The COVID-19 pandemic has raised concerns about potential links between SARS-CoV-2 infection and autoimmune diseases. This study investigated changes in the incidence rate (IR) of autoimmune diseases among children following the pandemic's onset.

A retrospective cross-sectional study analyzed data from Clalit Health Services, Israel's largest healthcare provider, examining the IR of different autoimmune diseases in children aged 0-18. The study compared pre-pandemic (2019) with pandemic/post-pandemic periods (2020-2023), encompassing a cohort of over 1.5 million children.

Significant IR increases were observed across multiple autoimmune diseases. Rheumatic diseases (Juvenile Idiopathic Arthritis, Systemic Lupus Erythematosus, Henoch Schoenlein Purpura (HSP)) showed consistent increases, with HSP demonstrating the most pronounced trend. Endocrine disorders exhibited diverse patterns, with autoimmune thyroid diseases and Type 1 diabetes showing overall increases, while diabetic ketoacidosis exhibited an initial spike followed by a decline. Gastrointestinal diseases displayed heterogeneous patterns; Celiac disease and Ulcerative colitis showed general increases, Crohn's disease showed a downward trend, and autoimmune hepatitis exhibited an initial significant decrease followed by a significant increase. Dermatological conditions, including Psoriasis and Vitiligo, demonstrated consistent elevations throughout 2020-2023. Immune Thrombocytopenia Purpura showed initial decreases followed by significant increases in 2022-2023.

This comprehensive analysis reveals significant changes in pediatric autoimmune disease incidence following the COVID-19 pandemic, suggesting potential associations between SARS-CoV-2 infection and autoimmune dysregulation. The diverse patterns observed across different conditions highlight the complex interplay between viral infection and autoimmunity, emphasizing the need for continued surveillance and investigation of long-term immunological consequences of COVID-19 in pediatric populations.

Graves disease (GD) is an autoimmune thyroid disorder characterized by hyperthyroidism and autoantibodies. The COVID-19 pandemic has raised questions about its potential relationship with autoimmune diseases like GD.

This study aims to investigate the causal association between COVID-19 and GD through Mendelian randomization (MR) analysis and assess the impact of COVID-19 on GD.

We conducted an MR study using extensive genome-wide association study data for GD and COVID-19 susceptibility and its severity. We used stringent single nucleotide polymorphism selection criteria and various MR methodologies, including inverse-variance weighting, MR-Egger, and weighted median analyses, to assess causal relationships. We also conducted tests for directional pleiotropy and heterogeneity, as well as sensitivity analyses.

The MR analysis, based on the largest available dataset to date, did not provide evidence supporting a causal relationship between COVID-19 susceptibility (odds ratio [OR] 0.989, 95% CI 0.405-2.851; P=.93), COVID-19 hospitalization (OR 0.974, 95% CI 0.852-1.113; P=.70), COVID-19 severity (OR 0.979, 95% CI 0.890-1.077; P=.66), and GD. Tests for directional pleiotropy and heterogeneity, as well as sensitivity analyses, supported these findings.

This comprehensive MR study does not provide sufficient evidence to support a causal relationship between COVID-19 and the onset or exacerbation of GD. These results contribute to a better understanding of the potential association between COVID-19 and autoimmune diseases, alleviating concerns about a surge in autoimmune thyroid diseases due to the pandemic. Further research is warranted to explore this complex relationship thoroughly.

Background Globally, the COVID-19 pandemic inflicted considerable morbidity and mortality. It has become a systemic illness that affects several body organs. The primary pathway for the SARS-CoV-2 virus to enter cells is the angiotensin-converting enzyme 2 (ACE2) receptor, and it uses transmembrane serine protease 2 (TMPRSS2) for S protein priming. Thyroid follicular cells have been found to express ACE2 and TMPRSS2 at even higher levels than those found in the lungs. The objective of the study was to assess and determine the six-month clinical outcome of thyroid dysfunction in COVID-19 patients. Methods This prospective, observational study was carried out in the COVID-19 unit of Bangabandhu Sheikh Mujib Medical University, Dhaka, Bangladesh. Forty-eight hospital-admitted COVID-19 reverse transcription-polymerase chain reaction (RT-PCR)-positive patients were included as per inclusion and exclusion criteria, and there was no control group. All admitted patients were classified into non-severe (mild, moderate) and severe (severe and critical) disease as per national guidelines. Baseline laboratory tests for thyroid-stimulating hormone (TSH), free T3, and free T4 were done on admission. The patients were again categorized according to their thyroid status. Further evaluation was done by performing autoantibody tests (TSH receptor Ab, anti-thyroid peroxidase Ab, anti-thyroglobulin Ab). The patients were followed up in the first month and sixth month to see disease progression and outcomes. Results Age and comorbidities were associated with an increased risk of severe disease. A total of 35 (73%) patients had comorbidities, 23 (49%) had multiple comorbidities, and 12 (24%) had single comorbidities. All patients (n=48) presented with fever and cough; 45 (94%) patients had fatigue, palpitations were present in 35 (73%) patients, and dyspnea in 32 (67%) patients. The difference in mean values of TSH, FT4, and FT3 among severe and non-severe groups was found to be significant. Most of the patients (n=36; 75%) were in a euthyroid state at baseline. Among the rest, 25% had thyroid dysfunction, including one (2.08%) who had subacute thyroiditis and eight (16.67%) who had euthyroid sick syndrome, which was higher in the severe group (14.59%). Three (6.24%) patients were autoantibody-positive and were diagnosed as having Hashimoto's thyroiditis in the form of primary hypothyroidism (2.08%; n=1) and subclinical hypothyroidism (4.16%; n=2). The Spearman correlation coefficient showed a strong negative correlation between severity and TSH (rs = -0.71) and moderate positive correlations between severity and free T3 (rs = 0.63) and free T4 levels (rs = 0.53). Follow-up at the first month showed that 44 (91.96%) returned to a euthyroid state, and at six months, 45 (93.7%) returned to a euthyroid state. Conclusion Thyroid hormone levels appear to change and recover gradually and spontaneously. Most patients have normal thyroid function status during COVID-19 infections, but a considerable number of patients can develop euthyroid sick syndrome in severe COVID-19 infections, from which they recover spontaneously.

Reports have highlighted thyroid abnormalities, including subacute thyroiditis and thyrotoxicosis, in COVID-19 patients, with a potential link between thyroid dysfunction and disease severity. However, population-level studies on COVID-19's impact on thyroid hormone levels are limited. We aimed to assess the impact of the COVID-19 pandemic on thyroid function tests at the population level.

We conducted a repeated cross-sectional study on consecutive patients who underwent thyroid function tests between March 1 and April 15, 2020, during the first wave of COVID-19 in northeastern France, and compared the results with those from the same period in 2018 and 2019.

The study analyzed 3968 tests, including 1534 in 2018, 1547 in 2019, and 887 in 2020. Patients tested in the first wave of COVID-19 had significantly lower TSH and FT3 levels and higher FT4 levels than those in reference periods. On ROC analysis, the optimal thresholds for FT3 and FT4 were ≤ 4.5 pmol/L and > 12 pmol/L, respectively. On multivariable analysis, FT3 ≤ 4.5 pmol/L and FT4 > 12 pmol/L were independently associated with the first wave of COVID-19. The proportion of subjects with concurrent changes in FT3 and FT4 levels was significantly higher in 2020 than in the reference periods, with an odds ratio of 3.62 (95 % CI, 2.77-4.73). A phenome-wide association study of 128 clinical and biological predictors identified an independent association between a low FT3/FT4 ratio and COVID-19, hypertension, or amiodarone therapy, suggesting the contribution of euthyroid sick syndrome to this presentation. This association remained significant after adjustment for potential confounders such as thyroid disease, steroids, and iodinated contrast injection.

