Graves’ Disease Caused by SARS-CoV-2 Infection

Sousa, Bruno; Santos, Catarina Pestana; Ferreira, Ana Paula Bonilauri; Judas, Tiago

doi:10.12890/2022_003470

Cited by 3 publications

(3 citation statements)

References 9 publications

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“…In a patient who started to present hyperthyroidism symptoms (fatigue, shortness of breath, palpitations, and weight loss) nearly 3 weeks after a mild SARS-CoV-2 infection, the ultrasound showed a diffusely heterogeneous and irregular thyroid and a nodular image below the sternal notch. Thyroid scintigraphy confirmed Graves' disease pattern (159). Not many studies have evaluated the post-mortem thyroid of patients who died of COVID-19.…”

Section: Thyroid Features In Covid-19 Patientsmentioning

confidence: 82%

COVID-19 and thyroid function: What do we know so far?

Rossetti

Cazarin²,

Hecht³

et al. 2022

Front. Endocrinol.

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Coronavirus disease 2019 (COVID-19) was characterized as a pandemic in March, 2020 by the World Health Organization. COVID-19 is a respiratory syndrome that can progress to acute respiratory distress syndrome, multiorgan dysfunction, and eventually death. Despite being considered a respiratory disease, it is known that other organs and systems can be affected in COVID-19, including the thyroid gland. Thyroid gland, as well as hypothalamus and pituitary, which regulate the functioning of most endocrine glands, express angiotensin-converting enzyme 2 (ACE2), the main protein that functions as a receptor to which SARS-CoV-2 binds to enter host cells. In addition, thyroid gland is extremely sensitive to changes in body homeostasis and metabolism. Immune system cells are targets for thyroid hormones and T3 and T4 modulate specific immune responses, including cell-mediated immunity, natural killer cell activity, the antiviral action of interferon (IFN) and proliferation of T- and B-lymphocytes. However, studies show that patients with controlled hypothyroidism and hyperthyroidism do not have a higher prevalence of COVID-19, nor do they have a worse prognosis when infected with the virus. On the other hand, retrospective observational studies, prospective studies, and case reports published in the last two years reported abnormal thyroid function related to acute SARS-CoV-2 infection or even several weeks after its resolution. Indeed, a variety of thyroid disorders have been documented in COVID-19 patients, including non-thyroidal illness syndrome (NTIS), subacute thyroiditis and thyrotoxicosis. In addition, thyroid disease has already been reported as a consequence of the administration of vaccines against SARS-CoV-2. Overall, the data revealed that abnormal thyroid function may occur during and in the convalescence post-COVID condition phase. Although the cellular and molecular mechanisms are not completely understood, the evidence suggests that the “cytokine storm” is an important mediator in this context. Thus, future studies are needed to better investigate the pathophysiology of thyroid dysfunction induced by COVID-19 at both molecular and clinical levels.

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Section: Thyroid Features In Covid-19 Patientsmentioning

confidence: 82%

COVID-19 and thyroid function: What do we know so far?

Rossetti

Cazarin²,

Hecht³

et al. 2022

Front. Endocrinol.

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“…SAT is probably secondary to the virus replication within the thyroid gland [49], whereas NTIS and thyrotoxicosis are not strictly related to a direct virus entry [82]. Some studies have also shown that COVID-19 may come before the onset of GD, supporting the theory of the potential thyroid tropism of SARS-CoV-2 [70][71][72][73][74][75]97]. A recent study [98] reported an association between low-level enterovirus infection and GD via the decreased transcription of the type I interferon (IFN), the cytokine pathways, and the simultaneous increased activity of the NFKB1/RELA, JAK1/STAT1, IFNAR1, CCL2 chemokine, and IL18 genes, which have a crucial pathogenic role in autoimmune conditions [99,100].…”

Section: Transcriptional Changes Of Immune Genesmentioning

confidence: 93%

“…Nonetheless, it has been reported that 70% of this cohort of patients during the hospital stay have been treated with interferon beta-1b therapy, which likely confounded the investigation of the autoimmunity appearance along SARS-CoV-2-related thyroid dysfunctions [69]. To date, several new cases of GD [70][71][72][73][74][75], including with Graves's ophthalmopathy (GO) [70], and of HT [75][76][77], following SARS-CoV-2 infection, have been reported in the literature. The time span between the infection and the onset of thyroid disease was heterogeneous, ranging from a concomitant appearance to more than 6 weeks, and all of these patients were managed with specific therapies.…”

Section: Autoimmune Thyroid Diseasesmentioning

confidence: 98%

Thyroid Autoimmunity and SARS-CoV-2 Infection

Fallahi,

Elia,

Ragusa

et al. 2023

JCM

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The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiological culprit of COronaVIrus Disease 19 (COVID-19), can enter the cells via the angiotensin-converting enzyme 2 (ACE2) receptor, which has been found in several tissues including in endocrine organs, such as the ovaries, testes, pancreas, and thyroid. Several thyroid disorders have been associated with SARS-CoV-2 infection [subacute thyroiditis (SAT), thyrotoxicosis, and non-thyroidal illness syndrome (NTIS)] and, in part, they are believed to be secondary to the local virus replication within the gland cells. However, as documented for other viruses, SARS-CoV-2 seems to interfere with several aspects of the immune system, inducing the synthesis of autoantibodies and triggering latent or new onset autoimmune disease (AID), including autoimmune thyroid disease (AITD), such as Hashimoto Thyroiditis (HT) and Graves’ disease (GD). Several mechanisms have been hypothesized to explain this induction of autoimmunity by SARS-CoV-2 infection: the immune system hyper-stimulation, the molecular mimicry between the self-antigens of the host and the virus, neutrophils extracellular traps, and finally, the virus induced transcriptional changes in the immune genes; nonetheless, more evidence is needed especially from large, long-term cohort studies involving COVID-19 patients, to establish or reject this pathogenetic relationship.

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Understanding autoimmune response after SARS-CoV-2 infection and the pathogenesis/mechanisms of long COVID

Guo,

Shang,

et al. 2024

Medical Review

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COVID-19 posed a major challenge to the healthcare system and resources worldwide. The popularization of vaccines and the adoption of numerous prevention and control measures enabled the gradual end of the COVID-19 pandemic. However, successive occurrence of autoimmune diseases in patients with COVID-19 cannot be overlooked. Long COVID has been the major focus of research due to the long duration of different symptoms and the variety of systems involved. Autoimmunity may play a crucial role in the pathogenesis of long COVID. Here, we reviewed several autoimmune disorders occurring after COVID-19 infection and the pathogenesis of long COVID.

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Graves’ Disease Caused by SARS-CoV-2 Infection

Cited by 3 publications

References 9 publications

COVID-19 and thyroid function: What do we know so far?

COVID-19 and thyroid function: What do we know so far?

Thyroid Autoimmunity and SARS-CoV-2 Infection

Understanding autoimmune response after SARS-CoV-2 infection and the pathogenesis/mechanisms of long COVID

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