West Nile virus (WNV) is an uncommon but serious case of encephalitis and meningitis, often presenting with nonspecific symptoms that can mimic a wide range of infectious, metabolic, and endocrine disorders. We present the case of a 61-year-old male with multiple comorbidities who arrived with 5 days of fever, chills, profuse diarrhea, black stools, and worsening confusion. Initial evaluation in the emergency department revealed hyponatremia, transaminitis, and concern for tick-borne illness, prompting empiric doxycycline. However, the patient denied any tick bites. Given his known thyroid nodule and Burch-Wartofsky screening score of 70, he was empirically treated for thyroid storm despite laboratory evidence of subacute hypothyroidism. During hospitalization, our patient developed acute hypoxic respiratory failure requiring emergent intubation, as well as second-degree heart block and supraventricular tachycardia following propranolol administration. Neurologic workup revealed moderate encephalopathy on EEG and an opening pressure of 36 cm H2O on lumbar puncture. CSF examination revealed pleocytosis with mixed neutrophilic and lymphocytic predominance. Despite broad-spectrum antibiotic coverage, initial testing, which included a tick panel, Monospot, respiratory studies, and viral PCR assays, was insignificant. On hospital day eight, CSF serologies were positive for WNV IgM with negative IgG, confirming acute WNV neuroinvasive disease presenting as meningitis. This case highlights the diagnostic complexity of WNV infection, which may initially resemble tick-borne illness, endocrine crisis, or bacterial meningitis. Early consideration of WNV in patients with unexplained encephalopathy, GI symptoms, hyponatremia, and CSF lymphocytic pleocytosis, especially during mosquito season, may reduce delays in diagnosis and prevent unnecessary interventions.

Background: Coronavirus disease 2019 (COVID-19) has been associated with thyroid dysfunction; however, evidence from primary care settings remains limited. Given that most patients with COVID-19 are managed outside hospital settings, understanding thyroid function changes in real-world primary care is clinically relevant. Methods: This retrospective study included 373 adult outpatients with confirmed COVID-19 and no prior thyroid disease, who were managed in a Family Medicine Clinic in Warsaw between January of 2022 and December of 2024. Thyroid function tests (yielding TSH, fT3, and fT4 levels) obtained within three months before and after infection were analyzed. Subacute thyroiditis (SAT) was assessed in symptomatic patients via thyroid ultrasound. Paired comparisons were performed, with p < 0.05 considered statistically significant. Results: A significant reduction in the mean TSH level was observed following COVID-19 compared with pre-infection values (mean 2.39 vs. 2.17 mIU/L; p < 0.05), while fT3 (2.93 vs. 2.98 pg/mL) and fT4 (1.31 vs. 1.30 ng/dL) concentrations remained unchanged. No significant associations were found between thyroid function changes and age or sex. Conclusions: In this real-world primary care population, lower TSH concentrations were observed following COVID-19 while peripheral thyroid hormone levels remained unchanged, suggesting predominantly modest changes in thyroid function parameters. Given the retrospective study design and the absence of a control group, these findings should be interpreted with caution. Further prospective studies are needed to clarify the clinical significance of post-COVID-19 thyroid function changes.

This Editorial introduces the series How to manage thyroid diseases: from autoimmunity to malignancy Special Issue: https://www.drugsincontext.com/special_issues/how-to-manage-thyroid-diseases-from-autoimmunity-to-malignancy.

Subacute thyroiditis (SAT) is a self-limited inflammatory thyroid disorder classically characterized by anterior neck pain, an enlarged tender thyroid, fever, fatigue, malaise, elevated inflammatory markers and a triphasic course from thyrotoxicosis through hypothyroidism to recovery. It can cause substantial morbidity and remains a frequent diagnostic challenge because it must be distinguished from acute suppurative thyroiditis, Graves' disease, painless thyroiditis, haemorrhage into a nodule and, rarely, malignant 'pseudothyroiditis' (rapidly growing carcinoma). In recent years, the recognized spectrum of triggers has expanded beyond the classical post-viral setting to include SARS-CoV-2 infection or vaccination. This review summarizes current understanding of SAT pathogenesis, including viral and post-viral mechanisms, and HLA-linked susceptibility. We outline the typical and variant clinical phenotypes, emphasising painful classical SAT, painless presentations, pregnancy-associated disease and therapy-related destructive thyroiditis. We then present a practical diagnostic framework based on clinical features, inflammatory markers, thyroid function tests, radionuclide imaging, ultrasound and fine-needle aspiration, when indicated. Management is discussed in a stepwise fashion, including NSAIDs and glucocorticoids for pain and inflammation, β-blockers for symptomatic thyrotoxicosis, selective levothyroxine replacement during the hypothyroid phase, and structured follow-up to detect recurrence and permanent hypothyroidism. Special attention is given to pregnancy and SARS-CoV-2-related SAT cases. Finally, we review long-term outcomes, recurrence risk and future research priorities. The aim is to provide a concise, clinically oriented guide to the contemporary management of SAT and to support rational, evidence-informed decision-making in routine endocrine practice.

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.