These findings suggest that COVID-19 is associated with significant population-level variation in thyroid function tests, which may have implications for managing COVID-19 patients.

Subacute thyroiditis (also known as granulomatous thyroiditis, giant cell thyroiditis, de Quervain's disease, or SAT) is an inflammatory disease of the thyroid gland, usually spontaneously remitting, that lasts for weeks to months. However, recurrent forms sometimes occur which may have a genetic basis. In our paper, we have focused on the pathogenetics, symptoms, and treatment of SAT. We have described the 17-month disease course of a woman with persistent recurrent steroid-resistant SAT. SAT was well established and the patient's symptoms were not only recurrent neck pain with fever, but also recurrent chronic urticaria, which are symptoms that fulfil the criteria for the diagnosis of Schnitzler syndrome. Schnitzler syndrome occurred after vaccination with COVID-19 in the mechanism of ASIA syndrome. In our patient, Schnitzler syndrome involved the thyroid gland, causing persistent subacute thyroiditis, and the pituitary gland, causing transient swelling of the pituitary, which, to our knowledge, is the first reported case in the literature. Also unprecedented, as far as we know, is the fact that we performed thyroidectomy in the above patient, which reduced systemic inflammation and caused SAT to resolve, although only the inclusion of anakinra treatment resulted in resolution of the underlying condition.

The novel coronavirus strain SARS-CoV-2 triggered the COVID-19 pandemic with severe economic and social ramifications. As the pathophysiology of SARS-CoV-2 infection in the respiratory system becomes more understood, growing evidence suggests that the virus also impacts the homeostasis-regulating neuroendocrine system, potentially affecting other organ systems.

This review explores the interactions between SARS-CoV-2 and the neuroendocrine system, highlighting the effect of this virus on various endocrine glands, including the brain, hypothalamus, pituitary, pineal, thyroid, parathyroid, adrenal glands, pancreatic islets, gonads, and adipose tissue. The viral invasion disrupts normal hormonal pathways, leading to a range of endocrine disorders, immune dysregulation, and metabolic disturbances.

There is potential for SARS-CoV-2 to induce autoimmune responses, exacerbate existing endocrine conditions, and trigger new-onset disorders. Understanding these interactions is crucial for developing treatment strategies that address not only the respiratory symptoms of COVID-19 but also its endocrine complications. The review emphasizes the need for further research to elucidate the long-term effects of SARS-CoV-2 on endocrine health.

Introduction  Long coronavirus disease (COVID) refers to the persistence of symptoms long after the recovery from the acute phase of the illness, and it is due to the interplay of various inflammatory mechanisms. This has led to emergence of new deficits, including otorhinolaryngological symptoms, in patients wo have recovered from COVID. The plethora of otorhinolaryngological symptoms associated with long COVID are tinnitus, sensorineural hearing loss (SNHL), vertigo, nasal congestion, sinonasal discomfort, hyposmia/anosmia, dysgeusia, sore throat, dry cough, dyspnea, dysphagia, and hoarseness of voice. Objective  To evaluate the possible ENT symptoms in patients wo have recovered from COVID and to combine those findings with our experience. Data Synthesis  We conducted a search on the PubMed, ENT Cochrane, Web of Science, and Google Scholar databases, and a total of 44 studies were selected for the present review. Conclusion  Otorhinolaryngological complications such as tinnitus, SNHL, vertigo, nasal congestion, sinonasal discomfort, hyposmia/anosmia, dysgeusia, sore throat, dry cough, dyspnea, dysphagia, and hoarseness of voice have been widely reported among in long-COVID patients.

Angiotensin-converting enzyme 2 receptors (ACE2R) are requisite to enter the host cells for severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). ACE2R is constitutive and functions as a type I transmembrane metallo-carboxypeptidase in the renin-angiotensin system (RAS). On thyroid follicular cells, ACE2R allows SARS-CoV-2 to invade the thyroid gland, impose cytopathic effects and produce endocrine abnormalities, including stiff back, neck pain, muscle ache, lethargy, and enlarged, inflamed thyroid gland in COVID-19 patients. Further damage is perpetuated by the sudden bursts of pro-inflammatory cytokines, which is suggestive of a life-threatening syndrome known as a "cytokine storm". IL-1β, IL-6, IFN-γ, and TNF-α are identified as the key orchestrators of the cytokine storm. These inflammatory mediators upregulate transcriptional turnover of nuclear factor-kappa B (NF-κB), Janus kinase/signal transducer and activator of transcription (JAK/STAT), and mitogen-activated protein kinase (MAPK), paving the pathway for cytokine storm-induced thyroid dysfunctions including euthyroid sick syndrome, autoimmune thyroid diseases, and thyrotoxicosis in COVID-19 patients. Targeted therapies with corticosteroids (dexamethasone), JAK inhibitor (baricitinib), nucleotide analogue (remdesivir) and N-acetyl-cysteine have demonstrated effectiveness in terms of attenuating the severity and frequency of cytokine storm-induced thyroid dysfunctions, morbidity and mortality in severe COVID-19 patients. Here, we review the pathogenesis of cytokine storms and the mechanisms and pathways that establish the connection between thyroid disorder and COVID-19. Moreover, cross-talk interactions of signalling pathways and therapeutic strategies to address COVID-19-associated thyroid diseases are also discussed herein.

Sodium imbalance is a common electrolyte disturbance in COVID-19, often linked to disruptions in hormonal regulation. This review explores the relationship between sodium dysregulation and endocrine disturbances, particularly focusing on primary and secondary hypothyroidism, hypocortisolism, and the renin-angiotensin-aldosterone system (RAAS). Hypocortisolism in COVID-19, due to adrenal insufficiency or secondary to pituitary dysfunction, can lead to hyponatremia through inadequate cortisol levels, which impair renal free water excretion and enhance antidiuretic hormone (ADH) secretion. Similarly, hypothyroidism is associated with decreased renal blood flow and the glomerular filtration rate (GFR), which also increases ADH activity, leading to water retention and dilutional hyponatremia. Furthermore, COVID-19 can disrupt RAAS (primarily through its interaction with the angiotensin-converting enzyme 2 (ACE2) receptor), diminishing aldosterone secretion and further contributing to sodium loss and hyponatremia. These hormonal disruptions suggest that sodium imbalance in COVID-19 is multifactorial and warrants further investigation into the complex interplay between COVID-19, endocrine function, and sodium homeostasis. Future research should focus on understanding these mechanisms to develop management algorithms that address both sodium imbalance and underlying hormonal disturbances in order to improve prognosis and outcomes in COVID-19 patients.

To assess the association between thyroid dysfunction and mortality among patients hospitalized with COVID-19. Design: This is a retrospective multi-center study, which examined all patients admitted with Covid-19 diagnoses, and thyroid function results in absence of known thyroid disease.

