Endocrinology and Diabetes Unit, Papa Giovanni XXIII Hospital, Bergamo, Italy.
Endocrinology Unit, San Raffaele Scientific Institute, Milan, Italy.
Front Endocrinol (Lausanne). 2023 Mar 8;14:1126683. doi: 10.3389/fendo.2023.1126683. eCollection 2023.
Thyroid dysfunctions associated with SARS-CoV-2 acute infection have been extensively described since the beginning of COVID-19 pandemics. Conversely, few data are available on the occurrence of thyroid autoimmunity after COVID-19 resolution. We assessed the prevalence of autoimmune thyroid disease (ATD) and thyroid dysfunctions in COVID-19 survivors three months after hospital admission.
Single-center, prospective, observational, cohort study performed at ASST Papa Giovanni XXIII Hospital, Bergamo, Italy. 599 COVID-19 survivors were prospectively evaluated for thyroid function and autoimmunity thyroperoxidase antibodies (TPOAb), thyroglobulin antibodies (TgAb). When a positive antibody concentration was detected, thyroid ultrasound was performed. Multiple logistic regression model was used to estimate the association between autoimmunity and demographic characteristics, respiratory support, and comorbidities. Autoimmunity results were compared to a cohort of 498 controls referred to our Institution for non-thyroid diseases before the pandemic onset. A sensitivity analysis comparing 330 COVID-19 patients with 330 age and sex-matched controls was performed.
Univariate and multivariate analysis found that female sex was positively associated (OR 2.01, SE 0.48, p = 0.003), and type 2 diabetes (T2DM) was negatively associated (OR 0.36, SE 0.16, p = 0.025) with thyroid autoimmunity; hospitalization, ICU admission, respiratory support, or COVID-19 treatment were not associated with thyroid autoimmunity (p > 0.05). TPOAb prevalence was greater in COVID-19 survivors than in controls: 15.7% vs 7.7%, p = 0.002. Ultrasonographic features of thyroiditis were present in 94.9% of the evaluated patients with positive antibodies. TSH was within the normal range in 95% of patients.
Autoimmune thyroid disease prevalence in COVID-19 survivors was doubled as compared to age and sex-matched controls, suggesting a role of SARS-CoV-2 in eliciting thyroid autoimmunity.
自 COVID-19 大流行开始以来,已经广泛描述了与 SARS-CoV-2 急性感染相关的甲状腺功能障碍。相反,关于 COVID-19 解决后发生甲状腺自身免疫的信息却很少。我们评估了 COVID-19 住院后三个月时 COVID-19 幸存者自身免疫性甲状腺疾病(ATD)和甲状腺功能障碍的发生率。
在意大利贝加莫的 ASST Papa Giovanni XXIII 医院进行了单中心、前瞻性、观察性队列研究。前瞻性评估了 599 例 COVID-19 幸存者的甲状腺功能和自身抗体甲状腺过氧化物酶抗体(TPOAb)、甲状腺球蛋白抗体(TgAb)。当检测到抗体浓度阳性时,进行甲状腺超声检查。多变量逻辑回归模型用于评估自身免疫与人口统计学特征、呼吸支持和合并症之间的关联。将自身免疫结果与大流行前在我们机构就诊的非甲状腺疾病的 498 例对照者进行比较。进行了一项敏感性分析,比较了 330 名 COVID-19 患者和 330 名年龄和性别匹配的对照组。
单变量和多变量分析发现,女性(OR 2.01,SE 0.48,p = 0.003)和 2 型糖尿病(T2DM)(OR 0.36,SE 0.16,p = 0.025)与甲状腺自身免疫呈正相关;住院、入住 ICU、呼吸支持或 COVID-19 治疗与甲状腺自身免疫无关(p > 0.05)。COVID-19 幸存者中 TPOAb 的患病率高于对照组:15.7%比 7.7%,p = 0.002。在评估的阳性抗体患者中,94.9%存在甲状腺炎的超声特征。95%的患者 TSH 在正常范围内。
与年龄和性别匹配的对照组相比,COVID-19 幸存者自身免疫性甲状腺疾病的患病率增加了一倍,这表明 SARS-CoV-2 在引发甲状腺自身免疫中起作用。