Background and Objectives: Thyroid dysfunction has been increasingly reported during and after SARS-CoV-2 infection, yet prospective longitudinal studies integrating biochemical and imaging assessments remain limited. The aim of this study was to evaluate the evolution of thyroid function and structural changes during a 12-month follow-up after COVID-19 hospitalization. Materials and Methods: This prospective single-center cohort study included adult patients hospitalized with laboratory-confirmed COVID-19 between December 2022 and December 2024. Thyroid-stimulating hormone (TSH), free thyroxine (FT4), free triiodothyronine (FT3), anti-thyroid peroxidase (anti-TPO), and anti-thyroglobulin antibodies (anti-TG) were assessed during hospitalization and at 1, 3, 6, and 12 months. Color Doppler thyroid ultrasound was performed at baseline and 6 and 12 months. Acute disease severity, vaccination status, and corticosteroid exposure were recorded. Results: Of the 71 enrolled patients, 67 completed the 12-month follow-up. Subacute thyroiditis occurred in 4/67 patients (6.0%; 95% CI: 1.7-12.6%). After excluding individuals with pre-existing disease, newly detected autoimmune thyroiditis was identified in 8/61 patients (13.1%; 95% CI: 5.8-24.2%). Most cases were mild and self-limited. Ultrasound patterns suggestive of autoimmune thyroiditis increased over time, even in patients with minimal biochemical abnormalities. Thyroid hormone trajectories showed interindividual variability, with most values remaining within reference ranges. Associations with inflammatory markers, disease severity, and vaccination status were weak. Conclusions: A subset of patients developed biochemical and structural thyroid changes during the 12 months following COVID-19 hospitalization. These findings highlight the value of targeted thyroid follow-up after COVID-19, particularly in patients with persistent symptoms, borderline TSH values, or ultrasound changes suggestive of autoimmune thyroiditis.

A 22-year-old woman developed palpitations, fatigue, and right leg pain 18 days after suffering from Mycoplasma pneumoniae (MP) pneumonia. Laboratory tests revealed severe hemolytic anemia with elevated lactate dehydrogenase levels, a C3b/C3d-positive direct antiglobulin test, and high cold agglutinin titers, confirming cold autoimmune hemolytic anemia. Thyroid studies showed asymptomatic thyrotoxicosis without tenderness, which was consistent with painless thyroiditis. Venous ultrasonography revealed deep vein thrombosis in the right popliteal and soleal veins. She improved with cold avoidance and apixaban treatment. This case underscores that multi-organ immune complications can emerge during the subacute phase of an MP infection.

Color Doppler ultrasonography was first used in 1988 by Ralls et al. to evaluate blood flow to the thyroid gland in patients with Graves' disease [1]. The "thyroid inferno" is the imaging demonstration of markedly increased vascularity and arteriovenous shunting seen with Graves' Disease (Fig. 2 and 1B) b[1]. This pattern consists of multiple small pulsatile areas of intrathyroidal flow seen diffusely throughout the gland in both systole and diastole. This hypervascularization reflects the hemodynamic changes of hyperfunctioning thyroid and/or an ongoing inflammatory process and is similar in color Doppler appearance to the homonymous "Inferno sign" in epididymo- orchitis [2]. Thyroid inferno is an imaging sign, which should not be mistaken with thyroid storm (hyperthyroid crisis) which is a clinical presentation of severe thyrotoxicosis. Though the clinical picture varies, the greyscale ultrasound picture of Graves' disease may be indistinguishable from Hashimoto's thyroiditis and de Quervain's thyroiditis as they often present with heterogenous and hypoechoic, diffuse glandular enlargement (Fig. 1A) [3]. Color Doppler has shown to help distinguish untreated Graves' disease from Hashimoto's thyroiditis, as marked hypervascularity is more characteristic of untreated Graves' disease [4]. It is notable that occasionally there might be hypervascularity in early Hashimoto thyroiditis. Additionally, in subacute thyroiditis, any degree of vascularization is possible [5]. Despite these overlaps, hypervascularization remains an important sonographic feature of Graves' disease [4]. Furthermore, in Graves' disease patients currently on treatment, increased blood flow detected prior to treatment cessation has shown to be a predictor of disease recurrence should treatment be stopped.

