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Plasma steroid concentrations reflect acute disease severity and normalise during recovery in people hospitalised with COVID-19.
Devine, Kerri; Russell, Clark D; Blanco, Giovanny R; Walker, Brian R; Homer, Natalie Z M; Denham, Scott G; Simpson, Joanna P; Leavy, Olivia C; Elneima, Omer; McAuley, Hamish J C; Shikotra, Aarti; Singapuri, Amisha; Sereno, Marco; Saunders, Ruth M; Harris, Victoria C; Houchen-Wolloff, Linzy; Greening, Neil J; Lone, Nazir I; Thorpe, Mathew; Greenhalf, William; Chalmers, James D; Ho, Ling-Pei; Horsley, Alex; Marks, Michael; Raman, Betty; Moore, Shona C; Dunning, Jake; Semple, Malcolm G; Andrew, Ruth; Wain, Louise V; Evans, Rachael A; Brightling, Christopher E; Kenneth Baillie, John; Reynolds, Rebecca M.
Afiliação
  • Devine K; BHF/University Centre for Cardiovascular Science, Queen's Medical Research Institute, Edinburgh Bioquarter, University of Edinburgh, Edinburgh, UK.
  • Russell CD; Translational and Clinical Research Institute, Newcastle University, Newcastle upon Tyne, UK.
  • Blanco GR; University of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, Edinburgh, UK.
  • Walker BR; Edinburgh Cancer Research UK Centre, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK.
  • Homer NZM; BHF/University Centre for Cardiovascular Science, Queen's Medical Research Institute, Edinburgh Bioquarter, University of Edinburgh, Edinburgh, UK.
  • Denham SG; Translational and Clinical Research Institute, Newcastle University, Newcastle upon Tyne, UK.
  • Simpson JP; BHF/University Centre for Cardiovascular Science, Queen's Medical Research Institute, Edinburgh Bioquarter, University of Edinburgh, Edinburgh, UK.
  • Leavy OC; Mass Spectrometry Core, Edinburgh Clinical Research Facility, Centre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
  • Elneima O; Mass Spectrometry Core, Edinburgh Clinical Research Facility, Centre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
  • McAuley HJC; Mass Spectrometry Core, Edinburgh Clinical Research Facility, Centre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
  • Shikotra A; Department of Population Health Sciences, University of Leicester, Leicester, UK.
  • Singapuri A; NIHR Leicester Biomedical Research Centre, University of Leicester, Leicester, UK.
  • Sereno M; NIHR Leicester Biomedical Research Centre, University of Leicester, Leicester, UK.
  • Saunders RM; NIHR Leicester Biomedical Research Centre, University of Leicester, Leicester, UK.
  • Harris VC; NIHR Leicester Biomedical Research Centre, University of Leicester, Leicester, UK.
  • Houchen-Wolloff L; NIHR Leicester Biomedical Research Centre, University of Leicester, Leicester, UK.
  • Greening NJ; NIHR Leicester Biomedical Research Centre, University of Leicester, Leicester, UK.
  • Lone NI; NIHR Leicester Biomedical Research Centre, University of Leicester, Leicester, UK.
  • Thorpe M; NIHR Leicester Biomedical Research Centre, University of Leicester, Leicester, UK.
  • Greenhalf W; NIHR Leicester Biomedical Research Centre, University of Leicester, Leicester, UK.
  • Chalmers JD; Centre for Medical Informatics, The Usher Institute, University of Edinburgh, Edinburgh, UK.
  • Ho LP; Centre for Medical Informatics, The Usher Institute, University of Edinburgh, Edinburgh, UK.
  • Horsley A; University of Liverpool, Liverpool, UK.
  • Marks M; Ninewells Hospital and Medical School, University of Dundee, Dundee, UK.
  • Raman B; MRC Human Immunology Unit, University of Oxford, Oxford, UK.
  • Moore SC; Division of Infection, Immunity and Respiratory Medicine, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, UK.
  • Dunning J; Department of Clinical Research, London School of Hygiene and Tropical Medicine, London, UK.
  • Semple MG; Hospital for Tropical Diseases, University College London Hospital, London, UK.
  • Andrew R; Division of Infection and Immunity, University College London, London, UK.
  • Wain LV; Radcliffe Department of Medicine, University of Oxford, Oxford, UK.
  • Evans RA; NIHR 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, UK.
  • Brightling CE; Pandemic Sciences Institute, University of Oxford, Oxford, UK.
  • Kenneth Baillie J; NIHR 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, UK.
  • Reynolds RM; BHF/University Centre for Cardiovascular Science, Queen's Medical Research Institute, Edinburgh Bioquarter, University of Edinburgh, Edinburgh, UK.
Clin Endocrinol (Oxf) ; 100(4): 317-327, 2024 04.
Article em En | MEDLINE | ID: mdl-38229583
ABSTRACT

OBJECTIVE:

Endocrine systems are disrupted in acute illness, and symptoms reported following coronavirus disease 2019 (COVID-19) are similar to those found with clinical hormone deficiencies. We hypothesised that people with severe acute COVID-19 and with post-COVID symptoms have glucocorticoid and sex hormone deficiencies. DESIGN/PATIENTS Samples were obtained for analysis from two UK multicentre cohorts during hospitalisation with COVID-19 (International Severe Acute Respiratory Infection Consortium/World Health Organisation [WHO] Clinical Characterization Protocol for Severe Emerging Infections in the UK study), and at follow-up 5 months after hospitalisation (Post-hospitalisation COVID-19 study). MEASUREMENTS Plasma steroids were quantified by liquid chromatography-mass spectrometry. Steroid concentrations were compared against disease severity (WHO ordinal scale) and validated symptom scores. Data are presented as geometric mean (SD).

RESULTS:

In the acute cohort (n = 239, 66.5% male), plasma cortisol concentration increased with disease severity (cortisol 753.3 [1.6] vs. 429.2 [1.7] nmol/L in fatal vs. least severe, p < .001). In males, testosterone concentrations decreased with severity (testosterone 1.2 [2.2] vs. 6.9 [1.9] nmol/L in fatal vs. least severe, p < .001). In the follow-up cohort (n = 198, 62.1% male, 68.9% ongoing symptoms, 165 [121-192] days postdischarge), plasma cortisol concentrations (275.6 [1.5] nmol/L) did not differ with in-hospital severity, perception of recovery, or patient-reported symptoms. Male testosterone concentrations (12.6 [1.5] nmol/L) were not related to in-hospital severity, perception of recovery or symptom scores.

CONCLUSIONS:

Circulating glucocorticoids in patients hospitalised with COVID-19 reflect acute illness, with a marked rise in cortisol and fall in male testosterone. These findings are not observed 5 months from discharge. The lack of association between hormone concentrations and common post-COVID symptoms suggests steroid insufficiency does not play a causal role in this condition.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: COVID-19 Tipo de estudo: Guideline Limite: Female / Humans / Male Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: COVID-19 Tipo de estudo: Guideline Limite: Female / Humans / Male Idioma: En Ano de publicação: 2024 Tipo de documento: Article