10,933 hospitalized COVID-19 positive patients were included in the study. These patients were without prior diagnosis or treatment of thyroid disease. Outcomes assessed were mortality, ICU admission, Ventilator use, length of stay, readmission and complications during hospital stay. Patients with low TSH and Low free T4 had odds of mortality of 10.07(95% CI [7.44-13.6]) compared to patients with Normal TSH and any free T4 levels. Patients with Low TSH and High free T4 also had odds of mortality of 1.38 (95% CI [1.19-1.59]) compared to patients with Normal TSH and Any free T4 level. Patients with Low TSH and Normal free T4 levels also had an Odds of mortality of 1.46 (95% CI [1.31-1.62]) compared to patients with Normal TSH and any free T4 level. Patients with Low TSH also had higher odds of ICU admission and Ventilator use when compared to patients with normal TSH.

This study shows that patients with low TSH, regardless of free T4 level, indicates poor prognosis for hospitalized patients with SARS-CoV-2 infection and offers further insights into possible prognostic value of TSH levels for severe COVID-19 outcomes.

Previous studies suggest that patients' thyroid status might directly impact the course of Coronavirus disease 2019 (COVID-19). The objective of the study was to determine the clinical profile of COVID-19 patients with hypothyroidism and compare it with that of COVID-19 patients without hypothyroidism.

Retrospective observational study.

The study was conducted in a tertiary healthcare centre in Tamil Nadu between May and June 2021.

The study included 117 patients admitted with hypothyroidism and COVID-19 as well as 117 age and Gender matched COVID-19 patients without hypothyroidism.

Data regarding the demography, comorbidities, presenting symptoms, method of diagnosis of COVID-19, computed tomography (CT) severity score, Interleukin 6 (IL-6), D-dimer, oxygen requirement, number of days in hospital and outcome were collected for both groups. Data analysis was conducted, and p<0.05 was considered statistically significant.

The study comprised 234 patients over two months, from May to June 2021. Distribution of presenting symptoms showed that the hypothyroidism group presented with a higher incidence of fever (66.67%), loose stool (18.80%) and myalgia (7.69%). Results show that RTPCR+, O2 Requirement, death, D-dimer, IL-6, number of days admitted as well as CT-severity did not show any statistically significant differences (p>0.05) between both groups. The outcomes also showed that both groups reported four mortalities.

The results of the study help conclude that the hypothyroidism status of a COVID-19 patient is not associated with higher severity of clinical symptoms, deranged laboratory values as well as mortality.

None declared.

The coronavirus disease 2019 (COVID-19) pandemic poses an enormous threat to public health worldwide. Many retrospective studies and case reports to date have shown associations between severe COVID-19 and diseases of multi-organs. However, the research on the causal mechanisms behind this phenomenon is neither extensive nor comprehensive. We conducted a proteome-wide Mendelian randomization (MR) study using summary statistics from a Genome-Wide Association Studies (GWAS) of severe COVID-19 and diseases related to seven organs: lung, spleen, liver, heart, kidney, testis, and thyroid, based on the European ancestry. The primary analytical method used is the radial inverse variance-weighted (radial IVW) method, supplemented with the inverse variance-weighted (IVW), weighted-median (WM), MR-Egger methods. Our findings have confirmed the association between severe COVID-19 and multiple organ-related diseases, such as Hypothyroidism, strict autoimmune (HTCBSA), Thyroid disorders (TD), and Graves' disease (GD). And we have also identified certain proteins that are associated with organ-related diseases, such as Superoxide Dismutase 2 (SOD2) and TEK Receptor Tyrosine Kinase (TEK), which are also considered potential drug targets. Phenotype scanning and sensitivity analyses were implemented to consolidate the results for Mendelian randomization. This study provides a compelling foundation for investigating COVID-19 caused diseases in future studies.

This study aimed to determine the frequency of thyroid gland involvement in chest CT scans of patients with COVID-19 admitted to university-affiliated hospitals and assess its relationship with the severity of lung involvement and patient survival in 2020.

In this retrospective cross-sectional study, 1000 PCR-positive patients with COVID-19 who were referred to University-affiliated Hospital in 2020 and had chest CT performed within 72 hours of admission to the hospital were examined. The data was collected by patient file information and CT findings recorded in the PACS system, including thyroid involvement, the severity of lung involvement, and findings related to the death and recovery of patients.

The mean age of the examined patients was 56 years. 525 people (52.5%) were men, and 475 (47.5%) were women. 14% had severe pulmonary involvement, and 9.3% had very severe involvement. Moreover, 15.9 percent of them had deceased. 19.7% had focal thyroid involvement, 14% had diffuse involvement, and 66.3% were healthy subjects. Male gender and older age showed a significant relationship with thyroid gland involvement. The severity of lung involvement, the death rate in patients, and hospitalization in ICU were also significantly related to thyroid gland involvement in patients with COVID.

This study highlights the importance of considering thyroid-gland involvement in the comprehensive management of COVID-19 patients. Routine screening and monitoring of thyroid-function may facilitate earlier detection and appropriate management of thyroid-related complications, potentially improving clinical outcomes. This study suggests that in COVID-19 infection the monitoring of thyroid function is prudent, particularly in cases of more serious disease.

SARS-CoV-2 is a highly contagious pathogen that predominantly caused the COVID-19 pandemic. The persistent effects of COVID-19 are defined as an inflammatory or host response to the virus that begins four weeks after initial infection and persists for an undetermined length of time. Chronic effects are more harmful than acute ones thus, this review explored the long-term effects of the virus on various human organs, including the pulmonary, cardiovascular, and neurological, reproductive, gastrointestinal, musculoskeletal, endocrine, and lymphoid systems and found that SARS-CoV-2 adversely affects these organs of older adults. Regarding diagnosis, the RT-PCR is a gold standard method of diagnosing COVID-19; however, it requires specialized equipment and personnel for performing assays and a long time for results production. Therefore, to overcome these limitations, artificial intelligence employed in imaging and microfluidics technologies is the most promising in diagnosing COVID-19. Pharmacological and non-pharmacological strategies are the most effective treatment for reducing the persistent impacts of COVID-19 by providing immunity to post-COVID-19 patients by reducing cytokine release syndrome, improving the T cell response, and increasing the circulation of activated natural killer and CD8 T cells in blood and tissues, which ultimately reduces fever, nausea, fatigue, and muscle weakness and pain. Vaccines such as inactivated viral, live attenuated viral, protein subunit, viral vectored, mRNA, DNA, or nanoparticle vaccines significantly reduce the adverse long-term virus effects in post-COVID-19 patients; however, no vaccine was reported to provide lifetime protection against COVID-19; consequently, protective measures such as physical separation, mask use, and hand cleansing are promising strategies. This review provides a comprehensive knowledge of the persistent effects of COVID-19 on people of varying ages, as well as diagnosis, treatment, vaccination, and future preventative measures against the spread of SARS-CoV-2.

Many cases of subacute thyroiditis (SAT) have been described related to SARS-CoV-2 infection, but no prospective data about follow-up are known. This prospective, longitudinal, 3-year, multicentre study aims to explore the clinical peculiarities and outcome of SAT in relation to SARS-CoV-2 infection, ascertained with antibody dosage.

All patients receiving SAT diagnosis from November 2020 to May 2022 were enrolled. Data on anamnesis, physical examination, blood tests (TSH, freeT4, freeT3, thyroglobulin, anti-thyroid antibodies, C-reactive protein, erythrocyte sedimentation rate, complete blood count), and thyroid ultrasound were collected. At baseline, the presence of IgG against the SARS-CoV-2 spike protein or nucleocapsid was investigated. Patients were evaluated after 1, 3, 6, and 12 months.

