COVID-19 and thyroid function: What do we know so far?

Coronavirus disease 2019 (COVID-19) was characterized as a pandemic in March, 2020 by the World Health Organization. COVID-19 is a respiratory syndrome that can progress to acute respiratory distress syndrome, multiorgan dysfunction, and eventually death. Despite being considered a respiratory disease, it is known that other organs and systems can be affected in COVID-19, including the thyroid gland. Thyroid gland, as well as hypothalamus and pituitary, which regulate the functioning of most endocrine glands, express angiotensin-converting enzyme 2 (ACE2), the main protein that functions as a receptor to which SARS-CoV-2 binds to enter host cells. In addition, thyroid gland is extremely sensitive to changes in body homeostasis and metabolism. Immune system cells are targets for thyroid hormones and T3 and T4 modulate specific immune responses, including cell-mediated immunity, natural killer cell activity, the antiviral action of interferon (IFN) and proliferation of T- and B-lymphocytes. However, studies show that patients with controlled hypothyroidism and hyperthyroidism do not have a higher prevalence of COVID-19, nor do they have a worse prognosis when infected with the virus. On the other hand, retrospective observational studies, prospective studies, and case reports published in the last two years reported abnormal thyroid function related to acute SARS-CoV-2 infection or even several weeks after its resolution. Indeed, a variety of thyroid disorders have been documented in COVID-19 patients, including non-thyroidal illness syndrome (NTIS), subacute thyroiditis and thyrotoxicosis. In addition, thyroid disease has already been reported as a consequence of the administration of vaccines against SARS-CoV-2. Overall, the data revealed that abnormal thyroid function may occur during and in the convalescence post-COVID condition phase. Although the cellular and molecular mechanisms are not completely understood, the evidence suggests that the "cytokine storm" is an important mediator in this context. Thus, future studies are needed to better investigate the pathophysiology of thyroid dysfunction induced by COVID-19 at both molecular and clinical levels.

Thyroid Function Abnormalities and Outcomes in Hospitalized Patients with COVID-19 Infection: A Cross-Sectional Study.

Thyroid gland can be affected by the COVID-19 infection. The pattern of thyroid function abnormality reported in COVID-19 is variable; in addition, some drugs used in COVID-19 patients like glucocorticoids and heparin can affect the thyroid function tests (TFT). We conducted an observational, cross-sectional study of thyroid function abnormalities with thyroid autoimmune profile in COVID-19 patients with varying severity from November 2020 to June 2021. Serum FT4, FT3, TSH, anti-TPO, and anti-Tg antibodies were measured before the initiation of treatment with steroids and anti-coagulants. A total of 271 COVID-19 patients were included in the study, of which 27 were asymptomatic and remaining 158, 39, and 47 were classified to mild, moderate and severe categories, respectively, according to MoHFW, India criteria. Their mean age was 49±17 years and 64.9% were males. Abnormal TFT was present in 37.2% (101/271) patients. Low FT3, low FT4, and low TSH were present in 21.03%, 15.9% and 4.5% of patients, respectively. Pattern corresponding to sick euthyroid syndrome was the most common. Both mean FT3 and FT3/FT4 ratio decreased with increasing severity of COVID-19 illness (p=0.001). In multivariate analysis, low FT3 was associated with increased risk of mortality (OR 12.36, 95% CI: 1.23-124.19; p=0.033). Thyroid autoantibodies were positive in 58 (27.14%) patients; but it was not associated with any thyroid dysfunction. Thyroid function abnormality is common among COVID-19 patients. Both low FT3 and FT3/FT4 ratio are indicators of disease severity while low FT3 is a prognostic marker of COVID-19 associated mortality.

[The role of systemic immune activation in the development of thyroid dysfunction in COVID-19].

