Search Results (65)

Objectives: This study aimed to estimate the prevalence of Post-COVID-19 Syndrome among older adults in Indonesia, using time-based definitions of symptoms persisting beyond >4 weeks, >8 weeks, and >12 weeks. Methods: A retrospective cohort study was conducted among 329 older patients (≥60 years) hospitalized with COVID-19 in two tertiary hospitals in Jakarta from January to December 2021. Data on risk factors and persistent symptoms were collected from medical records and interviews. Results: The prevalence of Post-COVID-19 Syndrome was 31% (>4 weeks), 18.24% (>8 weeks), and 10.64% (>12 weeks). Significant predictors included frailty (OR 2.814), immobility during hospitalization (OR up to 4.767), higher number of initial symptoms (OR 2.043), constipation, instability, and sensory impairment during follow-up. Conclusions: Frailty, symptom burden, and geriatric syndromes, particularly immobility are strongly associated with Post-COVID-19 Syndrome in older adults. Clinical Implications: Early identification of frailty, geriatric syndromes (especially immobility), and high initial symptom burden is essential for risk stratification, targeted monitoring, and implementation of preventive and rehabilitative interventions to reduce long-term post-COVID-19 complications in older populations. Full article

Background: Globally, around 400 million people are estimated to be affected by long COVID, yet treatment options remain scarce. A systematic review published in 2025 indicated that non-invasive brain stimulation may help reduce some long COVID symptoms. If repetitive transcranial magnetic stimulation (rTMS) has therapeutic potential for these patients, then a clear synthesis of the evidence is necessary to determine efficacy and potential for implementation. Methodology: This systematic review and narrative synthesis was conducted in accordance with PRISMA guidelines. The search, completed on the 4th of December 2025, covered four databases and grey literature. Studies were included if they examined long COVID and rTMS. Findings: A meta-analysis was not possible due to insufficient reported data across studies. Instead, a structured narrative synthesis was conducted on four included studies. The structured narrative synthesis of four studies indicates that rTMS is feasible and is associated with reported improvements in fatigue, mood, and cognitive symptoms in individuals with long COVID. However, all included evidence is based on uncontrolled case series and retrospective analyses, meaning no causal conclusions can be drawn and findings should be interpreted as exploratory. Conclusions: Taken together, the evidence remains preliminary and highlights the need for well-designed randomised controlled trials to assess efficacy. Full article

Background: Hypertension is one of the most prevalent comorbidities in patients with COVID-19 and a major contributor to chronic kidney disease (CKD). Traditional kidney injury markers, including creatinine, estimated glomerular filtration rate (eGFR) and microalbuminuria, reflect renal injury only after substantial nephron loss has already occurred. Urinary podocyte proteins, such as nephrin (nephrinuria), have been suggested as early markers of glomerular barrier dysfunction; however, their clinical behavior and diagnostic value in hypertensive patients with previous SARS-CoV-2 infection are unknown. Aim: To assess urinary nephrinuria, microalbuminuria, transforming growth factor β1 (TGF-β1), aldosterone, vascular endothelial growth factor A (VEGF-A) and renal hemodynamics across different stages of hypertension in patients with and without a history of COVID-19 and to assess the response to conventional antihypertensive and nephroprotective treatment. Methods: In a prospective comparative cohort study, 120 patients (aged 30–60 years) with stage I–III essential hypertension were stratified by COVID-19 history into a post-COVID-19 group (n = 60) and a non-COVID-19 group (n = 60); within each group, 20 patients were assigned to each hypertension stage. Comparisons were performed between the post-COVID-19 and non-COVID-19 subgroups at the same hypertension stage. Serum creatinine, cystatin-C, aldosterone, TGF-β1 and VEGF-A, urinary microalbumin and nephrin and intrarenal Doppler hemodynamics were measured at baseline and after six months of guideline-based treatment. Results: Nephrinuria was markedly increased in post-COVID-19 patients in all stages of hypertension, including stage I, where serum creatinine, cystatin-C and eGFR were within the normal range (126.5 ± 9.1 vs. 91.9 ± 8.3 pg/mL, p < 0.01). Nephrinuria was strongly correlated with renal functional reserve (r = −0.824, p < 0.001), eGFR (r = −0.797, p < 0.001), microalbuminuria (r = 0.758, p < 0.001), aldosterone (r = 0.613, p < 0.001) and VEGF-A (r = 0.589, p < 0.001). Antihypertensive and nephroprotective treatment for six months decreased nephrinuria, blood pressure and TGF-β1, with more limited effects in stage III disease. Conclusions: Nephrinuria was found to be an early marker of renal involvement in COVID-19, occurring before microalbuminuria and conventional functional markers and with a greater relative difference than these markers in stage I disease, suggesting podocyte injury as an early and potentially reversible mechanism of post-COVID renal involvement in hypertensive patients. Nephrinuria seems to be a potential biomarker for early renal surveillance in this population and its prognostic role for incident CKD needs to be validated in longitudinal outcome studies. Full article