Sixty-six subjects were enrolled. At baseline, 54 presented with pain, 36 (67%) for at least 15 days. Serum SARS-CoV-2 IgG measurements documented that 7 out of 52 subjects (13.5%) had infection before SAT diagnosis (COVID+). No significant differences between the COVID+ and COVID- groups were found at baseline, except for respiratory symptoms and fever, which were more common in COVID+ (P = 0.039 and P = 0.021, respectively). Among the 41 subjects who completed follow-up, COVID+ and COVID- did not differ for therapeutic approach to SAT or outcome, all having an improvement in neck pain, inflammation parameters, and ultrasound features.

This is the first prospective study investigating any difference both at diagnosis and at follow-up between SAT presentation in patients with previous SARS-CoV-2 infection and those without. Our data demonstrate that SARS-CoV-2 does not impact on SAT onset, evolution, and outcome.

A rare and intractable case of apathetic Graves' disease (GD) with severe liver and kidney damage induced by coronavirus disease 2019 (COVID-19) carries a certain risk of missing diagnosis and delayed treatment during the COVID-19 pandemic.

A 60-year-old female patient developed anorexia, exhaustion, jaundice, nausea, and vomiting 10 days after COVID-19 infection. She was admitted to the Infectious Diseases Department because of recurring symptoms for more than a month.

Based on the patient's epidemiological history, clinical symptoms, and prior history, she was preliminarily diagnosed with GD induced by COVID-19 with severe hyperthyroid-related liver injury and chronic kidney disease stage 4. Drug-induced and radiation-induced liver injuries occurred sequentially throughout the therapy.

Methimazole (MMI) (10 mg/d) was administered for 1 week, and the patient's symptoms, thyroid function, and liver and kidney function improved. Nevertheless, the aforementioned symptoms and liver and kidney function deteriorated 20 days after increasing the MMI dose (20 mg/d). Therefore, in the presence of an artificial liver, hemodialysis, and other medical conditions, the treatment schedule was adjusted to individualized 131I anti-hyperthyroidism therapy.

After 131I treatment, the patient's liver function returned to almost normal levels after a month, but worsened when the hepatoprotective drugs were stopped. Renal function did not deteriorate significantly and returned to baseline after 3 months. Thyroid function was restored to normal approximately 4 months later.

COVID-19 may induce GD. Multidisciplinary collaboration can be initiated as early as possible. Individualized 131I therapy or long-term low-dose MMI (10 mg/d) can be considered to manage hyperthyroidism in GD patients with liver and kidney dysfunction and to prolong liver protection therapy appropriately.

We report a case of overlooked Subacute Thyroiditis (SAT) potentially induced by the administration of a COVID-19 vaccine. This case prompted a thorough review of the existing literature to elucidate possible mechanisms by which immune responses to the COVID-19 vaccine might precipitate thyroid damage. The primary objective is to enhance the clinical understanding and awareness of SAT among healthcare professionals. Subacute thyroiditis is a prevalent form of self-limiting thyroid disorder characterized by fever, neck pain or tenderness, and palpitations subsequent to viral infection. The development of numerous SARS-CoV-2 vaccines during the COVID-19 pandemic was intended to mitigate the spread of the virus. Nevertheless, there have been documented instances of adverse reactions arising from SARS-CoV-2 vaccines, such as the infrequent occurrence of subacute thyroiditis. While the majority of medical practitioners can discern classic subacute thyroiditis, not all cases exhibit typical characteristics, and not all systematic treatments yield positive responses. In this study, we present a rare case of subacute thyroiditis linked to the administration of the SARS-CoV-2 vaccine. A previously healthy middle-aged female developed fever and sore throat 72 h post-inoculation with the inactivated SARS-CoV-2 vaccine. Initially attributing these symptoms to a common cold, she self-administered ibuprofen, which normalized her body temperature but failed to alleviate persistent sore throat. Suspecting a laryngopharyngeal disorder, she sought treatment from an otolaryngologist. However, the pain persisted, accompanied by intermittent fever over several days. After an endocrinology consultation, despite the absence of typical neck pain, her examination revealed abnormal thyroid function, normal thyroid antibodies, heterogeneous echogenicity on thyroid ultrasonography, and elevated levels of Erythrocyte Sedimentation Rate (ESR) and C-Reactive Protein (CRP). These findings led to a consideration of the diagnosis of SAT. Initially, she was treated with non-steroidal anti-inflammatory drugs (NSAIDs) for her fever, which proved effective, but her neck pain remained uncontrolled. This suggested a poor response to NSAIDs. Consequently, steroid therapy was initiated, after which her symptoms of fever and neck pain rapidly resolved.

Autoimmune thyroid diseases (AITDs) include a wide spectrum of thyroid diseases affecting more commonly women than men. The most frequent forms are Graves' Disease (GD) and Hashimoto's thyroiditis / Autoimmune Thyroiditis (AIT), but there are also other immunogenic destructive forms of thyroiditis, that is, silent and postpartum thyroiditis. In the last decade, AITDs and other inflammatory thyroid diseases related to anti-tumor molecular drugs are more frequently seen due to the widespread use of tyrosine kinase inhibitors (TKIs) and immune checkpoint inhibitors (ICPIs). Autoimmune thyroiditis related to SARS-CoV-2 infection has been a novel entity in recent years. Graves' Disease and AIT may shift from hyperthyroidism to hypothyroidism, which may complicate the differential diagnosis and further treatment strategy. Moreover, all AITDs may manifest with thyrotoxicosis (a clinical condition marked with high serum levels of thyroid hormones) which has to be distinguished from hyperthyroidism (increased thyroid hormone production and secretion as a result of hyperfunctioning thyroid gland) due to different therapeutic approaches. Nuclear medicine techniques, such as radioiodine uptake (RAIU) and thyroid scintigraphy, using 99mTc- pertechnetate (Na[99mTc]TcO4) or 123-Iodine (Na[123I]I), have a crucial role in the differential diagnosis. Measurement of thyroid antibodies, e.g. thyroid peroxidase antibodies (TPO) and thyrotropin receptor antibodies (TRAb), as well as thyroid ultrasound, are complementary methods in the evaluation of thyroid disorders.

As an increased body of COVID-19 related research is now available, it becomes apparent that the effects of COVID-19 extend beyond that of the respiratory system. Among others, the endocrine system is particularly vulnerable to perturbation from the COVID-19 infection. The present scoping review summarizes the bidirectional relationship between COVID-19 and endocrine system in children and adolescents, by describing both the possible susceptibility of children and adolescents without endocrinopathies to endocrine disorders following COVID-19 infection, but also the potential susceptibility to COVID-19 infection and severe infection, or the aggravation of endocrine dysfunction in patients with pre-existing endocrine diseases. Data suggest increased obesity and diabetes rates, as well as increased severity and frequency of diabetic ketoacidosis following COVID-19 infection. Conversely, patients with diabetes and obesity may experience a more severe course of COVID-19 infection. However, in the majority of cases, children and adolescents with well-managed and regulated endocrine disorders do not appear to be at increased risk of infection or severe infection from COVID-19. Thus, adhering to the appropriate "sick day management rules", maintaining adequate supply of medications and supplies, keeping close contact with the therapeutic team and seeking medical help without delay when needed, are the main recommendations for a safe outcome. Additional lessons learnt during the pandemic include the risk for mental health diseases caused by children's disrupted routine due to COVID-19 related protective measures and the importance of adopting alternative communication options, such as telehealth visits, in order to ensure uninterrupted endocrine care.