BACKGROUND: The research of cytokine-induced thyropathies in the midst of continuing coronavirus infection (COVID-19) pandemic is a very important and urgent problem. On the one hand, COVID-19 is often accompanied by a massive overproduction of cytokines, so we can expect an enhanced cytokines effects impact on the thyroid gland. On the other hand, it is possible that biological therapy with tocilizumab, which has a powerful immunosuppressive effect, plays a protective role to the development of cytokines-induced thyropathies amidst COVID-19. The results of the study should be the starting point for understanding the mechanisms of possible compromise of thyroid function during COVID-19. AIM: The primary endpoint is to assess the relationship between the levels of thyroid-stimulating hormone (TSH), free triiodothyronine (FT3), and free thyroxine (FT4) with the inflammatory process markers. The secondary endpoint is the identification of an association between TSH, FT3 and FT4 values, and patient survival. MATERIALS AND METHODS: This retrospective, single-center study included 122 patients hospitalized at the National Medical Research Center for Endocrinology with a clinical and laboratory analysis of COVID-19 and bilateral polysegmental viral pneumonia. To assess the functional status of the thyroid gland all patients underwent observation of the TSH, FT3, FT4, antibodies to thyroid peroxidase, antibodies to the TSH receptor (AT-recTSH). The markers of the inflammatory process were assessed: interleukin-6, C-reactive protein, the degree of lung tissue damage according to multispiral computed tomography of the lungs, the percentage of blood oxygen saturation (SpO2), the treatment outcomes. RESULTS: Five (4%) patients were found with subclinical thyrotoxicosis. Serum TSH values were inversely correlated with interleukin-6 (r=-0.221; p=0.024). Analysis of the level of hospital mortality, stratified by TSH, revealed statistically significantly lower TSH values in the group of deceased patients (p=0.012). The median TSH in surviving patients was 1.34 [0.85; 1.80], for the deceased 0.44 [0.29; 0.99]. CONCLUSION: Our research shows that the trigger of thyropathies in coronavirus infection is most likely thyroid tissue damage by the proinflammatory cytokines. This study shows some specific clinical aspects regarding the clinical relevance in patients with thyrotoxicosis and COVID-19, namely, the high hospital mortality rate.

Isolated thyroid abscess in early childhood.

Isolated thyroid abscess is a rare entity in early childhood. Among thyroid disorders, thyroid abscess or acute suppurative thyroiditis constitutes about 0.7%-1% of all cases. The thyroid gland is normally resistant to infections due to its well-enveloped capsule, rich blood supply, and high iodine content.A child presented with tender neck swelling accompanied by fever for 3 days. Ultrasound of the neck showed features suggestive of left parapharyngeal abscess. Laboratory parameters including thyroid function test were within normal limits. Contrast-enhanced CT of the neck was done and showed an isolated thyroid abscess with no other abnormalities. The patient was started on intravenous antibiotics followed by incision and drainage of the abscess. The child improved symptomatically. This report discusses the differential diagnosis and management of this rare entity.

The effect of COVID-19 on the presentation of thyroid disease in children.

Introduction: Although studies suggest a potential link between COVID-19 and thyroid dysfunction in adults, there are insufficient data to confirm that association in children, and whether there is any effect on presentation to healthcare services. Aims: To identify whether presentations of thyroid dysfunction in children to a tertiary paediatric hospital changed as a result of the COVID-19 pandemic. Methods: A retrospective case note review was conducted of all children with abnormal thyroid function tests between 1st January 2016 and 31st December 2021 at a tertiary paediatric endocrine centre in the United Kingdom. Results: Overall, 244 children whose first presentation was within the timeframe of interest were included in this study, with a median age (range) of 11.5 (6.1, 16.8) years. Of these, 43 (18%) were hyperthyroid and 201 (82%) were hypothyroid. The greatest number of thyroid presentations occurred in 2021 (n=60, 25% of total over time period) and the fewest in 2020 (n=10, 4% of total over time period). Prior to this, the median (range) number of presentations per year was 34 (28, 39). There were no statistically significant differences in biochemistry, antibody status or other clinical characteristics between those who presented with hyperthyroidism prior to the pandemic or after. In those with hypothyroidism, baseline biochemistry was similar between the 2 groups, but the presence of other autoimmune conditions was greater pre-pandemic (17.2% vs 15.0%, p=0.03). In addition, patients were more likely to have transient thyroid dysfunction, which did not require treatment post-pandemic (70.0% vs 49.6%, p=0.0086). Conclusions: Although overall rates of presentation with thyroid dysfunction have not altered since the first wave of the COVID-19 pandemic, presentations with transient thyroid dysfunction, not requiring ongoing treatment have increased. Further research regarding the relationship between COVID-19 and thyroid function in children and young people, is needed.

Association of thyroid dysfunction and COVID-19: A systematic review and meta-analysis.

