Developed by Shray Alag, The Harker School
Sections: Correlations,
Clinical Trials, and HPO
Navigate: Clinical Trials and HPO
| Name (Synonyms) | Correlation | |
|---|---|---|
| drug4099 | Two COVID-19 vaccine candidate (TMV-083) administrations - High dose Wiki | 0.50 |
| drug2691 | One COVID-19 vaccine candidate (TMV-083) administration - High dose Wiki | 0.50 |
| drug3590 | Serological testing Wiki | 0.50 |
| Name (Synonyms) | Correlation | |
|---|---|---|
| drug1472 | Extracorporeal blood purification using the oXiris® (AN69ST) hemofilter Wiki | 0.50 |
| drug4100 | Two COVID-19 vaccine candidate (TMV-083) administrations - Low dose Wiki | 0.50 |
| drug1007 | Complete thrombophilic profile testing by multiplex PCR Wiki | 0.50 |
| drug2185 | Low Molecular Weight Heparin Wiki | 0.50 |
| drug4406 | blood sampling Wiki | 0.20 |
| drug2916 | Placebo Wiki | 0.02 |
Navigate: Correlations HPO
There are 4 clinical trials
Coronavirus COVID-19 is an emerging virus also called Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). Eighty percent of patients are poor or asymptomatic. However, there are major respiratory complications for some patients, requiring intensive care hospitalization and possibly leading to death in 5% of cases. One of the hypotheses put forward is that much of the pathophysiology is due to endothelial dysfunction associated with disseminated intravascular coagulation. The covid-19 pathology could induce coagulation impairment as observed during sepsis. An increase in D-dimer levels during covid-19 disease is itself associated with excess mortality. While D-dimers are highly sensitive, they are not specific for clotting activity. They may be increased in many other circumstances, particularly in inflammation. On the other hand, the infection stimulates the release of extracellular vesicles. These vesicles, of multiple cellular origin, are an actor of vascular homeostasis, and participate in the state of hyperactivation of coagulation. They have a major role in the prothrombotic state and the development of coagulopathy associated with sepsis. The aim of our monocentric prospective study would be to study early and more specific markers of hypercoagulability and markers of routine endothelial dysfunction, as soon as the patient is hospitalized, in order to predict the risk of hospitalization in intensive care.
Description: Biological analysis using initial blood sampling
Measure: D-DIMERS plasma levels in blood Time: 1 hour after admissionDescription: Biological analysis using initial blood sampling
Measure: Fibrin monomers plasma levels in blood Time: 1 hour after admissionDescription: Biological analysis using initial blood sampling
Measure: Antithrombin plasma levels in blood Time: 1 hour after admissionDescription: Biological analysis using initial blood sampling
Measure: Prothrombin Fragment 1 plasma levels in blood Time: 1 hour after admissionDescription: Biological analysis using initial blood sampling
Measure: Prothrombin Fragment 2 plasma levels in blood Time: 1 hour after admissionDescription: Biological analysis using initial blood sampling
Measure: Thrombin generation test plasma levels in blood Time: 1 hour after admissionDescription: Biological analysis using initial blood sampling
Measure: Microvesicles of platelet plasma levels in blood Time: 1 hour after admissionDescription: Biological analysis using initial blood sampling
Measure: Cross-linked platelets plasma levels in blood Time: 1 hour after admissionDescription: Biological analysis using initial blood sampling
Measure: Willebrand Factor plasma levels in blood Time: 1 hour after admissionDescription: Biological analysis using initial blood sampling
Measure: Factor VIII plasma levels in blood Time: 1 hour after admissionThe HETHICO study aims to collect retrospectively documented clinical information on patients hospitalized in Veneto Region (Italy) for SARS-COVID-2 infection in 2 types of settings, medical environment (COORTE MED), and intensive / sub-intensive (COORTE ICU), to assess the safety and possible efficacy of the anticoagulant treatments used for thromboprophylaxis, or in preventing thrombotic complications related to hospitalization from COVID-19.
Description: Collect and evaluate in real-life the safety data of the anti-coagulant treatments used by estimating the incidence of bleeding complications during hospitalization.
Measure: Bleeding Time: 28 daysDescription: Collect and evaluate in real-life the efficacy data of the anti-coagulant treatments used by estimating the incidence of deep vein thrombosis and/or pulmonary embolism during hospitalization.