Long COVID-19, also known as post-acute sequelae of SARS-CoV-2 infection, is a condition where individuals who have recovered from the acute phase of COVID-19 continue to experience a range of symptoms for weeks or even months afterward. While it was initially thought to primarily affect the respiratory system, it has become clear that Long COVID-19 can involve various organs and systems, including the endocrine system, which includes the pituitary gland. In the context of Long COVID-19, there is a growing understanding of the potential implications for the pituitary gland. The virus can directly affect the pituitary gland, leading to abnormalities in hormone production and regulation. This can result in symptoms such as fatigue, changes in appetite, and mood disturbances. Long COVID-19, the persistent and often debilitating condition following acute COVID-19 infection, may be explained by deficiencies in ACTH and Growth hormone production from the pituitary gland. Corticotropin insufficiency can result in the dysregulation of the body's stress response and can lead to prolonged feelings of stress, fatigue, and mood disturbances in Long COVID-19 patients. Simultaneously, somatotropin insufficiency can affect growth, muscle function, and energy metabolism, potentially causing symptoms such as muscle weakness, exercise intolerance, and changes in body composition. Recently, some authors have suggested the involvement of the pituitary gland in Post COVID-19 Syndrome. The exact mechanisms of viral action on infected cells remain under discussion, but inflammatory and autoimmune mechanisms are primarily implicated. The aim of our study will be to review the main pituitary complications following COVID-19 infection. Moreover, we will explain the possible involvement of the pituitary gland in the persistence of Post COVID-19 Syndrome.

Background and Objectives: The interaction between thyroid and SARS-CoV-2 is complex and not yet fully understood. This study aimed to identify a predictive value of serum TSH levels on the short-term and middle-term outcomes of patients hospitalized for COVID-19. Materials and Methods: We retrospectively analyzed electronic records (ERs) data for hospitalized COVID-19 patients between March 2020 and June 2021 and their ERs during outpatient visits, 6-8 weeks post-discharge, in cases of known serum TSH levels and no previous thyroid disorder. The short-term (length of hospital stay, MSCT findings of lung involvement, required level of oxygen supplementation, admission to the ICU, and death) and middle-term outcomes after 6 to 8 weeks post-discharge (MSCT findings of lung involvement) were analyzed. Results: There were 580 patients included: 302 males and 278 females, average age of 66.39 ± 13.31 years, with no known thyroid disease (TSH mean 1.16 ± 1.8; median 0.80; no value higher than 6.0 mIU/L were included). Higher TSH was observed in patients with less severe outcomes and was associated with significantly higher SpO2 during hospitalization. Patients who required overall more oxygen supplementation or HFOT, mechanical ventilation, and patients who were more frequently admitted to the ICU or were more often treated with corticosteroids had lower TSH than those who did not show these indicators of disease severity. Lower TSH was also present in non-survivors when compared to survivors (all p < 0.01). Patients with low TSH during hospitalization more often had persistent lung involvement during the post-COVID-19 period (p = 0.028). In the post-COVID-19 period, there was an overall, statistically significant increase in the TSH levels when compared to TSH during hospitalization (p < 0.001). Conclusions: Low/suppressed serum TSH levels during acute COVID-19 may be an additional laboratory test that should be included in the prediction of unfavorable short- and middle-term outcomes.

The coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has led to the development of various vaccines. Reports have emerged suggesting a possible association between SARS-CoV-2 vaccination and the onset of thyroid diseases. This review explores the clinical aspects of thyroid disorders following SARS-CoV-2 vaccination, including a case report of a patient with concomitant subacute thyroiditis (SAT) and Graves' disease (GD) with blocking thyrotropin receptor autoantibodies (TSH-R-Ab) following SARS-CoV-2 vaccination. SAT, characterized by transient inflammation of the thyroid gland, has been reported after SARS-CoV-2 vaccination. GD, an autoimmune hyperthyroidism, has also been observed post-vaccination, often with stimulating TSH-R-Ab. Graves' orbitopathy (GO) has been associated with SARS-CoV-2 vaccination in patients with a history of immune thyroid disease. The unique case underscores a very rare thyroid condition of functional hypothyroidism in possible relation to SARS-CoV-2 vaccination and the usefulness of functional analysis of TSH-R-Ab that can provide valuable insights into disease pathogenesis and help to guide treatment. This review highlights the need for continued monitoring and awareness of potential thyroid-related complications following SARS-CoV-2 vaccination.

Lymphocytic hypophysitis is an underestimated disease and the pathogenesis is still poorly elucidated. Post-coronavirus lymphocytic hypophysitis is a new emerging entity.

A 16-year-old previously healthy girl presented with pituitary tumor syndrome. She suffered from frontal headaches, polyuria-polydipsic syndrome, and impaired visual acuity. She was diagnosed with COVID-19 infection three weeks before. Contrast-enhanced magnetic resonance imaging (MRI) revealed pituitary enlargement with intense homogenous enhancement postgadolinium on T1 weighted images. The diagnosis of lymphocytic hypophysitis was made after ruling out other differential diagnosis. She was started on methylprednisolone. Improvement of clinical symptoms was seen on day 5 with a significant decrease in headache intensity.

The article summarizes data from cases reported in the literature and our case to highlight coronavirus as a new trigger of lymphocytic hypophysitis. Despite the rarity of this complication, patients with a suspicion of hypophysitis after a recent COVID-19 infection should be carefully evaluated.

COVID-19 infection can cause lymphocytic hypophysitis. However, it seems premature to conclude on the causal link between COVID-19 and endocrine diseases. Further studies on larger samples are needed to comprehend the pathogenesis of autoimmune endocrinopathies after COVID-19 infection.

SARS-CoV-2 infection and Covid-19 vaccines have been associated with thyroid disorders.

We analyzed the risk of thyroid eye disease (TED) following Covid-19 vaccination. This was a self-controlled case series study at a tertiary referral center for TED. A total of 98 consecutive patients with newly developed (n = 92) or reactivated (n = 6) TED occurring between January 1, 2021, and August 31, 2022, were included. TED was assessed in patients undergoing Covid-19 vaccination. Person-days were defined as exposed if TED occurred 1 to 28 days after vaccination, and unexposed if occurring outside this time window. Conditional Poisson regression models were fitted to calculate incidence rate ratio (IRR) and 95% CI of exposed vs unexposed. Sensitivity analyses were conducted considering different exposed periods, and effect modification by potential TED risk factors.

Covid-19 vaccines were administered in 81 people, 25 (31%) of whom developed TED in exposed and 56 (69%) in unexposed periods. The IRR for TED was 3.24 (95% CI 2.01-5.20) and 4.70 (95% CI 2.39-9.23) in patients below 50 years of age. Sex, smoking, and radioiodine treatment did not modify the association between TED and vaccination. TED risk was unrelated to the number of vaccine doses, and progressively decreased over time following vaccination (P trend = .03).

The risk of TED was significantly increased after Covid-19 vaccination, especially in people below 50 years of age. Possible mechanisms include spike protein interaction with the angiotensin-converting enzyme II receptor, cross-reactivity with thyroid self-proteins, and immune reactions induced by adjuvants. We suggest monitoring of individuals undergoing Covid-19 vaccination, especially if young and at risk for autoimmunity.

In some patients, symptoms may persist after COVID-19, defined as long COVID. Its pathogenesis is still debated and many hypotheses have been raised.