Subacute thyroiditis is an inflammatory thyroid disorder that typically presents with anterior neck pain, thyroid tenderness and transient thyrotoxicosis. Presentation as pyrexia of unknown origin (PUO) without classical thyroid symptoms is uncommon and may lead to diagnostic delay.We report a case of a patient in their late 50s who presented with persistent evening febrile spikes, weight loss and markedly elevated inflammatory markers, fulfilling the criteria for PUO. Extensive evaluation for infectious, malignant and autoimmune causes was unrevealing. Careful repeat clinical examination revealed mild thyroid enlargement, prompting thyroid function testing, which demonstrated suppressed thyroid-stimulating hormone with elevated thyroid hormone levels. Technetium-99m thyroid scintigraphy showed markedly reduced uptake, consistent with subacute thyroiditis.The patient was treated with corticosteroids, resulting in rapid defervescence of fever within 48 hours. This case highlights that subacute thyroiditis, although uncommon, should be considered in patients presenting with persistent unexplained fever and elevated inflammatory markers, even in the absence of classical thyroid symptoms.

Autoimmune cerebellar ataxia (ACA) is an immune-mediated cerebellar disorder arising from various underlying conditions. Because ACA is potentially treatable, identifying associated neuronal antibodies is important for diagnosis. We report the case of a 55-year-old woman with subacute progressive ataxia who presented with dysarthria and impaired handwriting and gait. Her scale for the assessment and rating of ataxia (SARA) score was 20.5, with particularly high subscores for gait and stance. She had a history of Hashimoto's thyroiditis. Laboratory testing showed markedly elevated antithyroid antibody levels with normal thyroid function, initially suggesting the cerebellar ataxic subtype of Hashimoto's encephalopathy (HE). Cerebral blood flow single-photon emission computed tomography revealed cerebellar hypoperfusion, which was most prominent in the superior cerebellar vermis. Intravenous methylprednisolone (1000 mg/day for 3 days) was administered; however, her response was poor. Further evaluation revealed positivity for anti-Ma2 antibodies, leading to a diagnosis of anti-Ma2-associated ACA. Subsequent intravenous immunoglobulin therapy improved the clinical symptoms and imaging findings, and the follow-up SARA score decreased to 10. Comprehensive imaging revealed no underlying malignancy. This case is unique not only because both rare diseases were key considerations in the differential diagnosis, but also because it is instructive in two respects: the construct of HE remains insufficiently specific and should not preclude consideration of alternative immune-mediated etiologies, and patients positive for anti-Ma2 antibody require sustained oncological surveillance, even in the absence of malignancy at presentation.

No evidence suggests that women receiving a vaccine against SARS-CoV-2, the virus that causes COVID-19, is harmful to either the nursing mother or the breastfed infant. Antibodies appear in the milk after maternal vaccination, which may protect the infant against COVID-19. Professional organizations and governmental health authorities have recommended that COVID-19 vaccines be offered to those who are breastfeeding because the potential benefits of maternal vaccination during lactation outweigh any theoretical risks, including mothers with diabetes mellitus.[1-12] Nursing mothers experienced minimal disruption of breastfeeding after vaccination and noticed no serious adverse effects in their infants.[13,14]

Severe acute respiratory syndrome coronavirus-2 infection is a systemic disease associated with metabolic and hormonal disturbances, including thyroid dysfunction such as primary hypothyroidism, subacute thyroiditis, and non-thyroidal illness syndrome. This study aimed to investigate the association between severe acute respiratory syndrome coronavirus-2 infection and changes in thyroid function during hospitalization and follow-up and evaluate whether these alterations are related to disease severity. We retrospectively analyzed a random cohort of 500 patients admitted to the Medicine Department of a central hospital between March 2020 and 2022. After excluding deaths, prior thyroid disease, and cases without thyroid evaluation, 218 patients were included. Serum thyroid-stimulating hormone, free triiodothyronine and free thyroxine values were measured at admission and after hospitalization. Patients were classified as having thyrotoxicosis, hypothyroidism, isolated hypothyroxinemia, and non-thyroidal illness syndrome. Thyroid dysfunction was defined by compatible biochemical findings with serological and/or imaging evidence of thyroid pathology and/or the need for therapy. COVID-19 cases were grouped by severity. Non-thyroidal illness syndrome was the most frequent abnormality, followed by isolated hypothyroxinemia and primary hypothyroidism. Non-thyroidal illness syndrome was more common in severe cases of COVID-19, although no statistically significant association was found between disease severity and type of thyroid abnormality. Most reassessed patients showed normalization of thyroid function during follow-up. The small sample size may have limited statistical power. Thyroid function alterations are common in severe acute respiratory syndrome coronavirus-2 infection, transient, and more frequent in severe disease. These findings suggest an adaptive response to systemic stress and inflammation. Larger prospective studies are needed to clarify evolution and clinical impact.

