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American Family Physician Dec 2021Thyroiditis is a general term for inflammation of the thyroid gland. The most common forms of thyroiditis encountered by family physicians include Hashimoto, postpartum,...
Thyroiditis is a general term for inflammation of the thyroid gland. The most common forms of thyroiditis encountered by family physicians include Hashimoto, postpartum, and subacute. Most forms of thyroiditis result in a triphasic disease pattern of thyroid dysfunction. Patients will have an initial phase of hyperthyroidism (thyrotoxicosis) attributed to the release of preformed thyroid hormone from damaged thyroid cells. This is followed by hypothyroidism, when the thyroid stores are depleted, and then eventual restoration of normal thyroid function. Some patients may develop permanent hypothyroidism. Hashimoto thyroiditis is an autoimmune disorder that presents with or without signs or symptoms of hypothyroidism, often with a painless goiter, and is associated with elevated thyroid peroxidase antibodies. Patients with Hashimoto thyroiditis and overt hypothyroidism are generally treated with lifelong thyroid hormone therapy. Postpartum thyroiditis occurs within one year of delivery, miscarriage, or medical abortion. Subacute thyroiditis is a self-limited inflammatory disease characterized by anterior neck pain. Treatment of subacute thyroiditis should focus on symptoms. In the hyperthyroid phase, beta blockers can treat adrenergic symptoms. In the hypothyroid phase, treatment is generally not necessary but may be used in patients with signs and symptoms of hypothyroidism or permanent hypothyroidism. Nonsteroidal anti-inflammatory drugs and corticosteroids are indicated for the treatment of thyroid pain. Certain drugs may induce thyroiditis, such as amiodarone, immune checkpoint inhibitors, interleukin-2, interferon-alfa, lithium, and tyrosine kinase inhibitors. In all cases of thyroiditis, surveillance and clinical follow-up are recommended to monitor for changes in thyroid function.
Topics: Hashimoto Disease; Humans; Thyroiditis
PubMed: 34913664
DOI: No ID Found -
Frontiers in Endocrinology 2022Coronavirus 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... (Review)
Review
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.
Topics: Humans; COVID-19; SARS-CoV-2; COVID-19 Vaccines; Prospective Studies; Retrospective Studies; Peptidyl-Dipeptidase A; Thyroid Diseases
PubMed: 36601011
DOI: 10.3389/fendo.2022.1041676 -
Reviews in Endocrine & Metabolic... Dec 2021Subacute thyroiditis (SAT) is a thyroid inflammatory disease, whose pathogenesis and determinants of the clinical course were unclear for many decades. The last few... (Review)
Review
Subacute thyroiditis (SAT) is a thyroid inflammatory disease, whose pathogenesis and determinants of the clinical course were unclear for many decades. The last few years have brought many clinically significant new data on the epidemiology, pathogenesis and management of SAT. Several human leukocyte antigen (HLA) alleles were demonstrated not only to increase the risk of SAT, but also to correlate with SAT clinical course and determine the risk of recurrence. The world-wide epidemic of the coronavirus disease 19 (COVID-19) has provided new observations that the severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) can be a potent SAT-triggering factor, and that the clinical course of SAT in patients affected by COVID-19 is different from a typical one. Additionally, many new trends in the clinical course are emerging. In the last years, painless course of SAT is more and more often described, constituting a special challenge in patients hospitalized due to COVID-19. Despite an excellent availability of diagnostic methods, several difficulties in SAT differential diagnosis can be currently encountered and the proper diagnosis and treatment is frequently delayed. False positive diagnoses of SAT in patients with malignancies of poor prognosis constitute a life-threatening problem. Taking into account all the new aspects of SAT pathogenesis and of its clinical course, the new - modified - SAT diagnosis criteria have been proposed.