Our primary objective was to evaluate the corticotroph and somatotroph functions of patients previously infected with SARS-CoV-2 and experiencing post-COVID-19 syndrome to detect any deficiencies that may explain long COVID.

A cross-sectional study was conducted including patients who had previously contracted SARS-CoV-2 with a postinfection period of 3 months or less to 15 months, divided into 2 groups. The first group (G1) comprised fully recovered patients, while the second group (G2) included patients experiencing long COVID. The primary outcome was the comparison of corticotroph and somatotroph functions.

A total of 64 patients were divided into 2 groups, each consisting of 32 patients. G2 exhibited more frequently anterior pituitary deficits compared to G1 (P = .045): for the corticotroph axis (G1: 6.3% vs G2: 28.1%) and for the somatotroph axis (G1: 31.3% vs G2: 59.4%). Baseline cortisol level was significantly lower in G2 (G1: 13.37 µg/dL vs G2: 11.59 µg/dL) (P = .045). The peak cortisol level was also lower in G2 (G1: 23.60 µg/dL vs G2: 19.14 µg/dL) (P = .01). For the somatotroph axis, the insulin growth factor-1 level was lower in G2 (G1: 146.03 ng/mL vs G2: 132.25 ng/mL) (P = .369). The peak growth hormone level was also lower in G2 (G1: 4.82 ng/mL vs G2: 2.89 ng/mL) (P = .041).

The results showed that long COVID patients in our cohort were more likely to have anterior pituitary deficiencies. The endocrine hypothesis involving anterior pituitary insufficiency can be considered to explain long COVID.

Coronavirus disease 2019 (COVID-19) affects thyroid function. These changes are due to the direct impact of the virus on thyroid cells via angiotensin-converting-enzyme 2 (ACE2) receptors, inflammatory reaction, apoptosis in thyroid follicular cells, suppression of hypothalamus-pituitarythyroid axis, an increase in activity of adrenocortical axis, and excess cortisol release due to cytokine storm of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Euthyroid sick syndrome (ESS), thyroiditis, clinical and subclinical hypothyroidism, central hypothyroidism, exacerbation of underlying autoimmune thyroid disease, and clinical and subclinical hyperthyroidism can be associated with coronavirus. Adjuvants in coronavirus vaccines induce autoimmune/inflammatory syndrome known as vaccine adjuvants (ASIA) syndrome. Thyroiditis and Graves' disease have been reported to be associated with ASIA syndrome after some coronavirus vaccinations. Some coronavirus medications, such as hydroxychloroquine, monoclonal antibodies, lopinavir/ritonavir, remdesivir, naproxen, anticoagulants, and glucocorticoids can also affect thyroid tests, and correct diagnosis of thyroid disorders will be more difficult. Changes in thyroid tests may be one of the most important manifestations of COVID-19. These changes can be confusing for clinicians and can lead to inappropriate diagnoses and decisions. Prospective studies should be conducted in the future to increase epidemiological and clinical data and optimize the management of thyroid dysfunctions in patients with COVID-19.

Since most endocrine glands express ACE-2 receptors and can be infected by SARS-CoV-2 virus, this retrospective multicentre observational study aims to assess the metabolic activity of thyroid and adrenal glands of COVID-19 patients by 18F-FDG PET/CT.

We retrospectively evaluated the 18F-FDG PET/CT scans of COVID-19 patients admitted by three different centres, either in a low-intensity department or in the intensive care unit (ICU). A visual assessment and a semi-quantitative evaluation of areas of interest in thyroid and adrenal glands were performed by recording SUVmax and SUVmean. The 18F-FDG PET/CT uptake in COVID-19 patients was compared with those observed in normal age-matched controls.

Between March 2020 and March 2022, 33 patients from three different centres (twenty-eight patients in a low-intensity department and five patients in ICU), were studied by 18F-FDG PET/CT during active illness. Seven of them were also studied after clinical remission (3-6 months after disease onset). Thirty-six normal subjects were used as age-matched controls. In the thyroid gland, no statistically significant differences were observed between control subjects and COVID-19 patients at diagnosis. However, at the follow-up PET/CT study, we found a statistically higher SUVmax and SUVmean (p = 0.009 and p = 0.004, respectively) in the thyroid of COVID-19 patients. In adrenal glands, we observed lower SUVmax and SUVmean in COVID-19 patients at baseline compared to control subjects (p < 0.0001) and this finding did not normalize after clinical recovery (p = 0.0018 for SUVmax and p = 0.002 for SUV mean).

In our series, we observed persistent low 18F-FDG uptake in adrenal glands of patients at diagnosis of COVID-19 and after recovery, suggesting a chronic hypofunction. By contrast, thyroid uptake was comparable to normal subjects at disease onset, but after recovery, a subgroup of patients showed an increased metabolism, thus possibly suggesting the onset of an inflammatory thyroiditis. Our results should alert clinicians to investigate the pituitary-adrenal axis and thyroid functionality at the time of infection and to monitor them after recovery.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiological culprit of COronaVIrus Disease 19 (COVID-19), can enter the cells via the angiotensin-converting enzyme 2 (ACE2) receptor, which has been found in several tissues including in endocrine organs, such as the ovaries, testes, pancreas, and thyroid. Several thyroid disorders have been associated with SARS-CoV-2 infection [subacute thyroiditis (SAT), thyrotoxicosis, and non-thyroidal illness syndrome (NTIS)] and, in part, they are believed to be secondary to the local virus replication within the gland cells. However, as documented for other viruses, SARS-CoV-2 seems to interfere with several aspects of the immune system, inducing the synthesis of autoantibodies and triggering latent or new onset autoimmune disease (AID), including autoimmune thyroid disease (AITD), such as Hashimoto Thyroiditis (HT) and Graves' disease (GD). Several mechanisms have been hypothesized to explain this induction of autoimmunity by SARS-CoV-2 infection: the immune system hyper-stimulation, the molecular mimicry between the self-antigens of the host and the virus, neutrophils extracellular traps, and finally, the virus induced transcriptional changes in the immune genes; nonetheless, more evidence is needed especially from large, long-term cohort studies involving COVID-19 patients, to establish or reject this pathogenetic relationship.

Rapidly evolving clinical data suggest that the novel coronavirus (SARS-CoV-2) and vaccination against COVID-19 might be associated with thyroid disturbances. However, studies remain limited among the pediatric population. Our aim was to assess the prevalence and permanence of thyroid autoimmunity (TA) and dysfunction in children after an acute infection and its potential association with vaccination. A prospective, multicenter registry analysis was performed among 458 children (mean age: 12.4 ± 3,8 years, 45.4% male) with preceding COVID-19. Patient inclusion lasted from 24th March, 2021 to 23rd March, 2022 at three pediatric outpatient facilities at Semmelweis University, Budapest. Primary outcomes were the rate of thyroid disturbances assessed by laboratory parameters (thyroid function tests, antithyroglobulin [ATG] and anti-thyroid peroxidase [ATPO] antibodies) and thyroid ultrasound. TA rate among vaccinated and unvaccinated children was determined. Children with newly diagnosed thyroid alterations were followed up for 12.7 ± 4.3 months. Six children had previous thyroid disease. Out of 452 children, 30 cases (6.6%) of newly diagnosed TA (six of them had abnormal thyroid-stimulating hormone [TSH] levels) and eight cases (1.8%) of isolated TSH elevation were observed. Ultrasound-proven autoimmune thyroiditis (AIT) was 4.0%. No association was found between COVID-19 vaccination and thyroid autoimmunity (χ2(1,N = 452) = 0.138, p = 0.815). Among children with TA, 73.3% had long-lasting alterations.  Conclusion: Vaccination had no effect on the prevalence of TA. Until further controlled studies state otherwise, children with preceding COVID-19 might benefit from thyroid screening. What is Known: • Numerous case reports implicate that coronavirus disease-2019 (COVID-19) and vaccination against SARS-CoV-2 can be responsible for thyroid disturbances. • Thyroid alterations discovered during acute COVID-19 tend to cease by time and only incidental thyroid autoimmunity (TA) is diagnosed after COVID-19. In adults, no increase in vaccine-related hyper- or hypothyroidism was found. What is New: • TA rate after COVID-19 vaccination among children was not increased. TA had no role in long COVID syndrome. • We discovered a considerable rate of TA (6.6%) and ultrasound-proven autoimmune thyroiditis (AIT) (4.0%) after SARS-CoV-2 infection, and the majority of these alterations remained positive after 6 months.