This systematic review and meta-analysis was conducted to evaluate the effect of COVID-19 on thyroid function and the role of thyroid hormones alterations in predicting the severity of COVID-19. Online databases, including Scopus, Medline/PubMed, EMBASE, Google Scholar, and Cochrane were searched up to August 2, 2022. After screening titles, abstracts, and full manuscripts, respectively, 30 reports were enrolled. The risk of bias (ROB) was evaluated using the QUADAS-2 tool. In addition, odds ratio (OR) and hazard ratio (HR) analysis for assessing the OR of abnormal thyroid function tests (TFT) in predicting the COVID-19 severity and poor outcomes. Among 30 enrolled studies, ROB of the current study is estimated low to moderate. The average number of patients in each study was 325 (range: 40-3,703), with an overall mean age of 57.6, and the female proportion of 40.4%. Overall, the pooled analysis showed that the prevalence of thyroid dysfunction among 9,707 COVID-19 cases was 15%. Among mild to moderate COVID-19 patients, 6.2% had abnormal TFT, and among patients who experienced severe to critical COVID-19, 20.8% had abnormal TFT. The pooled OR for abnormal TFT and the severity of COVID-19 obtained from 3,865 COVID-19 patients was 3.77 (2.03, 6.99). The pooled HR of TSH level of COVID-19 mortality was 1.57 (0.91, 2.72). Our results demonstrate a high prevalence of thyroid dysfunction in COVID-19, and that among patients severe cases had a 3.77-fold higher risk of abnormal TFT compared to mild to moderate COVID-19. Further studies are required to evaluate the longer-term prognostic role of thyroid dysfunction in severe COVID-19, and investigate potential therapeutic strategies.

Thyroid diseases are associated with coronavirus disease 2019 infection.

Background: In 2019, there was a global outbreak of new coronary pneumonia. Studies have found that the severity of patients with new coronary pneumonia may be related to their comorbidities. This article discusses the impact of thyroid disease on the severity of new coronary pneumonia through a meta-analysis and provides new treatment ideas for the later treatment and recovery of new coronary pneumonia. Methods: Databases including PubMed, Embase, Cochrane Library, SINOMED, China national knowledge infrastructure (CNKI), and Wanfang for coronavirus disease 2019 (COVID-19) infection and thyroid diseases were searched. Reference lists of all eligible articles and related previous review articles were handsearched. Fifty-three articles were included to conduct the meta-analysis. Results: Fifty-three articles with 12,022 COVID-19 infection patients were included in this meta-analysis. The proportion of patients with thyroid diseases in all COVID-19 infection patients fluctuates between 0% and 88.46%. Of the 53 included studies, 22 studies reported the severity of COVID-19 infection and grouped. The fixed-effects model was used to merge odds ratio (OR) values, and the pooled effect size in favor of non-severe patients is 2.62 (95% CI = 1.96-3.49, P < 0.0001), which means that patients with severe COVID-19 infection are more likely to have thyroid diseases. The analysis subgrouped into Asia and Europe shows that patients with COVID-19 severe infection in Asia are 3.77 times more likely to have thyroid diseases than non-severe patients (fixed-effects model: OR = 3.77, 95% CI = 2.66-5.35, P < 0.00001). No significant statistical heterogeneity was found by the heterogeneity analysis (chi-square = 19.85, P = 0.34, I 2 = 9%). Severe COVID-19 infection patients are more likely to be complicated by hypothyroidism and low T3 syndrome. The pooled ORs with fixed-effects model are 3.72 (95% CI = 1.62-8.58, P = 0.002) and 5.86 (95% CI = 2.79-12.33, P < 0.00001), respectively. Conclusion: COVID-19 infection patients with thyroid diseases are very common, and severe patients are more likely to have thyroid diseases. Asian COVID-19 infection, hypothyroidism patients, and patients with low T3 syndrome are more likely to progress to severe condition. Systematic Review Registration: https://inplasy.com, identifier INPLASY202190079.

Thyroid Function, Inflammatory Response, and Glucocorticoids in COVID-19.

