Department of Internal Medicine and Radboud Center for Infectious Diseases, Radboud University Medical Center, 6500 HB, Nijmegen, the Netherlands.
4th Department of Internal Medicine, National and Kapodistrian University of Athens, 124 62, Athens, Greece.
J Clin Endocrinol Metab. 2021 Jun 16;106(7):1994-2009. doi: 10.1210/clinem/dgab148.
Lymphopenia is a key feature of immune dysfunction in patients with bacterial sepsis and coronavirus disease 2019 (COVID-19) and is associated with poor clinical outcomes, but the cause is largely unknown. Severely ill patients may present with thyroid function abnormalities, so-called nonthyroidal illness syndrome, and several studies have linked thyrotropin (thyroid stimulating hormone, TSH) and the thyroid hormones thyroxine (T4) and 3,5,3'-triiodothyronine (T3) to homeostatic regulation and function of lymphocyte populations.
This work aimed to test the hypothesis that abnormal thyroid function correlates with lymphopenia in patients with severe infections.
A retrospective analysis of absolute lymphocyte counts, circulating TSH, T4, free T4 (FT4), T3, albumin, and inflammatory biomarkers was performed in 2 independent hospitalized study populations: bacterial sepsis (n = 224) and COVID-19 patients (n = 161). A subgroup analysis was performed in patients with severe lymphopenia and normal lymphocyte counts.
Only T3 significantly correlated (ρ = 0.252) with lymphocyte counts in patients with bacterial sepsis, and lower concentrations were found in severe lymphopenic compared to nonlymphopenic patients (n = 56 per group). Severe lymphopenic COVID-19 patients (n = 17) showed significantly lower plasma concentrations of TSH, T4, FT4, and T3 compared to patients without lymphopenia (n = 18), and demonstrated significantly increased values of the inflammatory markers interleukin-6, C-reactive protein, and ferritin. Remarkably, after 1 week of follow-up, the majority (12 of 15) of COVID-19 patients showed quantitative recovery of their lymphocyte numbers, whereas TSH and thyroid hormones remained mainly disturbed.
Abnormal thyroid function correlates with lymphopenia in patients with severe infections, like bacterial sepsis and COVID-19, but future studies need to establish whether a causal relationship is involved.
淋巴细胞减少是细菌性败血症和 2019 年冠状病毒病（COVID-19）患者免疫功能障碍的一个关键特征，与不良临床结局相关，但病因在很大程度上尚不清楚。重症患者可能出现甲状腺功能异常，即所谓的非甲状腺疾病综合征，几项研究已经将促甲状腺激素（甲状腺刺激激素，TSH）和甲状腺激素甲状腺素（T4）和 3,5,3'-三碘甲状腺原氨酸（T3）与淋巴细胞群的稳态调节和功能联系起来。
本研究旨在检验以下假设，即严重感染患者的甲状腺功能异常与淋巴细胞减少相关。
对 2 个独立住院研究人群（细菌性败血症患者，n=224；COVID-19 患者，n=161）的绝对淋巴细胞计数、循环 TSH、T4、游离 T4（FT4）、T3、白蛋白和炎症生物标志物进行回顾性分析。在严重淋巴细胞减少和正常淋巴细胞计数的患者中进行亚组分析。
只有 T3 与细菌性败血症患者的淋巴细胞计数显著相关（ρ=0.252），且严重淋巴细胞减少患者的 T3 浓度低于非淋巴细胞减少患者（每组 n=56）。17 例严重淋巴细胞减少的 COVID-19 患者（n=17）的 TSH、T4、FT4 和 T3 血浆浓度明显低于无淋巴细胞减少的患者（n=18），并且炎症标志物白细胞介素-6、C 反应蛋白和铁蛋白的水平显著升高。值得注意的是，在 1 周的随访后，COVID-19 患者中的大多数（15 例中的 12 例）淋巴细胞数量恢复正常，而 TSH 和甲状腺激素仍主要受到干扰。
在严重感染患者中，如细菌性败血症和 COVID-19，甲状腺功能异常与淋巴细胞减少相关，但需要进一步的研究来确定是否存在因果关系。
