deficiency (AVP-D)’ for central etiologies, and ‘arginine vasopressin resistance (AVP-R)’ for nephrogenic etiologies. This article provides both the historical context and the rationale for this proposed name change.

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