Insights from a Prospective Follow-up of Thyroid Function and Autoimmunity among COVID-19 Survivors

Abstract

Background The occurrence of Graves’ disease and Hashimoto thyroiditis after coronavirus disease 2019 (COVID-19) raised concerns that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may trigger thyroid autoimmunity. We aimed to address the current uncertainties regarding incident thyroid dysfunction and autoimmunity among COVID-19 survivors. Methods We included consecutive adult COVID-19 patients without known thyroid disorders, who were admitted to Queen Mary Hospital from July 21 to September 21, 2020 and had serum levels of thyroid-stimulating hormone, free thyroxine, free triiodothyronine (fT3), and anti-thyroid antibodies measured both on admission and at 3 months. Results In total, 122 patients were included. Among 20 patients with abnormal thyroid function tests (TFTs) on admission (mostly low fT3), 15 recovered. Among 102 patients with initial normal TFTs, two had new-onset abnormalities that could represent different phases of thyroiditis. Among 104 patients whose anti-thyroid antibody titers were reassessed, we observed increases in anti-thyroid peroxidase (TPO) ( P <0.001) and anti-thyroglobulin ( P <0.001), but not anti-thyroid stimulating hormone receptor titers ( P =0.486). Of 82 patients with negative anti-TPO findings at baseline, 16 had a significant interval increase in anti-TPO titer by >12 U, and four became anti-TPO-positive. Worse baseline clinical severity ( P =0.018), elevated C-reactive protein during hospitalization ( P =0.033), and higher baseline anti-TPO titer ( P =0.005) were associated with a significant increase in anti-TPO titer. Conclusion Most patients with thyroid dysfunction on admission recovered during convalescence. Abnormal TFTs suggestive of thyroiditis occurred during convalescence, but infrequently. Importantly, our novel observation of an increase in anti-thyroid antibody titers post-COVID-19 warrants further follow-up for incident thyroid dysfunction among COVID-19 survivors.

Is Smaller Thyroid Gland Volume in COVID-19 Survivors Indicative of Chronic Thyroid Dysfunction?

“…Lui et al compared the anti-Tg and anti-TPO titers of 104 COVID-19 patients during the acute infection period and in 3 months after post-COVID-19. They revealed a signi cant increase in antibody titers [24]. We did not detect any difference with healthy subjects for antibody positivity.…”

Hashimoto’s thyroiditis following SARS-CoV-2 infection

“…An increase in anti-TOP and anti-Tg was observed 3 months after acute viral infection, which is similar to other presentations of viral infections such as T-lymphotropic virus type I. 14 The pathogenesis of Hashimoto's thyroiditis is an important subject of investigation because it has not been fully elucidated.…”

“…13 Autopsy patients showed changes in the structure and morphology of the epithelial cells of the glandular follicle, in addition to a decrease in TSH-producing cells in the pituitary gland, demonstrating the concomitant involvement of the hypothalamic-pituitary-adrenal axis. In the same context, a cohort study conducted in Seoul city in 2021 by Lui et al 14 followed 122 patients to check the presentation of thyroid autoimmunity after COVID-19. An increase in anti-TOP and anti-Tg was observed 3 months after acute viral infection, which is similar to other presentations of viral infections such as T-lymphotropic virus type I.…”

SARS-CoV-2: Emerging Role in the Pathogenesis of Various Thyroid Diseases

“… 25 In addition, thyroid dysfunction in ~15% of mild-to-moderate cases of COVID-19 and incident thyroid dysfunction and autoimmunity in COVID-19 survivors have recently been observed. 26 , 27 As illustrated in Figure 3 , the thyroid gland is likely dysfunctional as a consequence of either direct or indirect effects of SARS-CoV-2 infection. The thyroid gland can be directly infected by the SARS-CoV-2 as the ACE2, TMPRSS2, and other factors facilitating viral entry are highly expressed in it.…”

“…Initially, incident thyroid dysfunction and autoimmunity have been observed among 122 COVID cases during the convalescence phase. 27 Subsequently, the same group evaluated both the prevalence and predicting factors of long-COVID and possible functions of thyroid and autoimmunity in long-COVID. The study included 250 adults with no previous history of thyroid disorders and performed thyroid function tests and antithyroid antibody measurements in all cases prior to admission and at follow-up (median: 89 days).…”