The association between viral infections and subacute thyroiditis (SAT) has been recognized, yet whether a genetic causal relationship exists between them remains unclear. To address this, we conducted a two-sample Mendelian randomization (MR) study to investigate this relationship. Genetic instruments for exposure to common viruses were derived from published genome-wide association study summary statistics. Inverse-variance weighted was the primary analysis, supplemented by MR-Egger and weighted median methods. Sensitivity analyses included tests for heterogeneity and horizontal pleiotropy. Results from our MR analysis indicated no statistically significant causal associations between SAT and the following viral exposures: herpes simplex virus (OR = 0.90, 95% CI = 0.73-1.10, P = .294), Epstein-Barr virus (OR = 1.03, 95% CI = 0.90-1.18, P = .63), cytomegalovirus immunoglobulin G (OR = 1.01, 95% CI = 0.74-1.38, P = .934), varicella-zoster virus (OR = 1.02, 95% CI = 0.90-1.15, P = .76), COVID-19 (OR = 1.02, 95% CI = 0.83-1.27, P = .821), hepatitis B virus (OR = 0.98, 95% CI = 0.94-1.03, P = .518), human immunodeficiency virus (OR = 1.02, 95% CI = 0.89-1.17, P = .778), influenza (OR = 0.96, 95% CI = 0.77-1.21, P = .747), measles (OR = 0.95, 95% CI = 0.85-1.06, P = .35), and mumps (OR = 1.00, 95% CI = 0.92-1.10, P = .914). All sensitivity analyses consistently supported the robustness of these findings. In summary, this study provides no evidence for a substantial causal effect of genetic liability to viral infections on SAT risk. Further research in larger and more diverse populations, ideally incorporating both genetic and temporal data on acute infections, is needed to comprehensively understand the role of viruses in SAT pathogenesis.

Objective To analyze the accuracy of intraoperative frozen section diagnosis of thyroid lesions in Xizang and explore the methods and measures to improve the diagnosis accuracy. Methods The clinicopathological data of 371 patients with thyroid lesions surgically resected by four hospitals in Xizang from January 2020 to December 2024 were collected.With the paraffin section diagnosis after surgery as the standard,the accuracy,missed diagnosis rate,misdiagnosis rate,and delayed diagnosis rate of frozen section diagnosis were analyzed. Results The intraoperative frozen section diagnosis in 371 cases of thyroid lesions showed the accuracy of 95.42% (354/371),the missed diagnosis rate of 0.27% (1/371),the misdiagnosis rate of 0.54% (2/371),and the delayed diagnosis rate of 3.77% (14/371).One case was subjected to missed diagnosis,which was a papillary carcinoma of the thyroid gland.Two cases were misdiagnosed.One of them was diagnosed as malignant tumor during surgery but nodular goiter with atypical hyperplasia of follicular epithelium after surgery.The other case was diagnosed as medullary carcinoma during surgery but subacute thyroiditis after surgery. Conclusions Frozen section diagnosis is an important method for determining the benign or malignant nature of thyroid lesions during surgery.The diagnosis rates of follicular tumors and small lesions are low during surgery.Standardized sampling,improving the quality of frozen sections,and mastering the microscopic morphological characteristics and diagnostic criteria of frozen sections of thyroid lesions during surgery can improve the accuracy of intraoperative frozen section diagnosis.

Steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT) is a rare, potentially reversible neuropsychiatric syndrome linked to autoimmune thyroid disease. However, its clinical heterogeneity may stray from the most accepted diagnostic criteria often leading to a delay in its recognition. In this paper, we describe two patients who presented with subacute encephalopathy for which the diagnosis of SREAT was established after the detection of elevated antithyroid antibody titers and the exclusion of alternative etiologies. Notably, both cases exhibited atypical features, namely CSF lymphocytic pleocytosis and leptomeningeal enhancement in Case 1 and a complex differential confounded by multiple comorbidities in Case 2. Treatment strategies included corticosteroid-based immunosuppression, with one patient also receiving intravenous immunoglobulin and thyroid hormone replacement. Both patients demonstrated substantial neurological improvement following therapy, underscoring the reversibility of this condition when appropriately treated. Together, these cases highlight the importance of maintaining diagnostic suspicion for SREAT in patients with unexplained encephalopathy, even in the absence of overt thyroid dysfunction, atypical lab and imaging findings, and a complex past medical history. Early recognition and initiation of immunotherapy can significantly alter outcomes and prevent prolonged morbidity. By presenting these cases, we aim to add to the limited body of literature on SREAT and emphasize the critical role of maintaining suspicion for SREAT in atypical cases of probable autoimmune encephalitis to facilitate timely diagnosis and intervention in optimizing patient recovery.