The Old and the New in Subacute Thyroiditis: An Integrative Review

Lanzo, Nicola; Patera, Bohdan; Fazzino, Gaia Francesca Maria; Gallo, Daniela; Lai, Adriana; Piantanida, Eliana; Ippolito, Silvia; Tanda, Maria Laura

doi:10.3390/endocrines3030031

Cited by 11 publications

(8 citation statements)

References 155 publications

(209 reference statements)

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“…Although no HLA testing was performed on any of the cases we reviewed, Stasiak et al. suggest that the presence of novel high-risk alleles, including HLA-B*18:01 and HLA-DRB1*01 , may deteriorate the clinical course of SAT ( 62 , 63 ). Another hypothesis involves molecular mimicry; a recent in-vitro investigation revealed that antibodies against SARS-CoV-2 antigens may cross-react with self-tissue antigens, such as TPO.…”

Section: Discussionmentioning

confidence: 98%

“…As this theory states, HLAmediated tissue destruction occurs through either cross-reaction with host antigens or auto-antibody formation against the large amount of self-antigens released from the damaged thyroid tissue. Although no HLA testing was performed on any of the cases we reviewed, Stasiak et al suggest that the presence of novel high-risk alleles, including HLA-B*18:01 and HLA-DRB1*01, may deteriorate the clinical course of SAT (62,63). Another hypothesis involves molecular mimicry; a recent in-vitro investigation revealed that antibodies against SARS-CoV-2 antigens may cross-react with selftissue antigens, such as TPO.…”

Section: Discussionmentioning

confidence: 99%

“…Another hypothesis involves molecular mimicry; a recent in-vitro investigation revealed that antibodies against SARS-CoV-2 antigens may cross-react with self-tissue antigens, such as TPO. This mechanism is a putative pathogenic trigger for immune-mediated adverse effects following SARS-CoV-2 infection and immunization ( 63 ).…”

Section: Discussionmentioning

confidence: 99%

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Subacute thyroiditis following COVID-19: A systematic review

et al. 2023

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BackgroundSubacute thyroiditis (SAT) is a self-limiting thyroid inflammatory disease occurring specifically after upper respiratory tract infections. Since COVID-19 is a respiratory disease leading to multi-organ involvements, we aimed to systematically review the literature regarding SAT secondary to COVID-19.MethodsWe searched Scopus, PubMed/MEDLINE, Cochrane, Web of Science, ProQuest, and LitCovid databases using the terms “subacute thyroiditis” and “COVID-19” and their synonyms from inception to November 3, 2022. We included the original articles of the patients with SAT secondary to COVID-19. Studies reporting SAT secondary to COVID-19 vaccination or SAT symptoms’ manifestation before the COVID-19 infection were not included.ResultsTotally, 820 articles were retained. Having removed the duplicates, 250 articles remained, out of which 43 articles (40 case reports and three case series) with a total of 100 patients, were eventually selected. The patients aged 18–85 years (Mean: 42.70, SD: 11.85) and 68 (68%) were women. The time from the onset of COVID-19 to the onset of SAT symptoms varied from zero to 168 days (Mean: 28.31, SD: 36.92). The most common symptoms of SAT were neck pain in 69 patients (69%), fever in 54 (54%), fatigue and weakness in 34 (34%), and persistent palpitations in 31 (31%). The most common ultrasonographic findings were hypoechoic regions in 73 (79%), enlarged thyroid in 46 (50%), and changes in thyroid vascularity in 14 (15%). Thirty-one patients (31%) were hospitalized, and 68 (68%) were treated as outpatients. Corticosteroids were the preferred treatment in both the inpatient and outpatient settings (25 inpatients (81%) and 44 outpatients (65%)). Other preferred treatments were nonsteroidal anti-inflammatory drugs (nine inpatients (29%) and 17 outpatients (25%)) and beta-blockers (four inpatients (13%) and seven outpatients (10%)). After a mean duration of 61.59 days (SD: 67.07), 21 patients (23%) developed hypothyroidism and thus, levothyroxine-based treatment was used in six of these patients and the rest of these patients did not receive levothyroxine.ConclusionSAT secondary to COVID-19 seems to manifest almost similarly to the conventional SAT. However, except for the case reports and case series, lack of studies has limited the quality of the data at hand.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

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Subacute thyroiditis following COVID-19: A systematic review

et al. 2023

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“…TG is involved in the formation of thyroid hormones (T3 and T4) 90 . Elevated TG, T3, and T4 levels from ruptured follicles cause thyrotoxicosis in patients 91 . TSH is suppressed by a negative feedback loop of elevated thyroid hormones, 92 and symptoms of hyperthyroidism occur.…”

Section: Subacute Thyroiditis After Covid‐19 Infectionmentioning

confidence: 99%

“…90 Elevated TG, T3, and T4 levels from ruptured follicles cause thyrotoxicosis in patients. 91 TSH is suppressed by a negative feedback loop of elevated thyroid hormones, 92 and symptoms of hyperthyroidism occur. Before the euthyroid state, FT3 and FT4 decrease, and TSH increases moderately prompting hypothyroidism symptoms.…”

Section: Subacute Thyroiditis After Covid-19 Infectionmentioning

confidence: 99%

COVID‐19‐induced autoimmune thyroiditis: Exploring molecular mechanisms

Mohammadi

Dua

Saghafi

et al. 2023

Journal of Medical Virology

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Severe acute respiratory syndrome coronavirus‐2 (SARS‐CoV‐2) damages multiple organs, including the thyroid, by direct invasion and cell entry via angiotensin‐converting enzyme 2 or indirectly by promoting excessive inflammation in the body. The immune system is a critical factor in antiviral immunity and disease progression. In the context of SARS‐CoV‐2 infection, the immune system may become overly activated, resulting in a shift from regulatory to effector responses, which may subsequently promote the development and progression of autoimmune diseases. The incidence of autoimmune thyroid diseases, such as subacute thyroiditis, Graves' disease, and Hashimoto's thyroiditis, increases in individuals with COVID‐19 infection. This phenomenon may be attributed to aberrant responses of T‐cell subtypes, the presence of autoantibodies, impaired regulatory cell function, and excessive production of inflammatory cytokines, namely interleukin (IL)‐6, IL‐1β, interferon‐γ, and tumor necrosis factor‐α. Therefore, insights into the immune responses involved in the development of autoimmune thyroid disease according to COVID‐19 can help identify potential therapeutic approaches and guide the development of effective interventions to alleviate patients' symptoms.

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