SARS-COV-2-related immune-inflammatory thyroid disorders: facts and perspectives.

Introduction: During the COVID-19 pandemic thyroid gland alteration/dysfunction has been emerged as a possible endocrine complication. The present review is focused on inflammatory and autoimmune thyroid complications triggered by SARS-CoV-2 infection by searching through databases like MEDLINE and Scopus up to April 2021.Areas covered: Beside the occurrence of 'non-thyroidal illness' in severe clinical conditions, alterations of thyroid function and structure may occur during COVID-19 as a consequence of either direct or indirect effects of SARS-CoV-2 infection on the gland. On the one hand, SARS-CoV-2 uses ACE2 as a receptor to infect the host cells and ACE2 is highly expressed by follicular thyroid cells. On the other hand, COVID-19 is associated with a systemic inflammatory and immune response, involving Th1/Th17/Th2 lymphocytes and proinflammatory cytokines, which resembles the immune activation that occurs in immune-mediated thyroid diseases. COVID-19-related thyroid disorders include destructive thyroiditis and onset or relapse of autoimmune thyroid disorders, leading to a broad spectrum of thyroid dysfunction ranging from thyrotoxicosis to hypothyroidism, that may worsen COVID-19 clinical course and affect prognosis.Expert opinion: Physicians should be aware of the possible occurrence of thyroid dysfunction during and after SARS-CoV-2 infection. Further longitudinal studies are warranted to evaluate potential long-term sequelae.

Prevalence of thyroid dysfunction in patients with COVID-19: a systematic review.

PURPOSE: Currently, there is an increasing interest regarding the impact of COVID-19 on the thyroid function. As several recent reports have described the onset of thyroid dysfunction in patients diagnosed with COVID-19, we performed a systematic review to assess the prevalence of thyroid dysfunction in patients with COVID-19 as this information could be clinically relevant for the management of these patients. METHODS: A comprehensive computer literature search using PubMed/Medline and Cochrane databases was performed until November 14, 2020 to search original articles evaluating thyroid dysfunction in COVID-19 patients. Information about thyroid dysfunction assessed by thyroid function test was retrieved by the eligible articles. Qualitative analysis (systematic review) only was performed whether a significant heterogeneity of data was detected. RESULTS: Seven studies including 1237 patients with COVID-19 were included. A significant heterogeneity across the studies was found. Most COVID-19 patients were euthyroid with TSH levels in the normal range (from 44 to 94% of the COVID-19 patients assessed in the included studies). The prevalence of thyroid dysfunction in COVID-19 patients (defined as abnormal thyroid function tests) largely varies among the included studies between 13 and 64% of COVID-19 patients as well as clinical presentation. A positive correlation between thyroid dysfunction and clinical severity of COVID-19 was reported. CONCLUSION: Literature data show that thyroid dysfunction is present in a significant percentage of patients with COVID-19. Assessment of thyroid function may be considered in symptomatic COVID-19 patients to have a baseline before introducing thyroid-interfering drugs and those requiring high-intensity care. Further, well-designed studies are needed to better elucidate the impact of COVID-19 on thyroid function and inform thyroid function testing and thyroid dysfunction management in COVID-19 patients.

Subacute thyroiditis in a patient infected with SARS-COV-2: an endocrine complication linked to the COVID-19 pandemic.

PURPOSE: Subacute thyroiditis (SAT) is an inflammatory thyroid disorder of viral origin, generally preceded by an upper respiratory tract infection. Since the disorder is self-limiting, it is frequently underdiagnosed. However, the disease should not be overlooked since the associated thyrotoxicosis may worsen the clinical course of concomitant disorders (e.g., respiratory distress) and long-term sequelae, such as autoimmune hypothyroidism, have been reported. METHODS: Here we describe a woman who developed SAT with thyrotoxicosis after SARS-COV-2 infection. Coronavirus disease (COVID-19) symptoms were mild and the patient was managed with no specific treatment and recovered rapidly. RESULTS: Six weeks after the onset of the upper respiratory tract infection, the patient developed pain and tenderness in the anterior cervical region, fatigue, tremors, and palpitations. Physical examination revealed mild tremors of the extremities, a diffuse and painful goiter, and enlarged and tender cervical and submandibular lymph nodes. At biochemical evaluation, TSH was suppressed, FT3 and FT4 were high, and serum thyroglobulin was markedly increased (188 pg/mL; n.v. 0-40). Thyroid scintigraphy showed markedly reduced 99mTc-perthecnetate uptake in the gland. All findings were consistent with SAT, and treatment with oral prednisone (25 mg/day as the starting dose, gradually tapered) was started. Under the corticosteroid therapy, there was progressive resolution of symptoms and signs, and, within 4 weeks, all thyroid functional tests and inflammatory indexes normalized. CONCLUSION: Clinicians should be aware of thyroid manifestations potentially associated with COVID-19.