Background/Objectives: Admission hyperglycemia is frequent in COVID-19 and may serve as an early marker of severity. We assessed whether admission hyperglycemia predicts severe disease and poor outcomes in adults without diabetes. Methods: We performed a retrospective cohort study at the Clinical Hospital of Pneu-mophthisiology and Infectious Diseases, Brașov, Romania, including adults hospital-ized with RT-PCR/antigen–confirmed COVID-19 between August 2020 and July 2021. Patients < 18 or >80 years, with prior diabetes, or on corticosteroids were excluded. Hyperglycemia was defined as fasting glucose >106 mg/dL and classified as mild (107–180 mg/dL), moderate (181–300 mg/dL), and severe (>300 mg/dL). Clinical, laboratory, imaging, treatment, utilization, and cost parameters were analyzed. Results: Of 1,009 patients, 734 (72.7%) were hyperglycemic at admission. Compared with normoglycemic patients, hyperglycemics more often developed respiratory fail-ure (67.7% vs. 38.2%), required CPAP (9.4% vs. 1.5%), had severe/critical disease (46.9% vs. 25.1%), ICU transfer (6.5% vs. 1.5%), and mortality (3.8% vs. 1.1%) (all p≤0.0256). They also showed lymphopenia, eosinopenia, higher inflammatory and co-agulation markers, longer hospitalization (12.1 vs. 10.1 days), and increased costs (€1,846 vs. €1,043) (all p< 0.001). Severe hyperglycemia (>300 mg/dL) strongly corre-lated with inflammation, coagulopathy, tissue injury, and radiologic severity. Conclusions: Admission hyperglycemia is a robust, easily measurable predictor of se-vere COVID-19 and adverse outcomes in non-diabetic adults and is associated with greater resource utilization and higher costs. Early identification may improve risk stratification, while prospective studies should assess whether glycemic control modi-fies prognosis. Keywords: COVID-19; SARS-CoV-2; admission hyperglycemia; severity; mortality; ICU;

Background/Objectives: Admission hyperglycemia is frequent in COVID-19, reflecting stress hyperglycemia, systemic inflammation, and potential viral injury to pancreatic β-cells. It may serve as an early marker of severity. We assessed whether admission hyperglycemia predicts severe disease and poor outcomes in adults without diabetes. Methods: We performed a retrospective cohort study including adults hospitalized with RT-PCR/antigen-confirmed COVID-19 between August 2020 and July 2021. Patients < 18 or >80 years, with prior diabetes, or on corticosteroids were excluded. Hyperglycemia was defined as fasting glucose > 106 mg/dL and classified as mild (107–180 mg/dL), moderate (181–300 mg/dL), and severe (>300 mg/dL). Clinical, laboratory, imaging, treatment, utilization, and cost parameters were analyzed. Results: Of 1009 patients, 734 (72.7%) were hyperglycemic at admission. Compared with normoglycemic patients, hyperglycemics more often developed respiratory failure (67.7% vs. 38.2%), required CPAP (9.4% vs. 1.5%), and had severe/critical disease (46.9% vs. 25.1%), ICU transfer (6.5% vs. 1.5%), and mortality (3.8% vs. 1.1%) (all p ≤ 0.0256). They also showed lymphopenia, eosinopenia, higher inflammatory and coagulation markers, longer hospitalization (12.1 vs. 10.1 days), and increased costs (EUR 1846 vs. 1043) (all p < 0.001). Severe hyperglycemia (>300 mg/dL) strongly correlated with inflammation, coagulopathy, tissue injury, and radiologic severity. Conclusions: Admission hyperglycemia is a robust, easily measurable predictor of severe COVID-19 and adverse outcomes in non-diabetic adults and is associated with greater resource utilization and higher costs. Early identification may improve risk stratification. Future prospective studies should determine whether early detection and aggressive glycemic control can modify prognosis.

Background: Endocrine disturbances are increasingly recognized as components of long COVID, yet long-term data remain limited. This study evaluated the prevalence of dysglycemia and thyroid autoimmunity four years after SARS-CoV-2 infection in adults without previously known endocrine disease. Methods: We conducted a retrospective longitudinal 4-year evaluation of adults hospitalized for COVID-19 between 2020 and 2021. Of 1009 eligible patients without prior diabetes or thyroid disease, 96 completed a standardized 4-year post-infection evaluation. Acute-phase data included COVID-19 severity, admission glucose, inflammatory markers, imaging findings, and treatments. The 4-year evaluation comprised fasting plasma glucose, thyroid function tests, anti-thyroid antibodies (anti-TPO, anti-Tg), and thyroid ultrasonography. Baseline HbA1c, thyroid autoantibodies, and thyroid imaging were not available. Results: At four years post-infection, 27.1% of patients exhibited dysglycemia compatible with type 2 diabetes mellitus, 41.6% showed thyroid autoimmunity, and 15.6% presented with both conditions. Overall, 47.9% developed at least one endocrine alteration. Admission hyperglycemia strongly predicted long-term dysglycemia (OR 6.67; 95% CI: 1.45–30.58), and diabetes prevalence increased with acute disease severity. Thyroid autoimmunity was frequent but not associated with initial COVID-19 severity. Conclusions: Four years after SARS-CoV-2 infection, a substantial proportion of patients exhibited persistent metabolic and autoimmune alterations, supporting a long COVID immunometabolic phenotype. In the absence of baseline endocrine data, the reported findings reflect long-term endocrine alterations identified at the 4-year evaluation, with a potential role of SARS-CoV-2 infection. These findings highlight the importance of baseline metabolic and thyroid assessment—including HbA1c and thyroid autoantibodies—in hospitalized COVID-19 patients and underscore the need for structured long-term endocrine monitoring.