Excitotoxicity is one of the factors that participates in neurodegeneration, impairing neuronal and glial cells’ function, and leading to the development of chronic neurodegenerative diseases. The main mechanism of action lies in the overstimulation of excitatory receptors, especially the NMDA (N-methyl-D-aspartic acid) receptor, by glutamate, which promotes a massive influx of Ca²⁺ that is not sufficiently buffered by the intracellular machinery, or not released by mechanisms such as Ca²⁺ ATPase and plasma membrane Ca²⁺/Na⁺ exchanger promoting, among other toxic effects, mitochondrial damage and an increase in reactive oxygen species (ROS). Notably, many cases reported of long COVID-19 describe significant brain alterations and neuropsychiatric disorders, including delirium, depression, etc., and patients required increased use of antidepressant or anxiolytic drugs, for example. In addition, emerging evidence links neurodegeneration as a potential long-term sequelae associated with an increased number of patients with cognitive disorders. This review analyzes data from the literature regarding brain alterations associated with post-COVID-19 syndrome and explores a potential link to the excitotoxicity pathways, due to its participation in neurodegeneration by homeostatic failure, and it is clearly present in various brain conditions, such as Alzheimer’s and Parkinson’s diseases. Full article

Introduction: Coronavirus disease 2019 (COVID-19) can cause persistent cardiovascular alterations, including autonomic dysfunction. Heart rate (HR) recovery (HRR) after exercise is a simple marker of autonomic modulation associated with functional capacity and clinical prognosis. Evaluating HRR during the six-minute walk test (6MWT) may help identify residual functional limitations in diverse patients. Objective: To compare pulmonary function, maximal inspiratory pressure (MIP), functional capacity, dyspnea, fatigue, and functional status in post-COVID-19 patients. Methods: This cross-sectional study included 75 adults (mean age: 47.6 ± 13.1 years; 54.7% male) who recovered from COVID-19 divided into 2 groups based on HRR 1 min after the 6MWT: delayed (≤12 beats/min); and non-delayed (>12 beats/min). Pulmonary function, MIP, exercise capacity (via 6MWT), dyspnea, muscle fatigue, and functional status were assessed. Results: Based on HRR 1 min after 6MWT, 27 (36%) participants were classified with abnormal HRR and 48 (64%) with normal HRR. There were statistical differences between the groups regarding demographic or clinical characteristics, pulmonary function, MIP, muscle fatigue, or functional status (p > 0.05). The delayed HRR group exhibited a smaller reduction in HR in first minute of recovery (ΔHR = 6 vs. 23 beats/min), higher baseline HR (p = 0.010), and greater dyspnea (p = 0.020). Furthermore, this group exhibited worse functional performance in the 6MWT, with shorter distance walked (437.33 vs. 494.27 m; p = 0.019) and a lower percentage of predicted distance (74.66 ± 12.98% vs. 82.94 ± 15.71%; p = 0.023) compared with the non-delayed HRR group. Conclusion: Delayed HRR post-COVID-19 was associated with poorer functional performance and greater dyspnea, regardless of pulmonary function. The blunted reduction in HRR after exertion suggests impaired cardiovascular autonomic modulation, possibly related to attenuated vagal reactivation, which may contribute to exercise intolerance observed in this population. Full article

