tetano
Editor, Senior Moderator
Clin Endocrinol (Oxf)
. 2024 Jan 17.
doi: 10.1111/cen.15012. Online ahead of print. Plasma steroid concentrations reflect acute disease severity and normalise during recovery in people hospitalised with COVID-19
Kerri Devine[SUP] 1 2 [/SUP], Clark D Russell[SUP] 3 [/SUP], Giovanny R Blanco[SUP] 4 [/SUP], Brian R Walker[SUP] 1 2 [/SUP], Natalie Z M Homer[SUP] 1 5 [/SUP], Scott G Denham[SUP] 5 [/SUP], Joanna P Simpson[SUP] 5 [/SUP], Olivia C Leavy[SUP] 6 [/SUP], Omer Elneima[SUP] 7 [/SUP], Hamish J C McAuley[SUP] 7 [/SUP], Aarti Shikotra[SUP] 7 [/SUP], Amisha Singapuri[SUP] 7 [/SUP], Marco Sereno[SUP] 7 [/SUP], Ruth M Saunders[SUP] 7 [/SUP], Victoria C Harris[SUP] 7 [/SUP], Linzy Houchen-Wolloff[SUP] 7 [/SUP], Neil J Greening[SUP] 7 [/SUP], Nazir I Lone[SUP] 8 [/SUP], Mathew Thorpe[SUP] 8 [/SUP], William Greenhalf[SUP] 9 [/SUP], James D Chalmers[SUP] 10 [/SUP], Ling-Pei Ho[SUP] 11 [/SUP], Alex Horsley[SUP] 12 [/SUP], Michael Marks[SUP] 13 14 15 [/SUP], Betty Raman[SUP] 16 [/SUP], Shona C Moore[SUP] 17 [/SUP], Jake Dunning[SUP] 18 [/SUP], Malcolm G Semple[SUP] 17 [/SUP], Ruth Andrew[SUP] 1 5 [/SUP], Louise V Wain[SUP] 6 7 [/SUP], Rachael A Evans[SUP] 7 [/SUP], Christopher E Brightling[SUP] 7 [/SUP], John Kenneth Baillie[SUP] 19 [/SUP], Rebecca M Reynolds[SUP] 1 [/SUP]; ISARIC4C Investigators and PHOSP-COVID Study Collaborative Group
Affiliations
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.
Keywords: COVID 19; adrenal; cortisol; long COVID; testosterone.
. 2024 Jan 17.
doi: 10.1111/cen.15012. Online ahead of print. Plasma steroid concentrations reflect acute disease severity and normalise during recovery in people hospitalised with COVID-19
Kerri Devine[SUP] 1 2 [/SUP], Clark D Russell[SUP] 3 [/SUP], Giovanny R Blanco[SUP] 4 [/SUP], Brian R Walker[SUP] 1 2 [/SUP], Natalie Z M Homer[SUP] 1 5 [/SUP], Scott G Denham[SUP] 5 [/SUP], Joanna P Simpson[SUP] 5 [/SUP], Olivia C Leavy[SUP] 6 [/SUP], Omer Elneima[SUP] 7 [/SUP], Hamish J C McAuley[SUP] 7 [/SUP], Aarti Shikotra[SUP] 7 [/SUP], Amisha Singapuri[SUP] 7 [/SUP], Marco Sereno[SUP] 7 [/SUP], Ruth M Saunders[SUP] 7 [/SUP], Victoria C Harris[SUP] 7 [/SUP], Linzy Houchen-Wolloff[SUP] 7 [/SUP], Neil J Greening[SUP] 7 [/SUP], Nazir I Lone[SUP] 8 [/SUP], Mathew Thorpe[SUP] 8 [/SUP], William Greenhalf[SUP] 9 [/SUP], James D Chalmers[SUP] 10 [/SUP], Ling-Pei Ho[SUP] 11 [/SUP], Alex Horsley[SUP] 12 [/SUP], Michael Marks[SUP] 13 14 15 [/SUP], Betty Raman[SUP] 16 [/SUP], Shona C Moore[SUP] 17 [/SUP], Jake Dunning[SUP] 18 [/SUP], Malcolm G Semple[SUP] 17 [/SUP], Ruth Andrew[SUP] 1 5 [/SUP], Louise V Wain[SUP] 6 7 [/SUP], Rachael A Evans[SUP] 7 [/SUP], Christopher E Brightling[SUP] 7 [/SUP], John Kenneth Baillie[SUP] 19 [/SUP], Rebecca M Reynolds[SUP] 1 [/SUP]; ISARIC4C Investigators and PHOSP-COVID Study Collaborative Group
Affiliations
- PMID: 38229583
- DOI: 10.1111/cen.15012
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.
Keywords: COVID 19; adrenal; cortisol; long COVID; testosterone.