Topics: COVID-19; Humans; SARS-CoV-2; Thyroid Diseases; Thyroiditis, Subacute
PubMed: 33950404
DOI: 10.1007/s11154-021-09648-y -
Best Practice & Research. Clinical... Mar 2023Breakdown of self-tolerance to thyroid antigens (thyroperoxidase, thyroglobulin and the thyrotropin-receptor) is the driver of thyroid autoimmunity. It has been... (Review)
Review
Breakdown of self-tolerance to thyroid antigens (thyroperoxidase, thyroglobulin and the thyrotropin-receptor) is the driver of thyroid autoimmunity. It has been suggested that infectious disease might trigger autoimmune thyroid disease (AITD). Involvement of the thyroid has been reported during severe acute respiratory syndrome virus 2 (SARS-CoV-2) infection, in the form of subacute thyroiditis in subjects with mild coronavirus disease 19 disease (COVID-19) and of painless, destructive thyroiditis in hospitalized patients with severe infection. In addition, cases of AITD, both Graves' disease (GD) and Hashimoto's thyroiditis (HT), have been reported in association with (SARS-CoV-2) infection. In this review, we focus on the relationship between SARS-CoV-2 infection and occurrence of AITD. Nine cases of GD strictly related to SARS-CoV-2 infection and only three cases of HT associated to COVID-19 infection have been reported. No study has demonstrated a role of AITD as a risk factor for a poor prognosis of COVID-19 infection.
Topics: Humans; Autoimmunity; COVID-19; SARS-CoV-2; Hashimoto Disease; Autoimmune Diseases; Graves Disease
PubMed: 36813660
DOI: 10.1016/j.beem.2023.101742 -
Best Practice & Research. Clinical... Jul 2023At the end of 2019, the world began to fight the coronavirus disease 2019 (COVID-19) pandemic caused by the severe acute respiratory syndrome coronavirus-2. Many... (Review)
Review
At the end of 2019, the world began to fight the coronavirus disease 2019 (COVID-19) pandemic caused by the severe acute respiratory syndrome coronavirus-2. Many vaccines have quickly been developed to control the epidemic, and with the widespread use of vaccines globally, several vaccine-related adverse events have been reported. This review mainly focused on COVID-19 vaccination-associated thyroiditis and summarized the current evidence regarding vaccine-induced subacute thyroiditis, silent thyroiditis, Graves' disease, and Graves' orbitopathy. The main clinical characteristics of each specific disease were outlined, and possible pathophysiological mechanisms were discussed. Finally, areas lacking evidence were specified, and a research agenda was proposed.
Topics: Humans; COVID-19; COVID-19 Vaccines; Graves Disease; Graves Ophthalmopathy; Thyroiditis; Vaccination
PubMed: 36933997
DOI: 10.1016/j.beem.2023.101759 -
International Journal of Environmental... Sep 2020The outbreak of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has rapidly spread worldwide. A number of...
The outbreak of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has rapidly spread worldwide. A number of serious effects on various organs and systems have been reported in humans, and recently emerging evidence on the potential association between the infection and thyroid dysfunction are attracting attention from the scientific community. This editorial critically summarizes the main findings on this topic published so far and defines research lines according to the translational approach from the bench to the bed to epidemiological studies and back again, aimed at patient care and effective public health measures.
Topics: Betacoronavirus; COVID-19; Coronavirus Infections; Humans; Pandemics; Pneumonia, Viral; SARS-CoV-2; Thyroid Diseases
PubMed: 32932954
DOI: 10.3390/ijerph17186630 -
Endocrine May 2021The world is dealing with the Covid-19 pandemic due to the coronavirus SARS-CoV-2. Amongst the extra-pulmonary manifestations presented by Covid-19 patients, thyroiditis... (Review)
Review
The world is dealing with the Covid-19 pandemic due to the coronavirus SARS-CoV-2. Amongst the extra-pulmonary manifestations presented by Covid-19 patients, thyroiditis form part of the spectrum of visceral involvement linked to SARS-CoV-2. In this review, we will describe the various documented clinical forms of thyroiditis (inflammatory thyroiditis, subacute or de Quervain's thyroiditis, chronic lymphocytic thyroiditis or Hashimoto's disease, painless (silent) postpartum thyroiditis) to facilitate their diagnosis in more or less symptomatic Covid-19 patients and to provide guidance for patient treatment.
Topics: COVID-19; Female; Humans; Pandemics; SARS-CoV-2; Thyroiditis; Thyroiditis, Subacute
PubMed: 33774779
DOI: 10.1007/s12020-021-02689-y -
Journal of Clinical Medicine Oct 2023The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiological culprit of COronaVIrus Disease 19 (COVID-19), can enter the cells via the... (Review)
Review
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.
PubMed: 37835009
DOI: 10.3390/jcm12196365