Since the introduction of the Post-COVID-19 Functional Status (PCFS) scale early in the COVID-19 pandemic, the scale has been incorporated in research and clinical guidelines to assess and monitor functional status. In this explorative study, we aimed to evaluate characteristics of the PCFS scale based on its use during a 12-month follow-up of COVID-19 survivors to increase understanding of the scale over a longer period of time. Adult COVID-19 patients who were evaluated by multidisciplinary measures at 6 weeks and 12 months post-discharge at the Leiden University Medical Center (The Netherlands) were included. The distribution of PCFS scale grades, as well as descriptive patterns between PCFS grades and patient-reported outcome measures (PROMs), pulmonary function and physical function were evaluated with descriptive analyses; no statistical tests were performed due to data availability. Of the 79 included patients, 62% had a change in PCFS grade between the 6-week and 12-month follow-ups, of whom 63% improved over time. At 12 months, abnormal PROMs regarding psychological symptoms (according to clinical cut-offs), relatively lower quality of life (EQ VAS) scores, and MRC dyspnea grades ≥ 2 were observed in patients scoring PCFS grade ≥ 2. With increasing PCFS grade, a decrease in pulmonary function and physical function outcomes was observed. Higher PCFS grades (worse functional status) seemed related to worse outcomes at 12-month follow-up. Future studies are needed to investigate whether changes in PCFS grade reflect clinically relevant changes in patients’ self-perceived functioning. Full article

Background: Post-COVID-19 syndrome (PCS) is associated with impairments in mobility, balance, and physical function, which may reduce quality of life. The 30 s Sit-to-Stand (30STS) and Timed Up and Go (TUG) tests are widely used clinical measures; however, their intra-rater reliability in older adults with PCS has not been established. Reliable outcome measures are essential for clinical assessment and rehabilitation planning. Methods: In this single-center pilot study, nineteen older adults with PCS were recruited as a convenience sample. Participants completed three trials of the 30STS and TUG tests on day one, with the protocol repeated after three days. The 30STS evaluates lower-limb strength and functional performance, while the TUG assesses balance, gait, and fall risk. Intra-class correlation coefficient (ICC), standard error of measurement (SEM), and minimum detectable change (MDC) were calculated. Results: The TUG showed an ICC of 0.995 (95% CI: 0.991–0.998), SEM of 0.48 s, and MDC of 1.33 s. The 30STS showed an ICC of 0.986 (95% CI: 0.973–0.994), SEM of 0.26 repetitions, and MDC of 0.72 repetitions. Conclusions: The TUG and 30STS demonstrate excellent intra-rater reliability and appear to be feasible clinical tools for assessing functional performance in older adults with PCS. However, findings should be interpreted cautiously due to the small, single-center pilot design and single evaluator. Further research is needed to confirm generalizability across broader PCS populations and clinical settings. Full article

COVID-19 is increasingly recognized as a multisystemic disease with significant neurocognitive consequences. However, its specific impact on spatial memory, a cognitive domain essential for daily navigation and functional independence, remains insufficiently explored. This narrative review provides a critical synthesis of current evidence regarding spatial and visuospatial memory alterations across acute and post-acute phases, and post COVID-19 condition (PCC). Clinical findings, conventional and emerging assessment tools ranging from static tasks to immersive virtual reality environments, as well as potential neurobiological mechanisms, were considered. Results suggested that spatial memory is frequently compromised after COVID-19 disease, with deficits being most pronounced at longer retention intervals and within navigational contexts. Neuroimaging and biomarker data further reveal selective vulnerability in the medial temporal lobe, characterized by hippocampal atrophy, hypoperfusion, and disrupted functional connectivity. Importantly, traditional neuropsychological tools may underestimate these impairments due to limited ecological validity. Therefore, implementing multimodal assessment frameworks that integrate navigational paradigms is essential to enhance diagnostic sensitivity and facilitate the development of targeted rehabilitation strategies for PCC patients. Full article

