Silent thyroiditis following vaccination against COVID-19: report of two cases.

PURPOSE: It is well established that thyroiditis and other thyroid disorders can be induced by COVID-19 infection, but there is limited information about the autoimmune/inflammatory syndrome induced by adjuvants (ASIA) after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination. We report two cases of thyrotoxicosis following SARS-CoV-2 vaccine. METHODS AND RESULTS: Two young health care peoples (wife and husband) received a first dose of SARS-CoV-2 vaccine, and few weeks later developed clinical manifestations of thyroid hyperactivity, with increased thyroid hormone levels on thyroid function tests, suppressed thyroid-stimulating hormone and negative antithyroid antibodies, despite being healthy before vaccination. They were diagnosed at the 4th week after first dose of SARS-Cov-2 vaccine as silent thyroiditis and followed without treatment, since their symptoms were not severe. At the 6th week, the patients became wholly asymptomatic and their thyroid function returned to normal. CONCLUSIONS: Thyrotoxicosis can occur after SARS-CoV-2 vaccination probably related to silent thyroiditis.

Thyrotoxicosis following SARS-COV-2 vaccination: a case series and discussion.

AIM: To describe a case series of thyrotoxicosis likely triggered by SARS-CoV-2 vaccination and to warn physicians about this potential correlation. To report clinical, laboratory and imaging findings and provide further information that goes in line with the underlying mechanisms. METHODS: Single-center case series based on all the information collected in the hospital medical records, as well as the temporal sequence between the onset of symptoms and COVID-19 vaccination. RESULTS: We report 8 cases with thyrotoxicosis after SARS-CoV-2 vaccination. 4 cases of Graves' disease (GD), 2 cases of subacute painful thyroiditis (SAT), 1 case of concurrent GD and SAT and 1 case of atypical subacute thyroiditis. Five patients received BNT162b2 mRNA vaccine, 3 patients 1273 mRNA vaccine. The onset of symptoms following vaccination ranged from 10 to 14 days in six of eight patients and from 7 to 8 weeks in two patients. CONCLUSIONS: Several hypotheses have been proposed to explain the potential correlation between SARS-CoV-2 vaccination and thyrotoxicosis, including immune system hyper-stimulation, molecular mimicry and Autoimmune/Autoinflammatory Syndrome Induced by Adjuvants (ASIA). We should pay greater attention to thyroid disorders in patients receiving vaccine against SARS-CoV-2.

Two Cases of Severe Autoimmune Thyrotoxicosis Following SARS-CoV-2 Infection.

Since the start of the COVID-19 pandemic, there have been multiple reports of related thyroid dysfunction, most commonly, thyroiditis. The exact mechanism for this has not been elucidated, but it is known that thyroid gland cells have both angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2) receptors, which the SARS-CoV-2 virus uses to enter cells. While SARS-CoV-2 has also been shown to precipitate other autoimmune diseases, there are only a few reported cases of new onset Graves' disease in the setting of SARS-CoV-2 infection. We report 2 patients who presented with severe thyrotoxicosis (thyroid storm and impending storm) that was likely precipitated by SARS-CoV-2 infection. Both patients had no previous history of hyperthyroidism, and potentially also developed Graves' disease after getting COVID-19. The addition of these cases to the medical literature will further highlight the fact that SARS-CoV-2 infection should be considered a causative agent for thyrotoxicosis when no other cause can be found, and that SARS-CoV-2 may be a potential trigger for autoimmune thyroid disease. It is important to know the SARS-CoV-2 status of such patients for infection control purposes, and to identify patients who may have their hospital course complicated by this disease. These cases may also help further our understanding of the etiology of autoimmune thyroid disease following a viral infection.

Outcome of Sars-COV-2-related thyrotoxicosis in survivors of Covid-19: a prospective study.

PURPOSE: To evaluate the post- coronavirus disease-19 (COVID-19) outcome of thyroid function in patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-related thyrotoxicosis. METHODS: This was a single-center prospective study involving 29 patients (11 females, 18 males; median age 64 years, range: 43-85) with thyrotoxicosis diagnosed after hospitalization for COVID-19 and then followed-up for a median period of 90 days (range: 30-120) after hospital discharge. At follow-up, patients were evaluated for serum thyrotropin (TSH), free-thyroxine (FT4), free-triiodiothyronine (FT3), TSH receptor antibodies (TRAb), thyroglobulin antibodies (TgAb), thyroperoxidase antibodies (TPOAb) and ultrasonographic thyroid structure. RESULTS: After recovery of COVID-19, serum TSH values significantly increased (P < 0.001) and FT4 values significantly decreased (P = 0.001), without significant change in serum FT3 (P = 0.572). At follow-up, 28 subjects (96.6%) became euthyroid whereas overt hypothyroidism developed in one case. At the ultrasound evaluation of thyroid gland, hypoecogenicity was found in 10 patients (34.5%) and in these cases serum TSH values tended to be higher than those without thyroid hypoecogenity (P = 0.066). All subjects resulted to be negative for TgAb, TPOAb and TRAb. CONCLUSION: In a short-term follow-up, thyroid function spontaneously normalized in most subjects with SARS-CoV-2-related thyrotoxicosis. However, thyroid hypoecogenicity was found in a remarkable number of them and future longer-term studies are needed to clarify whether this ultrasonographic alteration may predispose to develop late-onset thyroid dysfunction.

Thyroid disorders and SARS-CoV-2 infection: From pathophysiological mechanism to patient management.

The World Health Organization (WHO) declared the COVID-19 epidemic to be a global pandemic in March 2020. COVID-19 is an infection caused by SARS-CoV-2, a coronavirus that utilizes the angiotensin-2 converting enzyme to penetrate thyroid and pituitary cells, and may result in a "cytokine storm". Based on the pathophysiological involvement of the pituitary-thyroid axis, the current review discusses the diagnosis of abnormal thyroid function test, and the management of patients presenting with thyrotoxicosis, thyroid-associated orbitopathy and hypothyroidism in the context of SARS-CoV-2 infection.