The ongoing COVID-19 pandemic calls for extensive research on various medical topics. Since the beginning of the pandemic, multiple studies investigated the impact of SARS CoV-2 on thyroid function. However, crucial data, such as trend progression over time or influence of commonly used drugs, might still be missing. We checked the thyroid function in 174 patients with PCR-confirmed COVID-19. Our research covered three separate time points of hospitalization (days 1, 4, and 10). We did not exclude patients treated with glucocorticoids but, instead, compared them with patients not treated with steroids. We correlated the results of thyroid function tests with markers of systemic inflammation. We checked if abnormal thyroid function can predict unfavorable outcomes defined as combined primary endpoint and/or secondary endpoints; the combined primary endpoint was the occurrence of death, mechanical ventilation, non-invasive ventilation, vasopressor infusion, or prolonged hospital stay, and the secondary endpoint was any of the listed events. In general, 80.46% of evaluated patients displayed abnormalities in thyroid function tests over at least one time point throughout the observation. We noticed a high prevalence of features typical for thyroid dysfunction in non-thyroidal illness (NTI). Free triiodothyronine (fT3) concentration was significantly lower in the group requiring glucocorticoids. Patients displaying abnormal thyroid function were statistically more likely to meet the predefined combined primary endpoint. We found that fT3 measured at admission could be perceived as an independent predictor of endpoint completion for all analyzed groups. Thyroid involvement is common in COVID-19. Our study supports the idea of thyroid function abnormalities being important clinical tools and allowing early recognition of possible detrimental outcomes of the disease.

Thyroid Dysfunction and COVID-19: The Emerging Role of Selenium in This Intermingled Relationship.

COVID-19 represents a worldwide public health emergency, and, beyond the respiratory symptoms characterizing the classic viral disease, growing evidence has highlighted a possible reciprocal relationship between SARS-CoV-2 infection and thyroid dysfunction. The updated data discussed in this review suggests a role of SARS-CoV-2 infection on the thyroid gland, with multiple thyroid pictures described. Conversely, no conclusion can be drawn on the association between pre-existing thyroid disease and increased risk of SARS-CoV-2 infection. In this scenario, selenium (Se), an essential trace element critical for thyroid function and known as an effective agent against viral infections, is emerging as a potential novel therapeutic option for the treatment of COVID-19. Large multicentre cohort studies are required to elucidate the mechanisms underlying thyroid dysfunction during or following recovery from COVID-19, including Se status. Meanwhile, clinical trials should be performed to evaluate whether adequate intake of Se can help address COVID-19 in Se-deficient patients, also avoiding thyroid complications that can contribute to worsening outcomes during infection.

The impact of pre-existing thyroid diseases on susceptibility to respiratory infections or self-reported sickness during the SARS-CoV-2 pandemic.

Introduction: This study aimed to evaluate the incidence, severity and presence of symptoms of respiratory tract infections and COVID-19, in patients with pre-existing thyroid dysfunction compared to individuals without thyroid diseases, during the peak month of the COVID-19 pandemic in the Netherlands. Subjects and methods: In this retrospective observational cohort study, all patients currently under follow-up at the Radboud UMC for thyroid dysfunction received a digital questionnaire. Primary outcomes were incidence of self-reported sickness and cases diagnosed with COVID-19. We compared these primary outcomes between these patients and individuals without thyroid diseases that received the same questionnaire, recruited from the Human Functional Genomics Cohort at the Radboud UMC. Results: In total, 238 patients with pre-existing thyroid dysfunction and 161 controls were included. Patients did not report more sickness (30.7% vs. 29.2%; p = 0.752) or microbiologically confirmed SARS-CoV-2 infections (1.7% vs. 0.6%; p = 0.351). COVID-19 clinical diagnosis was more frequently made in patients with thyroid diseases (4.2% vs. 0.6%; p = 0.032), despite overall lower incidence of self-reported respiratory related symptoms (52.8% vs. 63.8%; p = 0.028), compared to controls. Sub-group analysis between patients with autoimmune and not-autoimmune thyroid dysfunction did not reveal significant associations with respect to any of the outcome measures. Conclusion: This retrospective survey of a cohort of patients with from a tertiary academic hospital suggests that pre-existing thyroid dysfunction, independent from the aetiology, does not lead to an apparent risk to develop respiratory tract infections and COVID-19 related symptoms.

The prognostic values of thyroid disorders in predicting COVID-19 composite poor outcomes: A systematic review and meta-analysis.