Background: The COVID-19 pandemic has been associated with increased psychological distress globally. However, the independent psychological impact of prior COVID-19 infection remains heterogeneous, particularly in primary healthcare populations. This study aimed to examine differences in anxiety and depressive symptoms between individuals with and without a history of COVID-19 infection in a primary healthcare setting. Methods: A cross-sectional study was conducted in April 2022 in five family medicine practices in the primary health care facility of Sarajevo Canton. A total of 279 participants without previously diagnosed mental disorders completed an online questionnaire. Anxiety and depressive symptoms were assessed using the GAD-7 and PHQ-9 scales. Multivariable regression models were performed, and propensity score matching (1:1 nearest-neighbor matching, caliper = 0.2) was conducted to address baseline imbalance. Results: No statistically significant independent association was detected between prior COVID-19 infection and anxiety or depressive symptoms in multivariable models. Propensity score matching yielded 84 well-balanced pairs. In the matched sample, no significant differences were observed in GAD-7 (p = 0.229) or PHQ-9 scores (p = 0.139), nor in clinically relevant cut-offs. Female sex and chronic disease were independently associated with higher anxiety levels. Conclusions: In this primary healthcare population, we did not observe an independent association between prior COVID-19 infection and anxiety or depressive symptoms after covariate adjustment and propensity score matching. These findings should be interpreted cautiously given the cross-sectional design, possible exposure misclassification, and residual confounding. Full article

The neuroinvasive and neurotropic character of coronaviruses is a likely reason for neurological complications which may occur during acute COVID illness and sometimes persist or newly emerge in the post-acute phase. Terminology and temporal classification remain heterogeneous. A retrospective case series was conducted in a single center (Department of Neurology, Bielański Hospital, Warsaw, Poland). Medical records from March 2020 to December 2023 were screened. Inclusion criteria: (1) confirmed SARS-CoV-2 infection (polymerase chain reaction or antigen test and radiological findings), (2) new neurological syndrome within acute, post-acute, or post-COVID interval, and (3) diagnostic documentation. Exclusion criteria: alternative established etiology fully explaining the neurological condition. Six cases were selected for detailed analysis due to diagnostic completeness as well as etiological and temporal diversity. Cases included: (1) persistent neurocognitive and sensory symptoms (post-COVID), (2) acute ischemic stroke with internal carotid artery dissection during severe COVID-19, (3) cytotoxic lesion of the corpus callosum (CLOCC) during acute COVID-19, (4) Guillain–Barré syndrome (post-acute), (5) longitudinally extensive transverse myelitis (post-acute), and (6) delayed autoimmune cerebral vasculitis (post-COVID). Neurological presentations ranged from mild persistent symptoms to fatal outcome. Neurological complications span inflammatory, vascular, and autoimmune mechanisms across distinct temporal phases of SARS-CoV-2 infection. Precise temporal classification and systematic diagnostic protocols are essential. Prospective longitudinal studies integrating biomarkers and standardized neuroimaging are required. Full article

The COVID-19 pandemic has led to an unprecedented global health crisis, with millions recovering from acute infection but experiencing lingering symptoms, collectively referred to as post-acute sequelae of COVID-19 (PASC), or “long COVID.” While the precise mechanisms underlying long COVID remain elusive, one hypothesis gaining traction is the persistence of viral reservoirs in various tissues. Despite evidence of viral RNA and proteins detected in post-acute patients, the concept of viral reservoirs in the context of long COVID remains a subject of debate. This review explores the current scientific evidence for the existence of persistent SARS-CoV-2 in human tissues beyond the acute infection phase, focusing on the molecular mechanisms by which the virus may evade immune surveillance. We examine the role of immune dysregulation, chronic inflammation, and viral persistence in tissues such as the lungs, heart, brain, and gut. Additionally, we explore how these persistent viral elements may be associated with ongoing symptoms in long COVID and discuss the biological plausibility of these links. Finally, we discuss the clinical implications of viral persistence in post-COVID care, potential therapeutic strategies, and the need for further research to resolve the open questions surrounding this phenomenon. Full article

Long COVID is the disease entity triggered and potentially driven by SARS-CoV-2 infection. It is an heterogeneous condition characterized by dozens of different symptoms, signs and sequelae, which can affect all organs and body systems and evolve over the disease course. Clinical manifestations of Long COVID can vary from individual to individual and across the broader patient population. Pathology can range from asymptomatic and subclinical manifestations to fatal outcomes. Over 400 million people worldwide are estimated to suffer, or have suffered, from Long COVID, making the sequelae of SARS-CoV-2 infection one of the greatest public health challenges of the 21st century. This article provides an updated overview of epidemiology, definitions, main concepts and terminology for Long COVID. It also summarizes key evidence of pathology and disease mechanisms in major organs and body systems, such as the immune system, cardiovascular system, endothelium, heart, lungs, central nervous system, peripheral nervous system, gastrointestinal system, hapatobiliary system, pancreas and kidney. Heterogeneity in manifestations, potential risk of death and the degree of disability in several disease subsets call for timely diagnosis of each Long COVID types and a fuller understanding of their pathophysiological underpinnings. Further research is recommended to better understand pathobiology, develop effective clinical trials, and identify treatments and scalable biomarkers. Full article

