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/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: 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.

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.