SARS-CoV-2-related thyroid disorders: a synopsis for nuclear medicine thyroidologists

Abstract

The coronavirus disease-19 (COVID-19) is an infectious disease caused by the enveloped RNA β-severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2). The COVID-19 may have a variable presentation, from an asymptomatic disease to acute respiratory distress syndrome (ARDS) and multi-organ failure. Impairment of endocrine systems may also occur in COVID-19 patients and thyroid gland involvement was reported in a not negligible number of patients, as documented in several studies since the pandemic outbreak. Abnormal thyroid function tests (TSH and/or thyroid hormones) are frequently reported in COVID-19 patients with variable prevalence and mild to moderate severity in available studies, as recently reviewed by our group [1]. In addition, to provide thyroid imaging and radioiodine therapy, nuclear medicine physicians are also involved, especially in Europe, in clinical patients' management. Then, being aware of the multiple and complex interactions between SARS-CoV-2 infection and thyroid function is relevant to nuclear medicine physicians in order to provide adequate and high-quality diagnosis, treatment, and follow-up. SARS-CoV-2 effects on thyroid cellsTwo main mechanisms account for thyroid function perturbations in COVID-19 patients: (1) a viral effect on target cells and (2) an indirect effect of systemic inflammatory immune response (Fig. 1). A third condition, the so-called euthyroid sick syndrome (ESS), is typically observed in severely ill patients and represents an adaptive mechanism rather than a true thyroid dysfunction. Then, discriminating ESS from direct or indirect SARS-CoV-2 effects on thyroid function is relevant to avoid inappropriate treatments. Destructive thyroiditisDestructive thyroiditis usually manifests with initial thyrotoxicosis (1-2 months) followed by hypothyroidism (1-3 months) and, in most cases, a final restoration of euthyroidism [1]. Several cases of destructive thyroiditis are reported in COVID-19 patients, which is in line with the well-known association between many respiratory viruses and destructive thyroiditis (i.e., De Quervain's thyroiditis) [1,2]. It is This article is part of the Topical Collection on Endocrinology

The Association Between COVID-19 and Thyroxine Levels: A Meta-Analysis

“…Moreover, in a study based on severe cases in the UK, the proportion of thyroid follicular epithelial cells that were damaged was 22.2% ( 7 ). It is currently believed that COVID-19 has a direct effect on thyroid function and the thyroid hormone levels through the hypothalamus-pituitary-thyroid axis and can also affect the thyroid gland by autoimmune diseases through cytokines ( 8 ). It has been found that the TSH levels are negatively correlated with the mortality of COVID-19 in patients with normal FT3 and FT4 levels ( 9 ).…”

Low FT3 is an independent marker of disease severity in patients hospitalized for COVID-19

“…Hypothalamic–pituitary–thyroid (HPT) axis is an essential endocrine axis that regulates energy expenditure and homeostasis. Recent studies, reviews and epidemiological data have shed light on the involvement of HPT axis and thyroid gland in COVID-19 ( 1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 ). The changes in HPT axis associated with COVID-19 include impaired thyroid-stimulating hormone (TSH) secretion, decreased T3 and T4 (non-thyroidal illness; NTI), decreased activity of deiodinases and thyrotoxicosis ( 10 ).…”

“…Comorbid conditions included diabetes (119, 50.4%), hypertension (102, 43.2%), hypothyroidism (43, 18.2%), coronary artery disease (CAD) (19, 8%), respiratory disease (15, 6.4%), cancer (8, 3.4%) and chronic kidney disease (CKD) (6, 2.5%). The majority of patients (223, 94.5%) were symptomatic cases with a median symptom duration of 5 days(1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20). At baseline, a total of 222 (94.1%) patients had mild disease (no oxygen requirement in 181 and low flow oxygen requirement in 41) whereas 14 (5.9%) patients had severe disease (high flow oxygen-13 and intubation-1).…”

SARS-CoV-2: Emerging Role in the Pathogenesis of Various Thyroid Diseases

“…However, the current knowledge on Th17 and Th22 and their cytokines in the pathogenesis of autoimmune thyroid disease recommend revisiting the Th1 and Th2 role in the pathophysiology of thyroid disorders including Graves’ hyperthyroidism and Hashimoto thyroiditis. 53 Recently, the possible pathogenic mechanisms of immune-mediated thyroid disorders associated with SARS-CoV-2 infections are extensively discussed by Ruggeri et al 42 A clinical point of view on COVID-19-related thyroid disorders was precisely documented by Giovanella et al 55 They suggest for future longitudinal studies to rule out the long-term viral effect on the thyroid gland. Further, it would also be interesting if future studies recapitulate these clinical findings in experimental settings, in vitro and in vivo that may pave the way for new avenues towards molecular therapies targeting these disorders.…”