Respiratory viral infections such as influenza and SARS-CoV-2 induce complex immune responses characterized by dysregulated cytokine production, which may influence disease severity and lead to post-infection immunometabolic alterations. However, comparative data on local epithelial and systemic immune responses during acute infection and recovery remain limited. Objective: To evaluate the expression of IFN-γ, TNF-α, and interleukins IL-2, IL-4, IL-6, and IL-10 in nasopharyngeal epithelial cells from patients with influenza and SARS-CoV-2 infection, as well as in peripheral blood mononuclear cells (PBMCs) from individuals who recovered from COVID-19. Methods: A total of 120 participants were distributed into four groups (control, influenza, asymptomatic SARS-CoV-2 infection, and symptomatic COVID-19; n = 30 per group), in addition to 90 individuals who had recovered from COVID-19. COVID-19 and influenza diagnoses were established by the treating physician based on clinical presentation and confirmed by RT–qPCR. Cytokine gene expression was quantified by real-time PCR, and hematological and biochemical parameters were measured using automated analyzers. Results: The asymptomatic SARS-CoV-2 group showed significantly increased expression of IFN-γ (p = 0.0001), TNF-α (p = 0.0007), and IL-4 (p = 0.01). Individuals who recovered from COVID-19 exhibited elevated erythrocyte and leukocyte counts, along with increased glucose, glycated hemoglobin, triglycerides, and very-low-density lipoprotein levels, while no significant alterations in liver function markers were observed. Conclusions:Influenza and SARS-CoV-2 infections are associated with distinct epithelial cytokine expression profiles during acute infection, and COVID-19 recovery is characterized by persistent immunometabolic alterations, suggesting prolonged systemic effects beyond viral clearance. Full article

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. Full article

One of the challenges post-COVID-19 is reducing the negative impacts on quality of life, performance, and independence in activities of daily living. Assessing functional dependence in adults one year after acute infection can help to understand the long-term consequences, evaluate the impact on quality of life, plan rehabilitation and healthcare, identify the most vulnerable groups, measure the socioeconomic impact, and support public policies and clinical decisions. Objectives: The objectives of this study are as follows: (a) to assess the prevalence of functional dependence in Brazilian adults with COVID-19; (b) to analyze the association between the study variables; and (c) to determine the factors associated with functional dependence. Methods: This was an observational, cross-sectional study with 987 adults (18 to 59 years old) living in the State of Paraná (Brazil) hospitalized for COVID-19 between March and December 2020. Data were collected by telephone 12 months after the acute infection using an instrument to retrieve sociodemographic and health information, and a functional dependence scale to assess dependence before COVID-19 retrospectively (using participant recall information) and at the time of the interview. Data were analyzed using penalized logistic regression after imputing missing data. Data were analyzed using penalized logistic regression after imputing missing data. Results: Functional dependence after COVID-19 was 5.0% and was associated with low levels of education, not having a partner, living with someone, not owning a home, experiencing job changes, requiring care, obesity, smoking, multimorbidity, ICU admission in the acute phase, use of invasive ventilation, or having Long COVID. Individuals who required care or used invasive ventilation support were, respectively, 9.3 and 6.5 times more likely to develop dependence after COVID-19. Despite adjustment for multiple factors, the magnitude of the observed effects warrants cautious interpretation, as unmeasured or residual confounding effects may still be present. Sample recall bias due to collection after 12 months and the presence of the alpha variant without COVID-19 vaccination coverage may limit data generalization. Conclusions: The results highlight the need to emphasize the public health implications of identifying functional dependence. In this vein, it is necessary to implement preventive measures, identify and monitor more vulnerable groups, plan rehabilitation programs, and develop public health policies. Full article