BACKGROUND AND AIMS: In this meta-analysis, we aimed to evaluate the prognostic properties of thyroid disorder during admission on poor prognosis and factors that may influence the relationship in patients with COVID-19. METHODS: A systematic literature search of PubMed, EBSCO, and CENTRAL was conducted from inception to August 27, 2021. The main exposure was unspecified and specified thyroid disorders-hypothyroidism or hypothyroidism. The outcome of interest was the COVID-19 composite poor outcome that comprises of severity, mortality, ICU admission, and hospitalization. RESULTS: There were 24,734 patients from 20 studies. Meta-analysis showed that thyroid disorder was associated with composite poor outcome (OR 2.87 (95% CI 2.04-4.04), p < 0.001; I2 = 62.4%, p < 0.001). Meta regression showed that age (p = 0.047) and hypertension (p = 0.01), but not gender (p = 0.15), DM (p = 0.10), CAD/CVD (p = 0.38), obesity (p = 0.84), and COPD (p = 0.07) affected the association. Subgroup analysis showed that thyroid disorder increased risk of severe COVID-19 (OR 5.13 (95% CI 3.22-8.17), p < 0.05; I2 = 0%, p = 0.70) and mortality (OR 2.78 (95%CI 1.31-5.90), p < 0.05; I2 = 80%, p < 0.01). Pooled diagnostic analysis of thyroid disorder yielded a sensitivity of 0.22 (0.13-0.35), specificity of 0.92 (0.87-0.95), and AUC of 0.72. The probability of poor outcome was 38% in patients with thyroid disorder and 15% in patients without thyroid abnormality. CONCLUSION: On-admission thyroid disorder was associated with poor prognosis in COVID-19 patients.

Potential relationships between COVID-19 and the thyroid gland: an update.

In this review, I aim to provide a complete overview of recent advances in knowledge regarding severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2)-induced thyroid dysfunction. I discuss the findings regarding the role of SARS-CoV-2 in the development of thyroid dysfunction, including subacute thyroiditis, Graves' disease, non-thyroidal illness, thyrotoxicosis and Hashimoto's thyroiditis during and subsequent to coronavirus disease 2019 (COVID-19). The thyroid gland and the entire hypothalamic-pituitary-thyroid (HPT) axis may represent key targets of SARS-CoV-2. Thyroid dysfunction during and subsequent to COVID-19 has been documented in clinical studies and is usually reversible. Most of the thyroid disorders, including Graves' disease, euthyroid sick syndrome, Hashimoto's thyroiditis and subacute thyroiditis, have been documented as sequelae to COVID-19, and the SARS-CoV-2 virus has been implicated in the aetiology of each. COVID-19 has been suggested to trigger the activation of pre-existing thyroid disease or autoimmunity. Furthermore, patients with uncontrolled thyrotoxicosis are at risk of SARS-CoV-2 infection-related consequences. Because of the neutropenia caused by antithyroid medications, which may obscure the signs of COVID-19, this group of patients should receive special attention. It is suggested that thyroid dysfunction during COVID-19 is caused by direct infection of the thyroid or "cytokine storm"-mediated autoimmune effects on the thyroid.

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection and thyroid disease. An update.

PURPOSE OF REVIEW: Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection is associated with excess morbidity and mortality in patients with hypertension and diabetes but little is known about thyroid diseases. Thus, our goal was to review the literature with respect to: (i) Are patients with underlying hypo- or hyperthyroidism at increased risk of contracting SARS-CoV-2 infection? (ii) do underlying hypo- and hyperthyroidism impact the prognosis of SARS-CoV-2 infection? (iii) does SARS-CoV-2 infection cause de novo thyroid dysfunction? RECENT FINDINGS: Patients with hypo- or hyperthyroidism do not have an increased risk of contracting SARS-CoV-2, and a diagnosis of hypo- or hyperthyroidism is not associated with a worsened prognosis of SARS-CoV-2 infection. SARS-CoV-2 infection has been associated with subsequent thyrotoxicosis, euthyroid sick syndrome, subacute thyroiditis, and autoimmune thyroid disease. SUMMARY: These findings suggest that receiving treatment for thyroid dysfunction does not per se impact the patients' risk of acquiring SARS-CoV-2 infection, or the management of those who already contracted it. Additional studies with larger numbers of patients and long-term follow-up are required in order to clarify whether patients with SARS-CoV-2 infection are more or less prone to develop thyroid dysfunction and/or thyroid autoimmunity than patients recovering from other virus infections.

