Thyroid dysfunction in the wake of Omicron: understanding its role in COVID-19 severity and mortality

Qingfeng Zhang, Zongyue Zhang, Xu Liu, Yixuan Wang, Hao Chen, Yueying Hao, Shiqian Zha, Jingyi Zhang, Yang He, Beini Zhou, Ke Hu
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Abstract

SARS-CoV-2 can invade the thyroid gland. This study was to delineate the risk of thyroid dysfunction amidst the prevalence of the Omicron variant, and to investigate the correlation between thyroid function and Coronavirus disease 2019 (COVID-19) outcomes. The study also aimed to ascertain whether thyroid dysfunction persisted during COVID-19 recovery phase.This was a retrospective cohort study. COVID-19 patients from the Renmin Hospital of Wuhan University, China during the epidemic of Omicron variants were included, and their thyroid function were analyzed in groups.A history of thyroid disease was not associated with COVID-19 outcomes. COVID-19 can lead to a bimodal distribution of thyroid dysfunction. The severity of COVID-19 was inversely proportional to the levels of thyroid- stimulating hormone (TSH), free triiodothyronine (FT3) and free thyroxine (FT4), leading to a higher prevalence of thyroid dysfunction. Severe COVID-19 was a risk factor for euthyroid sick syndrome (ESS) (OR=22.5, 95% CI, 12.1 - 45.6). Neutrophil to lymphocyte ratio mediated the association between severe COVID-19 and ESS (mediation effect ratio = 41.3%, p < 0.001). ESS and decreased indicators of thyroid function were associated with COVID-19 mortality, while high levels of FT3 and FT4 exhibited a protective effect against death. This effect was more significant in women (p < 0.05). During the recovery period, hyperthyroidism was quite uncommon, while a small percentage of individuals (7.7%) continued to exhibit hypothyroidism.COVID-19 severity was linked to thyroid dysfunction. Severe COVID-19 increased the risk of ESS, which was associated with COVID-19 mortality. Post-recovery, hyperthyroidism was rare, but some individuals continued to have hypothyroidism.
奥米克龙事件后的甲状腺功能障碍:了解其在 COVID-19 严重程度和死亡率中的作用
SARS-CoV-2可侵入甲状腺。本研究旨在确定在Omicron变异体流行的情况下甲状腺功能障碍的风险,并调查甲状腺功能与冠状病毒病2019(COVID-19)结果之间的相关性。该研究还旨在确定甲状腺功能障碍是否会在COVID-19恢复阶段持续存在。研究纳入了中国武汉大学人民医院在奥米克隆变异体流行期间的COVID-19患者,并对他们的甲状腺功能进行了分组分析。COVID-19可导致甲状腺功能障碍的双峰分布。COVID-19的严重程度与促甲状腺激素(TSH)、游离三碘甲状腺原氨酸(FT3)和游离甲状腺素(FT4)的水平成反比,导致甲状腺功能障碍的发生率较高。严重的 COVID-19 是甲状腺疾病综合征(ESS)的风险因素(OR=22.5,95% CI,12.1 - 45.6)。中性粒细胞与淋巴细胞比值介导了严重 COVID-19 与 ESS 之间的关联(介导效应比 = 41.3%,p < 0.001)。ESS和甲状腺功能指标下降与COVID-19死亡率有关,而高水平的FT3和FT4则对死亡有保护作用。这种效应在女性中更为明显(P < 0.05)。在恢复期间,甲状腺功能亢进症并不常见,但仍有一小部分人(7.7%)表现出甲状腺功能减退症。严重的COVID-19会增加ESS的风险,而ESS与COVID-19的死亡率相关。康复后,甲状腺功能亢进症很少见,但仍有一些患者出现甲状腺功能减退。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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