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 Greenhalf, James 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, The ISARIC4C Investigators and PHOSP-COVID Study Collaborative Group
{"title":"血浆类固醇浓度反映了急性疾病的严重程度，并在 COVID-19 住院患者恢复期间趋于正常。","authors":"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 Greenhalf, James 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, The ISARIC4C Investigators and PHOSP-COVID Study Collaborative Group","doi":"10.1111/cen.15012","DOIUrl":null,"url":null,"abstract":"<div>\n \n \n <section>\n \n <h3> Objective</h3>\n \n <p>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.</p>\n </section>\n \n <section>\n \n <h3> Design/Patients</h3>\n \n <p>Samples were obtained for analysis from two UK multicentre cohorts during hospitalisation with COVID-19 (<i>International Severe Acute Respiratory Infection Consortium/World Health Organisation [WHO] Clinical Characterization Protocol for Severe Emerging Infections in the UK study</i>), and at follow-up 5 months after hospitalisation (<i>Post-hospitalisation COVID-19 study</i>).</p>\n </section>\n \n <section>\n \n <h3> Measurements</h3>\n \n <p>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).</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>In the acute cohort (<i>n</i> = 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, <i>p</i> < .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, <i>p</i> < .001). In the follow-up cohort (<i>n</i> = 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.</p>\n </section>\n \n <section>\n \n <h3> Conclusions</h3>\n \n <p>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.</p>\n </section>\n </div>","PeriodicalId":10346,"journal":{"name":"Clinical Endocrinology","volume":null,"pages":null},"PeriodicalIF":3.0000,"publicationDate":"2024-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cen.15012","citationCount":"0","resultStr":"{\"title\":\"Plasma steroid concentrations reflect acute disease severity and normalise during recovery in people hospitalised with COVID-19\",\"authors\":\"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 Greenhalf, James 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, The ISARIC4C Investigators and PHOSP-COVID Study Collaborative Group\",\"doi\":\"10.1111/cen.15012\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n \\n <section>\\n \\n <h3> Objective</h3>\\n \\n <p>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.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Design/Patients</h3>\\n \\n <p>Samples were obtained for analysis from two UK multicentre cohorts during hospitalisation with COVID-19 (<i>International Severe Acute Respiratory Infection Consortium/World Health Organisation [WHO] Clinical Characterization Protocol for Severe Emerging Infections in the UK study</i>), and at follow-up 5 months after hospitalisation (<i>Post-hospitalisation COVID-19 study</i>).</p>\\n </section>\\n \\n <section>\\n \\n <h3> Measurements</h3>\\n \\n <p>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).</p>\\n </section>\\n \\n <section>\\n \\n <h3> Results</h3>\\n \\n <p>In the acute cohort (<i>n</i> = 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, <i>p</i> < .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, <i>p</i> < .001). In the follow-up cohort (<i>n</i> = 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.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Conclusions</h3>\\n \\n <p>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.</p>\\n </section>\\n </div>\",\"PeriodicalId\":10346,\"journal\":{\"name\":\"Clinical Endocrinology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":3.0000,\"publicationDate\":\"2024-01-17\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cen.15012\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Clinical Endocrinology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1111/cen.15012\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"ENDOCRINOLOGY & METABOLISM\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical Endocrinology","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/cen.15012","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
Plasma steroid concentrations reflect acute disease severity and normalise during recovery in people hospitalised with COVID-19
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.
期刊介绍：
Clinical Endocrinology publishes papers and reviews which focus on the clinical aspects of endocrinology, including the clinical application of molecular endocrinology. It does not publish papers relating directly to diabetes care and clinical management. It features reviews, original papers, commentaries, correspondence and Clinical Questions. Clinical Endocrinology is essential reading not only for those engaged in endocrinological research but also for those involved primarily in clinical practice.
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号
