SFEBES2021 Poster Presentations Adrenal and Cardiovascular (45 abstracts)
Plasma steroid profiles in patients hospitalised with COVID-19 - an ISARIC/WHO CCP-UK cohort study
Kerri Devine 1,2 , Clark D Russell 3 , Shona C Moore 4 , Ryan S Thwaites 5 , Hayley E Hardwick 4 , Wilna Oosthuyzen 6 , Jake Dunning 7 , Lance Turtle 4 , Giovanny Rodriguez Blanco 8 , Alex von Kriegsheim 8 , Brian R Walker 1,2 , Natalie ZM Homer 1 , Peter JM Openshaw 5 , J Kenneth Baillie 9 , Malcolm G Semple 4 , Ruth Andrew 1 & Rebecca M Reynolds 1
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
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Endocrine Abstracts
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