We conducted this umbrella review to review the current evidence on the relationship between COVID-19 and sexual health in both men and women.

We conducted searches in Pubmed, Embase, and the Cochrane dataset for meta-analyses that met our pre-set inclusion criteria. We included studies with detailed information investigating the link between COVID-19 and sexual health in men/women. We did not limit the language.

The results of the included studies frequently relied on the Female Sexual Function Index to assess sexual health in women. For men, the International Index of Male Function and hospital diagnoses were commonly used to assess sexual health. Currently, there is conflicting evidence regarding the impact of COVID-19 on sexual health. However, since most studies were observational in nature, additional study designs are necessary to draw definitive conclusions across different contexts.

Our findings highlight the importance of sexual health among COVID-19 patients and people affected due to COVID-19. Further critical studies should investigate the mechanism underlying the association between COVID-19 and sexual health.

Infectious diseases are commonly implicated as potential initiators of autoimmune diseases (ADs) and represent the most commonly known factor in the development of autoimmunity in susceptible individuals. Epidemiological data and animal studies on multiple ADs suggest that molecular mimicry is one of the likely mechanisms for the loss of peripheral tolerance and the development of clinical disease. Besides molecular mimicry, other mechanisms such as defects in central tolerance, nonspecific bystander activation, epitope-determinant spreading, and/or constant antigenic stimuli, may also contribute for breach of tolerance and to the development of ADs. Linear peptide homology is not the only mechanism by which molecular mimicry is established. Peptide modeling (i.e., 3D structure), molecular docking analyses, and affinity estimation for HLAs are emerging as critical strategies when studying the links of molecular mimicry in the development of autoimmunity. In the current pandemic, several reports have confirmed an influence of SARS-CoV-2 on subsequent autoimmunity. Bioinformatic and experimental evidence support the potential role of molecular mimicry. Peptide dimensional analysis requires more research and will be increasingly important for designing and distributing vaccines and better understanding the role of environmental factors related to autoimmunity.

Thyroid storm is a severe form of thyrotoxicosis with a mortality rate of 8%-25% despite modern advancements in both early identification and treatment. It is more common in patients with a history of Graves' disease; however, its incidence remains as low as 0.57-0.76 cases per 100,000 per year. In the setting of newly diagnosed COVID-19 with subsequent development of thyroid storm, the presentation is increasingly rare with only two reported cases in the current literature.

Coronavirus disease 2019 (COVID-19) is a disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the seventh coronavirus to be linked to human disease. The SARS-CoV-2 virus may have several pathophysiologic interactions with endocrine systems, resulting in disruptions in glucose metabolism, hypothalamus and pituitary function, adrenal function, and mineral metabolism. An increasing amount of evidence demonstrates both the influence of underlying endocrine abnormalities on the outcome of COVID-19 and the effect of the SARS-CoV-2 virus on endocrine systems. However, a systematic examination of the link to pediatric endocrine diseases has been missing.

The purpose of this review is to discuss the impact of SARS-CoV-2 infection on endocrine systems and to summarize the available knowledge on COVID-19 consequences in children with underlying endocrine abnormalities. For this purpose, a literature search was conducted in EMBASE, and data that were discussed about the effects of COVID-19 on endocrine systems were used in the current study.

Treatment suggestions were provided for endocrinopathies associated with SARS-CoV-2 infection.

With the global outbreak of COVID-19, it is critical for pediatric endocrinologists to understand how SARS-CoV-2 interacts with the endocrine system and the therapeutic concerns for children with underlying problems who develop COVID-19. While children and adults share certain risk factors for SARS-CoV-2 infection sequelae, it is becoming obvious that pediatric responses are different and that adult study results cannot be generalized. While pediatric research gives some insight, it also shows the need for more study in this area.

SARS-CoV-2 infections have been associated with the onset of thyroid disorders like classic subacute thyroiditis (SAT) or atypical SAT upon severe COVID disease (COV-A-SAT). Little is known about thyroid anti-viral immune responses.

To define the role of T-cells in COV-A-SAT.

T-cells from COV-A-SAT patients were analyzed by multi-dimensional flow cytometry, UMAP and DiffusionMap dimensionality reduction and FlowSOM clustering. T-cells from COVID-naïve healthy donors, patients with autoimmune thyroiditis (ATD) and with SAT following COVID vaccination were analyzed as controls. T-cells were analyzed four and eight months post-infection in peripheral blood and in thyroid specimen obtained by ultrasound-guided fine needle aspiration. SARS-COV2-specific T-cells were identified by cytokine production induced by SARS-COV2-derived peptides and with COVID peptide-loaded HLA multimers after HLA haplotyping.

COV-A-SAT was associated with HLA-DRB1*13 and HLA-B*57. COV-A-SAT patients contained activated Th1- and cytotoxic CD4+ and CD8+ effector cells four months post-infection, which acquired a quiescent memory phenotype after eight months. Anti-SARS-CoV-2-specific T-cell responses were readily detectable in peripheral blood four months post-infection, but were reduced after eight months. CD4+ and CD8+ tissue-resident memory cells (TRM) were present in the thyroid, and circulating CXCR3+T-cells identified as their putative precursors. SARS-CoV-2-specific T-cells were enriched in the thyroid, and acquired a TRM phenotype eight months post-infection.

The association of COV-A-SAT with specific HLA haplotypes suggests a genetic predisposition and a key role for T-cells. COV-A-SAT is characterized by a prolonged systemic anti-viral effector T-cell response and the late generation of COVID-specific TRM in the thyroid target tissue.

Euthyroid sick syndrome (ESS) is characterized by low serum levels of free triiodothyronine (fT3) with normal or low levels of thyroid stimulating hormone (TSH) and free thyroxine (fT4) and is reported in different acute clinical situations, such as sepsis, diabetic ketoacidosis and after cardiac surgery. Our aim was to evaluate the predicting role of ESS for disease severity in patients with Multisystem Inflammatory Syndrome in children (MIS-C).

A single-centre observational study on consecutive patients with MIS-C. Before treatment clinical, and laboratory data were collected and, in a subset of patients, thyroid function tests were repeated 4 weeks later. Variables distribution was analyzed by Mann-Whitney U-test and correlations between different parameters were calculated by Spearman's Rho coefficient.

