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Immunothrombotic dysregulation in chagas disease and COVID-19: a comparative study of anticoagulation.

ABSTRACT: Chagas and COVID-19 are diseases caused by Trypanosoma cruzi and SARS-CoV-2, respectively. These diseases present very different etiological agents despite showing similarities such as susceptibility/risk factors, pathogen-associated molecular patterns (PAMPs), recognition of glycosaminoglycans, inflammation, vascular leakage hypercoagulability, microthrombosis, and endotheliopathy; all of which suggest, in part, treatments with similar principles. Here, both diseases are compared, focusing mainly on the characteristics related to dysregulated immunothrombosis. Given the in-depth investigation of molecules and mechanisms related to microthrombosis in COVID-19, it is necessary to reconsider a prompt treatment of Chagas disease with oral anticoagulants.

SUBMITTER: Perez-Campos Mayoral L

PROVIDER: S-EPMC8190527 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Immunothrombotic Dysregulation in COVID-19 Pneumonia Is Associated With Respiratory Failure and Coagulopathy.

Project description:BackgroundSevere acute respiratory syndrome corona virus 2 infection causes severe pneumonia (coronavirus disease 2019 [COVID-19]), but the mechanisms of subsequent respiratory failure and complicating renal and myocardial involvement are poorly understood. In addition, a systemic prothrombotic phenotype has been reported in patients with COVID-19.MethodsA total of 62 subjects were included in our study (n=38 patients with reverse transcriptase polymerase chain reaction-confirmed COVID-19 and n=24 non-COVID-19 controls). We performed histopathologic assessment of autopsy cases, surface marker-based phenotyping of neutrophils and platelets, and functional assays for platelet, neutrophil functions, and coagulation tests, as well.ResultsWe provide evidence that organ involvement and prothrombotic features in COVID-19 are linked by immunothrombosis. We show that, in COVID-19, inflammatory microvascular thrombi are present in the lung, kidney, and heart, containing neutrophil extracellular traps associated with platelets and fibrin. Patients with COVID-19 also present with neutrophil-platelet aggregates and a distinct neutrophil and platelet activation pattern in blood, which changes with disease severity. Whereas cases of intermediate severity show an exhausted platelet and hyporeactive neutrophil phenotype, patients severely affected with COVID-19 are characterized by excessive platelet and neutrophil activation in comparison with healthy controls and non-COVID-19 pneumonia. Dysregulated immunothrombosis in severe acute respiratory syndrome corona virus 2 pneumonia is linked to both acute respiratory distress syndrome and systemic hypercoagulability.ConclusionsTaken together, our data point to immunothrombotic dysregulation as a key marker of disease severity in COVID-19. Further work is necessary to determine the role of immunothrombosis in COVID-19.

| S-EPMC7497892 | biostudies-literature

Genome-wide PBMCs Profiling Reveals Early Detection of Immunothrombotic Dysregulation in COVID-19 based on Blood Routine Test: A Multi-Center Retrospective Study of 1219 Patients

Project description:The present study aimed to develop algorithms for early identification of patients who are at risk of being involved in abnormal immunothrombosis, enabling prompt interventions and averted progression of disease.

2021-10-06 | GSE167930 | GEO

covid-19 study

Project description:covid-19 study

| PRJEB43387 | ENA

Anticoagulation in COVID-19.

Project description: Not available

| S-EPMC8673870 | biostudies-literature

Anticoagulation in COVID-19: a single-center retrospective study.

Project description:Introduction: COVID-19 induces a pro-thrombotic state as evidenced by microvascular thrombi in the renal and pulmonary vasculature. Therapeutic anticoagulation in COVID-19 has been debated and data remain anecdotal. Hypothesis: We hypothesize that therapeutic anticoagulation is associated with a reduction in in-hospital mortality, upgrade to intensive care unit, invasive mechanical ventilation, and acute renal failure necessitating dialysis by decreasing the over-all clot burden. Methods: A retrospective cohort study was done to determine the impact of therapeutic anticoagulation in hospitalized COVID-19 patients. Independent t-test and multivariate logistic regression analysis were performed to calculate mean differences and adjusted odds ratios (aOR) with its 95% confidence interval (CI) respectively. Results: A total of 176 hospitalized COVID-19 patients were divided into two groups, therapeutic anticoagulation and prophylactic anticoagulation. The mean age, baseline comorbidities and other medications used during hospitalization were similar in both groups. The aOR for in-hospital mortality (OR 3.05, 95% CI 1.15-8.10, p = 0.04), upgrade to intensive care (OR 3.08, 95% CI 1.43-6.64, p = 0.006) and invasive mechanical ventilation (OR 4.27, 95% CI 1.95-9.34, p = 0.00) were significantly lower while there was no statistically significant difference in the rate of developing acute renal failure (OR 1.87 95% CI 0.46-7.63, p = 0.64) between two groups. Conclusions: In patients with COVID-19, therapeutic anticoagulation offers a significant reduction in the rate of in-hospital mortality, upgrade to intensive medical care, and invasive mechanical ventilation. It should be preferred over prophylactic anticoagulation in COVID-19 patients unless randomized controlled trials prove otherwise.

| S-EPMC7850331 | biostudies-literature

Test COVID-19 Study

Project description:Testing the uploader tool with COVID-19 data

| PRJEB38185 | ENA

Anticoagulation in COVID - 19: An Update.

