ECE2019 Poster Presentations Interdisciplinary Endocrinology 2 (37 abstracts)
Glucocorticoid receptor alpha and betaexpression, serum cortisol and cytokine levels in critical illness
Dimitra Argyro Vassiliadi 1 , Alice Vassiliou 2 , G Stamogiannos 3 , G Floros 3 , Efthymia Botoula 1 , Edison Jahaj 3 , Marinella Tzanela 1 , Stylianos E. Orfanos 2, , Anastasia Kotanidou 2, , Ioanna Dimopoulou 3 & Stylianos Tsagarakis 1
1Department of Endocrinology, Diabetes and Metabolism, Evangelismos Hospital, Athens, Greece; 21st Department of Critical Care Medicine & Pulmonary Services, GP Livanos and M Simou Laboratories, Evangelismos Hospital, Athens Medical School, National & Kapodistrian University of Athens, Athens, Greece; 31st Department of Critical Care Medicine & Pulmonary Services, Evangelismos Hospital, Athens Medical School, National & Kapodistrian University of Athens, Athens, Greece.
Purpose: HPA axis activation resulting in increased cortisol production by the adrenals is a crucial part of the response to critical illness. The action of cortisol may also be modulated at the tissue level, through changes in the availability of the free fraction and modifications of the glucocorticoid receptor activity. It has been proposed that tissue resistance to glucocorticoids may occur, at least in some patients, and relate to insufficient anti-inflammatory activity and development of shock, despite the high circulating levels of cortisol. Therefore, in the present project we assessed serum cortisol levels and the two isoforms of the intracellular signalling receptor for cortisol, the glucocorticoid receptor (GCR), in a cohort of critically ill patients at ICU admission.
Methods: A prospective observational study conducted on 42 critically ill adults not receiving steroids, in a university-affiliated, multidisciplinary intensive care unit (ICU). Blood samples were collected for measurement of glucocorticoid receptor expression and serum cortisol levels within 24-48 hours of admission to the ICU. Twenty-five age- and sex-matched healthy donors were used as controls.
Results: At ICU admission, critically ill patients expressed increased levels of both GCRs compared to healthy controls; GCR-αmRNA expression was 10-fold (P< 0.0001), while GCR-βmRNA levels were 3-fold the expression of controls (P< 0.0001). Patients with acute stress due to surgery or trauma had significantly higher GCR-αmRNA compared to medical patients. The increased levels of alpha and beta GCRmRNA at ICU admission, returned to control values over ICU stay. GCR-βmRNA and cortisol levels were highly elevated in septic shock patients compared to patients without septic shock.
Conclusions: GCR-αmRNA expression rises acutely in response to stress, suggesting that resistance to glucocorticoids, if it occurs, is a later event. Septic shock may represent an exception where increased expression of the GCR-βmay lead to glucocorticoid resistance despite elevated cortisol levels.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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