BHF/University Centre for Cardiovascular Science, Queen's Medical Research Institute, Edinburgh Bioquarter, University of Edinburgh, Edinburgh, UK.
Translational and Clinical Research Institute, Newcastle University, Newcastle upon Tyne, UK.
Clin Endocrinol (Oxf). 2024 Apr;100(4):317-327. doi: 10.1111/cen.15012. Epub 2024 Jan 17.
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).
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).
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.
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.
内分泌系统在急性疾病中会受到干扰，而新冠肺炎（COVID-19）后报告的症状与临床激素缺乏症相似。我们假设患有严重急性 COVID-19 和 COVID-19 后症状的人存在糖皮质激素和性激素缺乏症。
设计/患者：在 COVID-19 住院期间（国际严重急性呼吸感染联合会/世界卫生组织 [WHO] 英国严重新兴感染临床特征协议研究）和住院后 5 个月（COVID-19 后住院研究），从英国两个多中心队列中采集样本进行分析。
通过液相色谱-质谱法定量测定血浆类固醇。将类固醇浓度与疾病严重程度（WHO 序数量表）和验证症状评分进行比较。数据以几何均数（SD）表示。
在急性队列（n=239，66.5%为男性）中，血浆皮质醇浓度随疾病严重程度增加（皮质醇 753.3[1.6]与 429.2[1.7]nmol/L 相比，致命与最轻微，p<0.001）。在男性中，睾酮浓度随严重程度下降（致命与最轻微，睾酮 1.2[2.2]与 6.9[1.9]nmol/L 相比，p<0.001）。在随访队列（n=198，62.1%为男性，68.9%持续症状，出院后 165[121-192]天）中，血浆皮质醇浓度（275.6[1.5]nmol/L）与住院期间的严重程度、恢复感知或患者报告的症状无关。男性睾酮浓度（12.6[1.5]nmol/L）与住院期间的严重程度、恢复感知或症状评分无关。
COVID-19 住院患者的循环糖皮质激素反映了急性疾病，皮质醇明显升高，男性睾酮水平下降。这些发现在出院后 5 个月时并未观察到。激素浓度与常见 COVID-19 后症状之间缺乏关联表明，类固醇不足在这种情况下不起因果作用。
