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Endocrine Abstracts (2021) 77 P1 | DOI: 10.1530/endoabs.77.P1

1BHF Centre for Cardiovascular Science, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom; 2Clinical & Translational Research Institute, Newcastle University, Newcastle upon Tyne, United Kingdom; 3Centre for Inflammation Research, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom; 4NIHR Health Protection Research Unit in Emerging and Zoonotic Infections, Institute of Infection, Veterinary and Ecological Sciences, Faculty of Health and Life Sciences, University of Liverpool, Liverpool, United Kingdom; 5National Heart and Lung Institute, Imperial College London, London, United Kingdom; 6University of Edinburgh, Edinburgh, United Kingdom; 7Centre for Tropical Medicine and Global Health, University of Oxford, Oxford, United Kingdom; 8Deanery of Molecular, Genetic and Population Health Sciences, University of Edinburgh, Edinburgh, United Kingdom; 9Division of Genetics and Genomics, Roslin Institute, University of Edinburgh, Edinburgh, United Kingdom


Background: Secretion and metabolism of glucocorticoids and sex steroids is disrupted in critical illness, and may be further disrupted in COVID-19. The host receptor (ACE-2) is expressed in endocrine tissues including adrenal cortex and gonad, and its occupancy may dysregulate the renin-angiotensin system. We hypothesise that severe COVID-19 results in glucocorticoid and sex hormone deficiency, and aldosterone excess.

Methods: Plasma was obtained from 279 adults admitted to UK hospitals with COVID-19 between March and June 2020, at recruitment to the ISARIC/WHO CCP-UK prospective cohort study. 67% were male, median (interquartile range (IQR)) age was 63.0 (52.0-73.5) years, and time from symptom onset was 11.0 (6.0-16.5) days. These represented a spectrum of disease severity as per the WHO Ordinal Scale, with 19.7% in-hospital mortality. 22 steroid hormones, precursors and metabolites were quantified by LCMS/MS. Data are median (IQR).

Results: Compared with patients not requiring supplemental oxygen, those with fatal disease had higher cortisol concentrations (793.2 (552.7-957.9) vs. 465.9 (338.4-580.8) nmol/l, P <0.001) and cortisol:cortisone ratios (16.7 (12.2-23.7) vs. 8.6 (6.6-12.8), P <0.01), and (in males) lower testosterone concentrations (1.1 (0.6-2.1) vs. 6.8 (4.8-10.5) nmol/l, P <0.001). Testosterone correlated inversely with IL-6 (r = -0.62, P <0.01) and estrone (r = -0.3, P <0.01) in males, while estradiol was below detectable threshold (46 pmol/l) in 266/279 patients. Aldosterone levels were raised in those receiving invasive mechanical ventilation (586.0 (125.0-885.2) vs 136.1 (75.0-357.6) pmol/l, P <0.01). Findings remained significant after adjustment for confounders.

Conclusions: Amongst patients hospitalised with COVID-19, steroid responses are similar to other causes of critical illness, including elevated glucocorticoids and reduced male testosterone. The efficacy of glucocorticoid treatment is therefore unlikely related to any COVID-induced hypocortisolism. Re-evaluation of these hormone axes is important to determine if abnormalities persist beyond resolution of infection in people with ‘long COVID’.

Volume 77

Society for Endocrinology BES 2021

Edinburgh, United Kingdom
08 Nov 2021 - 10 Nov 2021

Society for Endocrinology 

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