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General Thermography
Published in James Stewart Campbell, M. Nathaniel Mead, Human Medical Thermography, 2023
James Stewart Campbell, M. Nathaniel Mead
Thyroiditis occurs in the autoimmune conditions such as Hashimoto's thyroiditis and Graves' disease.127 Subacute thyroiditis is a transient thyrotoxic state and results in temporary hyperthyroidism, generally lasting a few weeks but sometimes persisting for months (Figure 10.45).128 Postpartum thyroiditis is a thyroid dysfunction that manifests within one year of pregnancy. Hyperthyroidism and toxic nodular goiter are more commonly seen in older women.129 An inflammatory component is commonly present in most if not all cancers, and thyroid cancer is no exception.130 There may be an increased risk of thyroid cancer among patients with Hashimoto's thyroiditis.131
Acquired hypothyroidism
Published in Pallavi Iyer, Herbert Chen, Thyroid and Parathyroid Disorders in Children, 2020
Subacute thyroiditis presents with a tender, enlarged thyroid gland, likely due to viral mediated inflammation. Fever may be present along with other viral symptoms initially. Hyperthyroidism or hypothyroidism may be associated with subacute thyroiditis and typically lasts for 1–2 months. NSAIDS or corticosteroids may improve tenderness of the gland and beta-blockers can ameliorate symptoms of hyperthyroidism. Hypothyroidism is treated with levothyroxine as with AITD, but may be transient and short-lived.
Thyroid and Parathyroid Imaging
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
Brahm Shapiro, Milton D. Gross
Subacute thyroiditis classically presents as a self-limited course of transient hyperthyroidism followed by either euthyroidism or hypothyroidism with a return to the euthyroid state over weeks to months.146 The gland may be painful or painless (silent thyroiditis) to palpation.146 Occasionally occurring in the immediate postpartum interval, thyroiditis can be mistaken for postpartum depression, especially if the patient presents in the hypothyroid phase of the syndrome. The etiology of this thyroiditis is unknown but a causal relationship with antecedent viral illnesses has been made.146 Thyroid inflammation results in the release of stored hormone and impaired accumulation of radioiodine leading to the important finding of a low (usually less than 1–2% at 24 h) radioiodine uptake in the setting of an elevated T4 or T3 and a suppressed TSH level.27,38,39,40,42,86,146 Ultrasound may have a role in selected cases.14,102–106,146,146a The management of subacute thyroiditis is for the most part observation, but in some cases (3-blockade to relieve symptoms of hyperthyroxinemia and corticosteroids to relieve pain may be used. It is not uncommon for patients to have more than one episode of thyroiditis.10
Insights into the possible impact of COVID-19 on the endocrine system
Published in Archives of Physiology and Biochemistry, 2023
Adel Abdel-Moneim, Ahmed Hosni
Subacute thyroiditis (SAT) is a self-limiting thyroid inflammatory disease and can causes thyrotoxicosis-associated with the viral infection. SAT exhibits neck pain and overall signs that are commonly linked to thyroid dysfunction (Nishihara et al.2008). The aetiology and pathogenesis of SAT are not fully understood, although it is widely accepted that it arises because of viral infection or post-viral inflammatory response in people with genetic susceptibility (Nishihara et al.2008, Desailloud and Hober 2009). Based on the reported data about the relation of SAT with previous coronavirus infection, SAT may be aetiologically linked to SARS-CoV-2 infection (Brancatella et al.2020). Additionally, Brancatella et al. (2020), Asfuroglu-Kalkan and Ates (2020), and Ippolito et al. (2020) reported three cases of SAT associated with SARS-CoV-2 infection. Furthermore, Scappaticcio et al. (2020) reported that, among nine patients positive for SARS-CoV-2, SAT occurred after the remission of COVID-19 (disappearance of clinical manifestations and negative SARS-CoV-2 test) in six patients (about 65%), with a time interval ranging from 17 to 40 days from remission of COVID-19. The above evidence has been suggested that patients with COVID-19 may have thyroid gland illness (Figure 1).
Association between Thyroid Function and Prognosis of COVID-19: A Retrospective Observational Study
Published in Endocrine Research, 2021
Shan Lang, Ye Liu, Xue Qu, Ran Lu, Wei Fu, Wenhui Zhang, Haining Wang, Tianpei Hong
COVID-19’s impact on the thyroid gland remains largely unknown. Increasing evidence has demonstrated that angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2), which are the key entry sites for SARS-CoV-2, are highly expressed in the thyroid gland and are more abundant than in the lungs.4–7 The onset of subacute thyroiditis has been reported in patients with COVID-19, indicative of viral infections as an etiology.8–11 Data from the previous coronavirus pandemic caused by the SARS-associated coronavirus (SARS-CoV), a member of the Coronaviridae family, demonstrated that SARS-CoV could damage thyroid follicular and parafollicular cells and decrease the number of thyroid stimulating hormone (TSH)-positive cells in the pituitary.12,13 Thus, thyroid dysfunction may be a comorbidity in patients with COVID-19. Moreover, a low triiodothyronine (T3) state is considered an indicator of nonthyroidal illness syndrome (NTIs), also known as euthyroid sick syndrome,14–16 and is observed in critically ill patients. Therefore, changes in thyroid function during coronavirus infection have attracted attention.
A case of idiopathic thyroid abscess caused by Escherichia coli
Published in Journal of Community Hospital Internal Medicine Perspectives, 2019
Gurbaj Singh, Radhika Jaiswal, Neha Gulati, Elizabeth Campbell Granieri
Subacute thyroiditis and thyroid abscess were among the likely causes. Since imaging studies had not identified a concerning locus for infection, oral glucocorticoids were started for treatment of subacute thyroiditis. Antibiotics were also initiated, however, given the clinical concern for infectious etiology. The patient later spiked a fever to 101.1 Fahrenheit on day 4. Repeat CT scan of the neck with IV contrast showed increased retropharyngeal soft tissue edema, enlarged left lobe of thyroid and several nonenhancing foci within the gland concerning for abscesses. Antibiotics were broadened to target a wider pathogen spectrum, and a fine needle aspiration was performed which resulted in drainage of 1 cc of purulent fluid. The patient continued to have neck pain and eventually underwent incision and drainage of the lesion. Cultures demonstrated Escherichia coli sensitive to ceftriaxone. Urine culture and blood culture remained negative. The patient was discharged home on oral antibiotics. Underlying etiology for the infection remained unidentified with no obvious immunocompromised state or other source of infection like a urinary tract infection. On Otorhinolaryngology evaluation, there was no pyriform sinus fistula seen on direct laryngoscopy or upon review of neck imaging. HIV antigen/antibody screen was reported negative. There has been no evidence of recurrence since then on a follow up of 1 year.