Coronavirus Disease 2019-Induced Thyroiditis

Ramsay, Nicolas; Carizey, Rene; Popa, Daniela

doi:10.1016/j.jemermed.2021.01.012

Cited by 4 publications

(1 citation statement)

References 15 publications

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“…It is important to be aware of this particular complication of the COVID-19 infection and to differentiate it from other acute complications such as pneumonia or thromboembolism as some complications require investigations where iodine contrast is used for computer tomography. Such investigations might aggravate thyroid hormone anomalies, such as, for instance, in cases with primary hyperthyroidism [6]. Also, once SAT is recognized, specific anti-thyroid drugs are unnecessary since beta-blockers and non-steroidal anti-inflammatory drugs usually control the disease; glucocorticoids should be used as a last resort for cases with severe local symptoms [24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40][41].…”

Section: Subacute Thyroiditis Induced By Covid-19 Infectionmentioning

confidence: 99%

The New Entity of Subacute Thyroiditis amid the COVID-19 Pandemic: From Infection to Vaccine

et al. 2022

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This is a review of full-length articles strictly concerning subacute thyroiditis (SAT) in relation to the SARS-CoV-2 virus infection (SVI) and COVID-19 vaccine (COV) that were published between the 1st of March 2020 and the 21st of March 2022 in PubMed-indexed journals. A total of 161 cases were reported as follows: 81 cases of SAT–SVI (2 retrospective studies, 5 case series, and 29 case reports), 80 respective cases of SAT–COV (1 longitudinal study, 14 case series, 17 case reports; also, 1 prospective study included 12 patients, with 6 patients in each category). To our knowledge, this represents the largest cohort of reported cases until the present time. SAT–SVI was detected in adults aged between 18 and 85 years, mostly in middle-aged females. SAT–COVID-19 timing classifies SAT as viral (synchronous with infection, which is an original feature of SATs that usually follow a viral infection) and post-viral (during the recovery period or after infection, usually within 6 to 8 weeks, up to a maximum 24 weeks). The clinical spectrum has two patterns: either that accompanying a severe COVID-19 infection with multi-organ spreading (most frequent with lung involvement) or as an asymptomatic infection, with SAT being the single manifestation or the first presentation. Either way, SAT may remain unrecognized. Some data suggest that more intense neck pain, more frequent fever, and more frequent hypothyroidism at 3 months are identified when compared with non-SAT–SVI, but other authors have identified similar presentations and outcomes. Post-COVID-19 fatigue may be due to residual post-SAT hypothyroidism. The practical importance of SAT–SVI derives from the fact that thyroid hormone anomalies aggravate the general status of severe infections (particular concerns being tachycardia/arrhythmias, cardiac insufficiency, and ischemic events). If misdiagnosed, SAT results in unnecessary treatment with anti-thyroid drugs or even antibiotics for fever of unknown cause. Once recognized, SAT does not seem to require a particular approach when compared with non-COVID-19 cases, including the need for glucocorticoid therapy and the rate of permanent hypothyroidism. A complete resolution of thyroid hormone anomalies and inflammation is expected, except for cases with persistent hypothyroidism. SAT–COV follows within a few hours to a few weeks, with an average of 2 weeks (no particular pattern is related to the first or second vaccine dose). Pathogenesis includes molecular mimicry and immunoinflammatory anomalies, and some have suggested that this is part of ASIA syndrome (autoimmune/inflammatory syndrome induced by adjuvants). An alternative hypothesis to vaccine-related increased autoimmunity is vaccine-induced hyperviscosity; however, this is supported by incomplete evidence. From what we know so far concerning the risk factors, a prior episode of non-SVI–SAT is not associated with a higher risk of SAT–COV, nor is a previous history of coronavirus infection by itself. Post-vaccine SAT usually has a less severe presentation and a good outcome. Generally, the female sex is prone to developing any type of SAT. HLA susceptibility is probably related to both new types of SATs. The current low level of statistical evidence is expected to change in the future. Practitioners should be aware of SAT–COV, which does not restrict immunization protocols in any case.

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Section: Subacute Thyroiditis Induced By Covid-19 Infectionmentioning

confidence: 99%

The New Entity of Subacute Thyroiditis amid the COVID-19 Pandemic: From Infection to Vaccine

et al. 2022

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Electrochemical immunoassay for one-pot detection of thyroxin (T4) and thyroid-stimulating hormone (TSH) using magnetic and Janus nanoparticles

2023

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Subacute Thyroiditis in Active COVID-19 Infection: A Report of Two Cases With a Systematic Review of the Literature

Ganie,

Rashid,

Qadir

et al. 2024

Cureus

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Subacute thyroiditis (SAT) is a self-limiting inflammatory condition of the thyroid gland with distinct symptoms and a predictable outcome. During the current COVID-19 pandemic, there have been multiple isolated reports of SAT either during the active viral illness or following recovery. Here, we report two such cases of COVID-19 infection presenting with SAT. A 65-year-old male presented with a two-week history of anterior neck pain, odynophagia, high-grade fever (38.9°C), sweating, palpitations, and tremulousness. At physical examination, the patient presented with a slightly increased heart rate and a tender and enlarged thyroid on palpation. Laboratory examination showed high C-reactive protein levels, with elevated erythrocyte sedimentation rate, and thyroid function tests were suggestive of thyrotoxicosis. Ultrasonography showed a heterogeneous thyroid gland with ill-defined hypoechoic areas, and thyroid scintigraphy showed reduced uptake, confirming the diagnosis of SAT. In another case, a 52-year-old male presented with fever, cough, and myalgias, and was diagnosed with mild COVID-19 pneumonia, and managed conservatively. After two weeks, the patient had a recurrence of high-grade fever, odynophagia, palpitations, and tremors. Examination revealed tachycardia, hyperhidrosis, and a tender and enlarged thyroid on palpation. Thyroid function tests revealed low thyroid-stimulating hormone, with normal total T4 and total T3. Ultrasonography examination showed a heterogeneous thyroid gland with bilateral ill-defined hypoechoic areas. In our systematic review, including 103 SAT cases, it has been suggested that SAT should be recognized as an uncommon extra-pulmonary clinical manifestation of COVID-19 infection and clinicians need to be aware of the association. Pending larger multicentric studies, management of the condition has to be on a case-by-case basis.

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Coronavirus Disease 2019-Induced Thyroiditis

Cited by 4 publications

References 15 publications

The New Entity of Subacute Thyroiditis amid the COVID-19 Pandemic: From Infection to Vaccine

The New Entity of Subacute Thyroiditis amid the COVID-19 Pandemic: From Infection to Vaccine

Electrochemical immunoassay for one-pot detection of thyroxin (T4) and thyroid-stimulating hormone (TSH) using magnetic and Janus nanoparticles

Subacute Thyroiditis in Active COVID-19 Infection: A Report of Two Cases With a Systematic Review of the Literature

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