Plasma steroid concentrations reflect acute disease severity and normalise during recovery in people hospitalised with COVID-19

Kerri Devine, Clark D. Russell, Giovanny R. Blanco, Brian R. Walker, Natalie Z. M. Homer, Scott G. Denham, Joanna P. Simpson, Olivia C. Leavy, Omer Elneima, Hamish J. C. McAuley, Aarti Shikotra, Amisha Singapuri, Marco Sereno, Ruth M. Saunders, Victoria C. Harris, Linzy Houchen-Wolloff, Neil J. Greening, Nazir I. Lone, Mathew Thorpe, William GreenhalfJames D. Chalmers, Ling-Pei Ho, Alex Horsley, Michael Marks, Betty Raman, Shona C. Moore, Jake Dunning, Malcolm G. Semple, Ruth Andrew, Louise V. Wain, Rachael A. Evans, Christopher E. Brightling, John Kenneth Baillie, Rebecca M. Reynolds (Lead / Corresponding author), , PHOSP-COVID Collaborative Group

Research output: Contribution to journalArticlepeer-review

2 Downloads (Pure)


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.

Original languageEnglish
Pages (from-to)317-327
Number of pages11
JournalClinical Endocrinology
Issue number4
Early online date17 Jan 2024
Publication statusPublished - Apr 2024


  • COVID 19
  • adrenal
  • cortisol
  • long COVID
  • testosterone

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism


Dive into the research topics of 'Plasma steroid concentrations reflect acute disease severity and normalise during recovery in people hospitalised with COVID-19'. Together they form a unique fingerprint.

Cite this