Thyroid dysfunction in COVID-19 patients.

PURPOSE: "Non thyroidal illness syndrome" (NTIS) or "euthyroid sick syndrome" (ESS) is a possible biochemical finding in euthyroid patients with severe diseases. It is characterized by a reduction of serum T3 (fT3), sometimes followed by reduction of serum T4 (fT4). The relationship between thyroid hormones levels and mortality is well known and different studies showed a direct association between NTIS and mortality. The sudden spread of the 2019 novel coronavirus (SARS-CoV 2) infection (COVID-19) and its high mortality become a world healthcare problem. Our aim in this paper was to investigate if patients affected by COVID-19 presented NTIS and the relationship between thyroid function and severity of this infection. METHODS: We evaluated the thyroid function in two different groups of consecutive patients affected by COVID-19 with respect to a control group of euthyroid patients. Group A included patients hospitalized for COVID-19 pneumonia while patients requiring intensive care unit (ICU) for acute respiratory syndrome formed the group B. Group C identified the control group of euthyroid patients. RESULTS: Patients from group A and group B showed a statistically significant reduction in fT3 and TSH compared to group C. In group B, compared to group A, a further statistically significant reduction of fT3 and TSH was found. CONCLUSIONS: COVID-19 in-patients can present NTIS. FT3 and TSH serum levels are lower in patients with more severe symptoms.

Thyroid Function Abnormalities in COVID-19 Patients.

Purpose: The novel coronavirus COVID-19, has caused a worldwide pandemic, impairing several human organs and systems. Whether COVID-19 affects human thyroid function remains unknown. Methods: Eighty-four hospitalized COVID-19 patients in the First Affiliated Hospital, Zhejiang University School of Medicine (Hangzhou, China) were retrospectively enrolled in this study, among which 22 cases had complete records of thyroid hormones. In addition, 91 other patients with pneumonia and 807 healthy subjects were included as controls. Results: We found that levels of total triiodothyronine (TT3) and thyroid stimulating hormone (TSH) were lower in COVID-19 patients than healthy group (p < 0.001). Besides, TSH level in COVID-19 patients was obviously lower than non-COVID-19 patients (p < 0.001). Within the group of COVID-19, 61.9% (52/84) patients presented with thyroid function abnormalities and the proportion of thyroid dysfunction was higher in severe cases than mild/moderate cases (74.6 vs. 23.8%, p < 0.001). Patients with thyroid dysfunction tended to have longer viral nucleic acid cleaning time (14.1 ± 9.4 vs. 10.6 ± 8.3 days, p = 0.088). To note, thyroid dysfunction was also associated with decreased lymphocytes (p < 0.001) and increased CRP (p = 0.002). The correlation between TT3 and TSH level seemed to be positive rather than negative in the early stage, and gradually turned to be negatively related over time. Conclusion: Thyroid function abnormalities are common in COVID-19 patients, especially in severe cases. This might be partially explained by nonthyroidal illness syndrome.

Thyroid dysfunction may be associated with poor outcomes in patients with COVID-19.

BACKGROUND: Coronavirus disease (COVID-19) has resulted in considerable morbidity and mortality worldwide. Thyroid hormones play a key role in modulating metabolism and the immune system. However, the prevalence of thyroid dysfunction (TD) and its association with the prognosis of COVID-19 have not yet been elucidated. In this study, we seek to address this gap and understand the link between TD and COVID-19. METHODS: Herein, we enrolled patients who were hospitalized with COVID-19 and had normal or abnormal thyroid function test results at the West Court of Union Hospital in Wuhan, China, between 29 January and February 26, 2020. We carried out follow up examinations until April 26, 2020. Data on clinical features, treatment strategies, and prognosis were collected and analyzed. TD was defined as an abnormal thyroid function test result, including overt thyrotoxicosis, overt hypothyroidism, subclinical hypothyroidism, subclinical hyperthyroidism, and euthyroid sick syndrome. RESULTS: A total of 25 and 46 COVID-19 patients with and without TD, respectively, were included in the study. COVID-19 patients with TD had significantly higher neutrophil counts and higher levels of C-reactive protein, procalcitonin, lactate dehydrogenase, serum creatine kinase, aspartate transaminase, and high-sensitive troponin I and a longer activated partial thromboplastin time but lower lymphocyte, platelet, and eosinophil counts. A longitudinal analysis of serum biomarkers showed that patients with TD presented persistently high levels of biomarkers for inflammatory response and cardiac injury. COVID-19 patients with TD were more likely to develop a critical subtype of the disease. Patients with TD had a significantly higher fatality rate than did those without TD during hospitalization (20% vs 0%, P = 0.002). Patients with TD were more likely to stay in the hospital for more than 28 days than were those without TD (80% vs 56.52%, P = 0.048). CONCLUSIONS: Our preliminary findings suggest that TD is associated with poor outcomes in patients with COVID-19.