Forty-two patients were included and 36 (85.7%) presented ESS. fT3 values were significantly lower in patients requiring intensive care, a strong direct correlation was shown between fT3 and Hb, platelet count and ejection fraction values. A significant inverse correlation was retrieved between fT3 levels and C-reactive protein, brain natriuretic peptide, IL-2 soluble receptor and S-100 protein. Subjects with severe myocardial depression (EF < 45%) had lower fT3 values than subjects with higher EF. The thyroid function tests spontaneously normalized in all subjects who repeated measurement 4 weeks after admission.

ESS is a frequent and transient condition in acute phase of MIS-C. A severe reduction of fT3 must be considered as important prognostic factor for severe disease course, with subsequent relevant clinical impact in the management of these patients.

The outbreak of coronavirus disease 2019 (COVID-19) has caused a worldwide pandemic since 2019. A metabolic disorder is a contributing factor to deaths from COVID-19. However, the underlying mechanism of metabolic dysfunction in COVID-19 patients and the potential interventions are not elucidated. Here targeted plasma metabolomic is performed, and the metabolite profiles among healthy controls, and asymptomatic, moderate, and severe COVID-19 patients are compared. Among the altered metabolites, arachidonic acid and linolenic acid pathway metabolites are profoundly up-regulated in COVID-19 patients. Arginine biosynthesis, alanine, aspartate, and glutamate metabolism pathways are significantly disturbed in asymptomatic patients. In the comparison of metabolite variances among the groups, higher levels of l-citrulline and l-glutamine are found in asymptomatic carriers and moderate or severe patients at the remission stage. Furthermore, l-citrulline and l-glutamine combination therapy is demonstrated to effectively protect mice from coronavirus infection and endotoxin-induced sepsis, and is observed to efficiently prevent the occurrence of pulmonary fibrosis and central nervous system damage. Collectively, the data reveal the metabolite profile of asymptomatic COVID-19 patients and propose a potential strategy for COVID-19 treatment.

The correlation between acute coronavirus disease 2019 (COVID-19) and subacute thyroiditis (SAT) has not been clearly investigated in "long COVID" patients. We aimed to investigate the incidence of SAT during convalescence and after the acute phase of COVID-19, comparing with that of the general population.

Data from a total of 422,779 COVID-19 patients and a control group of 2,113,895 individuals were analyzed. The index date was defined as the date 3 months after confirmation of COVID-19. The incidence rate (IR) of SAT and hazard ratios (HRs) were calculated per 100,000 persons. Subgroup analysis included analysis of HRs 90-179 and 180 days post-COVID-19 diagnosis; and additional analysis was conducted according to hospitalization status, sex, and age group.

The IR of SAT was 17.28 per 100,000 persons (95% confidence interval [CI], 12.56 to 23.20) in the COVID-19 group and 8.63 (95% CI, 6.37 to 11.45) in the control group. The HR of COVID-19 patients was 1.76 (95% CI, 1.01 to 3.06; P=0.045). The HR of SAT was 1.39 (95% CI, 0.82 to 2.34; P=0.220) up to 6 months after the index date and 2.30 (95% CI, 1.60 to 3.30; P<0.001) beyond 6 months. The HR for SAT among COVID-19 patients was 2.00 (95% CI, 1.41 to 2.83) in hospitalized patients and 1.76 (95% CI, 1.01 to 3.06) in non-hospitalized patients compared to the control group. The IR of SAT was 27.09 (95% CI, 20.04 to 35.82) for females and 6.47 (95% CI, 3.34 to 11.30) for males. In the 19 to 64 age group, the IR of SAT was 18.19 (95% CI, 13.70 to 23.67), while the IR was 9.18 (95% CI, 7.72 to 10.84) in the 65 to 69 age group.

SAT could be a potential long-term complication of COVID-19. Long-term surveillance for thyroid dysfunction is needed especially in hospitalized, female and young-aged subjects.

The present severe acute respiratory syndrome-2 (SARS-CoV-2) mediated Coronavirus pandemic (COVID-19) and post-COVID-19 complications affect human life drastically. Patients who have been cured of COVID-19 infection are now experiencing post-COVID-19 associated comorbidities, which have increased mortality rates. The SARS-CoV-2 infection distresses the lungs, kidneys, gastrointestinal tract, and various endocrine glands, including the thyroid. The emergence of variants which includes Omicron (B.1.1.529) and its lineages threaten the world severely. Among different therapeutic approaches, phytochemical-based therapeutics are not only cost-effective but also have lesser side effects. Recently a plethora of studies have shown the therapeutic efficacy of various phytochemicals for the treatment of COVID-19. Besides this, various phytochemicals have been found efficacious in treating several inflammatory diseases, including thyroid-related anomalies. The method of the phytochemical formulation is quick and facile and the raw materials for such herbal preparations are approved worldwide for human use against certain disease conditions. Owing to the advantages of phytochemicals, this review primarily discusses the COVID-19-related thyroid dysfunction and the role of key phytochemicals to deal with thyroid anomaly and post-COVID-19 complications. Further, this review shed light on the mechanism via which COVID-19 and its related complication affect organ function of the body, along with the mechanistic insight into the way by which phytochemicals could help to cure post-COVID-19 complications in thyroid patients. Considering the advantages offered by phytochemicals as a safer and cost-effective medication they can be potentially used to combat COVID-19-associated comorbidities.

Subacute thyroiditis, a manifestation of Autoimmune/inflammatory syndrome induced by adjuvants that may develop after vaccination.

The aim of this study is to determine the importance of vaccination against COVID-19 in the etiology of subacute thyroiditis.

This case reports/series is an observational, descriptive research design.

Five of the thirty patients who applied to our clinic with subacute thyroiditis in the last 6 months had a history of inactivated and mRNA vaccines in the last four weeks, after exclusion of infection and comorbidities. We present three cases of mRNA-based vaccination and two cases of inactive SARS-CoV-2 vaccination that met ASIA criteria.

Our findings suggest that subacute thyroiditis may be a complication of vaccination against COVID-19.

Vaccine administration may led to autoimmune manifestation induction as well as autoantibody production. Adjuvant-induced autoimmune/inflammatory syndrome, an abnormal autoimmune response as a result of exposure to an adjuvant such as vaccine, appears likely in our cases.

Since the COVID-19 emergence as a global pandemic in March 2020, more than 5 million SARS-CoV-2-related deaths have been globally documented. As the pandemic progressed, it became clear that, although the infection is mainly characterized as a respiratory disease, it also affects other organs and systems, including the thyroid gland. Indeed, emerging evidence suggests that SARS-CoV-2 can act as a trigger for various thyroid disorders, for example, subacute thyroiditis (SAT), Grave's disease, and non-thyroidal illness syndrome. The entry of SARS-CoV-2 into the host cells is mainly mediated by the ACE2-receptor, making organs and systems with high expression of this receptor, such as the thyroid gland, highly vulnerable to COVID-19. Accumulating data propose that SAT may be an underestimated manifestation of COVID-19 infection. Importantly, if SAT remains unrecognized, it may trigger or aggravate potential other complications of the disease, for example, respiratory insufficiency and cardiovascular complications, and thus negatively influence prognosis. Moreover, recent case reports, case series, and systematic reviews highlight SAT as a potential side effect of the vaccination against SARS-CoV-2. The present review aims to raise awareness of SARS-CoV-2-associated- and post-vaccination subacute thyroiditis, to discuss recent evidence regarding its pathophysiology, and to present useful information for this special form of SAT related to daily clinical practice.