Subacute thyroiditis (SAT) is an inflammatory condition affecting the thyroid gland, usually triggered by a viral infection or occurring after a viral illness. It is characterized by neck tenderness, along with the typical symptoms of thyrotoxicosis and an elevated erythrocyte sedimentation rate. SAT has been identified as a potential complication associated with SARS-CoV-2 infection. The aim of this study is to present and discuss two cases of subacute thyroiditis that occurred following a viral infection, potentially linked to SARS-CoV-2 infection. We describe the clinical, biochemical, and imaging features of two cases of SAT that manifested six weeks after the onset of COVID-19-associated symptoms. Both cases involved female patients, aged 58 and 39, who developed subacute thyroiditis, characterized by neck pain, fever, and fatigue. These symptoms emerged three weeks after recovering from a viral episode marked by acute coryza, cough, and anosmia. Due to a persistent fever lasting three weeks, one of the patients required hospitalization to rule out other infectious causes of prolonged febrile syndrome. Laboratory analyses revealed elevated inflammatory markers, positive serology for SARS-CoV-2 infection, thyroid function tests showed thyroid over-activity and thyroid ultrasound confirmed the diagnosis of SAT. The patients received corticosteroid treatments and beta-blockers, resulting in the complete resolution of symptoms and normalization of inflammatory markers, within three weeks after the SAT diagnosis. Post-COVID-19 thyroiditis can emerge as a potential complication of SARS-CoV-2 infection. It is crucial for clinicians to be aware of this possibility, highlighting the importance of considering post-COVID-19 thyroiditis in patients presenting with relevant symptoms.

Introduction: Thyroid dysfunctions in the paediatric population can present with atypical and nonspecific systemic manifestations, making diagnosis particularly challenging. Viral infections, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), have increasingly been implicated in the onset or exacerbation of autoimmune thyroid diseases both in children and adults. This report describes a case of autoimmune thyroiditis with a transient hyperthyroid phase (hashitoxicosis) following prior exposure to SARS-CoV-2, highlighting the possible immune-mediated mechanisms of viral-induced endocrine autoimmunity that may extend to paediatric populations. Case report: A previously healthy 13-year-old boy presented with fever, asthenia, bicytopenia, and hepatic cytolysis. Extensive infectious workup, including tests for hepatitis viruses, Epstein–Barr virus, cytomegalovirus, Leptospira spp., and Coxiella burnetii, was negative, except for rhinovirus detection by reverse transcription-polymerase chain reaction. Thyroid function testing revealed elevated thyroid-stimulating hormone (11.9 µIU/ml) and positive anti-thyroid antibodies (anti-thyroid peroxidase >1000 IU/ml, anti- thyroglobulin, 2108 IU/ml). Anti–SARS-CoV-2 neutralizing antibodies were markedly increased, consistent with previous infection. Thyroid ultrasound showed diffuse inhomogeneous echotexture with a pseudonodular pattern and increased vascularity, consistent with autoimmune thyroiditis. Corticosteroid therapy led to fever resolution and normalization of laboratory parameters, followed by a transient hyperthyroid phase (hashitoxicosis) and subsequent progression to subclinical hypothyroidism. Conclusion: This case underscores the importance of thyroid function evaluation in paediatric or adult patients presenting with unexplained systemic inflammation or cytolysis following viral infections. The overlapping effects of SARS-CoV-2 and other respiratory viruses may unmask or accelerate autoimmune thyroid disorders.

Introduction: SARS-CoV-2 infection has been increasingly associated with thyroid involvement, likely mediated by post-viral immune–inflammatory mechanisms. However, prospective data on the incidence and medium-term evolution of post-COVID thyroid dysfunction remain limited. Methods: We conducted a prospective, observational, single-center study including adult patients hospitalized for COVID-19 between December 2022 and December 2024. Thyroid function tests, thyroid autoantibodies, inflammatory markers, and thyroid ultrasound were assessed during hospitalization and re-evaluated at 4–6 weeks, 3, 6, and 12 months. Acute disease severity and administered treatments, including corticosteroid therapy, were recorded. Results: A total of 71 patients were enrolled, of whom 67 completed the 12-month follow-up. During follow-up, 6.0% of patients developed subacute thyroiditis and 11.9% developed autoimmune thyroiditis, with most cases showing a mild or self-limited clinical course. Persistence of thyroid autoantibodies at 12 months was observed in a subset of patients. Longitudinal assessment of thyroid hormones revealed an overall trend toward gradual normalization, with marked interindividual variability. Associations between thyroid dysfunction, systemic inflammation, and acute COVID-19 severity were weak. Conclusions: Post-COVID thyroid dysfunction, particularly subacute and autoimmune thyroiditis, was relatively frequent within the first 12 months after SARS-CoV-2 infection, even following mild or moderate acute disease. These findings support the need for risk-adapted thyroid monitoring in the post-COVID period and suggest a triggering role of SARS-CoV-2 for both transient thyroid dysfunction and persistent autoimmune processes.