Project description:The novel coronavirus disease, 2019 (COVID - 19) evolved as an unprecedented pandemic. The severe acute respiratory syndrome-corona virus-2 (SARS-CoV-2) infection has been associated with significantly deranged coagulation parameters and increased incidence of thrombotic events. Deranged coagulation parameters, such as D-dimers and fibrin degradation products, can indicate a poor prognosis, and their measurement will help stratify the patients according to the disease severity, need of intensive care unit admission, and prediction of the clinical course. Gaps in understanding the natural history of the disease cause difficulties in tailoring therapies and optimizing the management of patients. Lack of specific treatment further complicates this situation. While thrombotic events can cause significant morbidity and mortality in patients, a focused approach to the prevention and treatment of venous thromboembolism (VTE) can, to a great extent, decrease the disease burden caused by thrombotic diseases. Pharmacological prophylactic anticoagulants and mechanical therapies such as pneumatic compression devices can help prevent venous thromboembolism and other thrombotic events. Thrombotic events due to COVID-19, their prevention and management, are the focus of this paper, with the prospect of providing insights into this relatively unexplored area.

| S-EPMC7648443 | biostudies-literature

SnoRNAs and miRNAs expression profiles underlying COVID-19 disease severity

Project description:The causative organism, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), exhibits a wide spectrum of clinical manifestations in disease-ridden patients. Differences in the severity of COVID-19 ranges from asymptomatic infections and mild cases to the severe form, leading to acute respiratory distress syndrome (ARDS) and multiorgan failure with poor survival. MiRNAs can regulate various cellular processes, including proliferation, apoptosis, and differentiation, by binding to the 3′UTR of target mRNAs inducing their degradation, thus serving a fundamental role in post-transcriptional repression. Alterations of miRNA levels in the blood have been described in multiple inflammatory and infectious diseases, including SARS-related coronaviruses. We used microarrays to delineate the miRNAs and snoRNAs signature in the peripheral blood of severe COVID-19 cases (n=9), as compared to mild (n=10) and asymptomatic (n=10) patients, and identified differentially expressed transcripts in severe versus asymptomatic, and others in severe versus mild COVID-19 cases. A cohort of 29 male age-matched patients were selected. All patients were previously diagnosed with COVID-19 using TaqPath COVID-19 Combo Kit (Thermo Fisher Scientific, Waltham, Massachusetts), or Cobas SARS-CoV-2 Test (Roche Diagnostics, Rotkreuz, Switzerland), with a CT value < 30. Additional criterion for selection was age between 35 and 75 years. Participants were grouped into severe, mild and asymptomatic. Classifying severe cases was based on requirement of high-flow oxygen support and ICU admission (n=9). Whereas mild patients were identified based on symptoms and positive radiographic findings with pulmonary involvement (n=10). Patients with no clinical presentation were labelled as asymptomatic cases (n=10).

2022-03-01 | E-MTAB-10970 | biostudies-arrayexpress

Complement system component dysregulation is a distinctive feature of COVID-19 disease: a prospective and comparative analysis of patients admitted to the emergency department for suspected COVID-19 disease.

Project description:The complement system (CS) plays a pivotal role in Coronavirus disease 2019 (COVID-19) pathophysiology. The objective of this study was to provide a comparative, prospective data analysis of CS components in an all-comers cohort and COVID-19 patients. Patients with suspected COVID-19 infection admitted to the Emergency department were grouped for definite diagnosis of COVID-19 and no COVID-19 accordingly. Clinical presentation, routine laboratory and von Willebrand factor (vWF) antigen as well as CS components 3, 4 and activated 5 (C5a) were assessed. Also, total complement activity via the classical pathway (CH50) was determined. Levels of calprotectin in serum were measured using an automated quantitative lateral flow assay. We included 80 patients in this prospective trial. Of those 19 (23.7%) were tested positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Patients with COVID-19 had higher levels of CS components 5a and 4 (54.79 [24.14-88.79] ng/ml vs. 35 [23.15-46.1] ng/ml; p = 0.0433 and 0.3772 [± 0.1056] g/L vs. 0.286 [0.2375-0.3748] g/L; p = 0.0168). COVID-19 patients had significantly higher levels of vWF antigen when compared to the control group (288.3 [± 80.26] % vs. 212 [151-320] %; p = 0.0469). There was a significant correlation between CS C3 and 5a with vWF antigen (rs = 0.5957 [p = 0.0131] and rs = 0.5015 [p = 0.042]) in COVID-19 patients. There was no difference in calprotectin plasma levels (4.786 [± 2.397] µg/ml vs. 4.233 [± 2.142] µg/ml; p = 0.4175) between both groups. This prospective data from a single centre all-comers cohort accentuates altered levels of CS components as a distinct feature of COVID-19 disease. Deregulation of CS component 3 and C5a are associated with increased vWF antigen possibly linking vascular damage to alternative CS activation in COVID-19.

| S-EPMC8668393 | biostudies-literature

COVID-19 Vaccine Immune Responses Study (COVIRS)

Project description:Blood collected from adults pre vaccination and post vaccination to study the immune effects of COVID-19 vaccination and how they relate to antibody and T-cell responses.

2023-01-12 | GSE199750 | GEO

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