Thyroid Function Before, During, and After COVID-19.

CONTEXT: The effects of COVID-19 on the thyroid axis remain uncertain. Recent evidence has been conflicting, with both thyrotoxicosis and suppression of thyroid function reported. OBJECTIVE: We aimed to detail the acute effects of COVID-19 on thyroid function and determine if these effects persisted on recovery from COVID-19. DESIGN: A cohort observational study was conducted. PARTICIPANTS AND SETTING: Adult patients admitted to Imperial College Healthcare National Health Service Trust, London, UK, with suspected COVID-19 between March 9 to April 22, 2020, were included, excluding those with preexisting thyroid disease and those missing either free thyroxine (FT4) or thyrotropin (TSH) measurements. Of 456 patients, 334 had COVID-19 and 122 did not. MAIN OUTCOME MEASURES: TSH and FT4 measurements were recorded at admission, and where available, in 2019 and at COVID-19 follow-up. RESULTS: Most patients (86.6%) presenting with COVID-19 were euthyroid, with none presenting with overt thyrotoxicosis. Patients with COVID-19 had a lower admission TSH and FT4 compared to those without COVID-19. In the COVID-19 patients with matching baseline thyroid function tests from 2019 (n = 185 for TSH and 104 for FT4), TSH and FT4 both were reduced at admission compared to baseline. In a complete case analysis of COVID-19 patients with TSH measurements at follow-up, admission, and baseline (n = 55), TSH was seen to recover to baseline at follow-up. CONCLUSIONS: Most patients with COVID-19 present with euthyroidism. We observed mild reductions in TSH and FT4 in keeping with a nonthyroidal illness syndrome. Furthermore, in survivors of COVID-19, thyroid function tests at follow-up returned to baseline.

Thyroid Dysfunction in Relation to Immune Profile, Disease Status, and Outcome in 191 Patients with COVID-19.

OBJECTIVE: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-related thyroiditis is increasingly recognized. The role of thyroid autoimmunity and SARS-CoV-2 viral load in SARS-CoV-2-related thyroid dysfunction is unclear. We evaluated the thyroid function of a cohort of coronavirus disease 2019 (COVID-19) patients, in relation to their clinical features, and biochemical, immunological, and inflammatory markers. METHODS: Consecutive adult patients, without known thyroid disorders, admitted to Queen Mary Hospital for COVID-19 from July 21 to August 21, 2020, were included. Serum levels of thyroid-stimulating hormone (TSH), free thyroxine, free triiodothyronine (fT3), and antithyroid antibodies were measured on admission. RESULTS: Among 191 patients with COVID-19 (mean age 53.5 ±â€…17.2 years; 51.8% male), 84.3% were mild, 12.6% were moderate, and 3.1% were severe. Abnormal thyroid function was seen in 13.1%. Ten patients had isolated low TSH, suggestive of subclinical thyrotoxicosis due to thyroiditis, although the contribution of autoimmunity was likely in 2 of them. Autoimmune thyroiditis probably also contributed to subclinical hypothyroidism in another patient. Ten patients had isolated low fT3, likely representing nonthyroidal illness syndrome. Lower SARS-Cov-2 polymerase chain reaction cycle threshold values and elevated C-reactive protein were independently associated with occurrence of low TSH (P = .030) and low fT3 (P = .007), respectively. A decreasing trend of fT3 with increasing COVID-19 severity (P = .032) was found. Patients with low fT3 had more adverse COVID-19-related outcomes. CONCLUSION: Around 15% of patients with mild to moderate COVID-19 had thyroid dysfunction. There may be a direct effect of SARS-CoV-2 on thyroid function, potentially leading to exacerbation of pre-existing autoimmune thyroid disease. Low fT3, associated with systemic inflammation, may have a prognostic significance.