Measure: Thrombosis Time: 28 daysDescription: Collect and evaluate in real-life the data by estimating incidence of intra-hospital death.
Measure: Mortality Time: 28 daysDescription: clinical worsening with transfer to the intensive/sub-intensive ward
Measure: Worsening Time: 28 daysDescription: length of stay
Measure: LOS Time: 60 daysSeveral studies have suggested a potential clinical benefit of controlling hyper inflammation triggered by SARS-CoV-2/COVID-19. Blood purification, the removal of excessive proinflammatory mediators may control disease progression and support clinical recovery. For this purpose, COVID-19 patients might benefit from treatment with AN69ST hemofilter based extracorporeal blood purification.
Description: Systemic levels of IL-6, IL-8 and TNF-α are evaluated to assess the effect of blood purification. Measurement points: at admission, "before and after a blood purification cycle" and before discharge
Measure: Changes in cytokine levels of Interleukin (IL) 6, IL-8 and Tumor Necrosis Factor-α (pg/mL) Time: Hospitalisation window, day 0 until day 14 or until hospital discharge (whichever comes first)Description: Systemic levels of proinflammatory mediators are measured as a marker for disease severity. Measurement points: at admission, "before and after a blood purification cycle" and before discharge.
Measure: Changes in inflammatory markers; C-Reactive Protein (CRP) (mg/L) Time: Hospitalisation window, day 0 until day 14 or until hospital discharge (whichever comes first)Description: Systemic levels of thrombocytes are measured as a marker for disease severity. Measurement points: at admission, "before and after a blood purification cycle" and before discharge.
Measure: Changes in thrombocyte counts (10^3 counts/microL) Time: Hospitalisation window, day 0 until day 14 or until hospital discharge (whichever comes first)Description: Coagulation markers will be followed to assess the effect of systemic heparinisation, Measurement points, at admission, "before and after a blood purification cycle" and before discharge
Measure: Changes in the coagulation marker Fibrinogen (g/L) Time: Hospitalisation window, day 0 until day 14 or until hospital discharge (whichever comes first)Description: Duration of intensive care will be determined in relation to the number of blood purification cycles Patients will be followed for the duration of ICU stay.
Measure: ICU length of stay after admission (days) Time: An expected average of 4 - 14 hospitalisation days or until hospital discharge (whichever comes first)Description: Systemic levels of proinflammatory mediators are measured as a marker for disease severity. Measurement points: at admission, "before and after a blood purification cycle" and before discharge.
Measure: Changes in Neutrophil-to-Lymphocyte Ratio Time: Hospitalisation window, day 0 until day 14 or until hospital discharge (whichever comes first)Description: Coagulation markers will be followed to assess the effect of systemic heparinisation, Measurement points, at admission, "before and after a blood purification cycle" and before discharge
Measure: Changes in the coagulation marker D-Dimers (ng/mL) Time: Hospitalisation window, day 0 until day 14 or until hospital discharge (whichever comes first)Description: Coagulation markers will be followed to assess the effect of systemic heparinisation, Measurement points, at admission, "before and after a blood purification cycle" and before discharge
Measure: Changes in the Activation Clotting Time (seconds). Time: Hospitalisation window, day 0 until day 14 or until hospital discharge (whichever comes first)An estimated 22% of the global population is at an increased risk of a severe form of COVID-19, while one in four coronavirus patients admitted to intensive care unit will develop a pulmonary embolism. A major public health question remains to be investigated: why COVID-19 is mild for some, critically severe for others and why only a percentage of COVID-19 patients develop thrombosis, despite the disease's proven hypercoagulable state? Patients' intrinsic characteristics might be responsible for the deep variety of disease forms. Our study aims to assess the validity of the hypothesis according to which underlining genetic variations might be responsible for different degrees of severity and thrombotic events risks in the novel coronavirus disease. Moreover, we suspect that prothrombotic genotypes occuring in the genes that encode angiotensin-converting enzyme (ACE-DEL/INS) and angiotensinogen (AGT M235T) are involved in the unpredictable evolution of COVID-19, both in terms of severity and thrombotic events, due to the strong interactions of SARS-CoV-2 with the renin-angiotensin-aldosterone system (RAAS). Therefore, we also aim to assess the validity of the theory according to which there is a pre-existing atypical modulation of RAAS in COVID-19 patients that develop severe forms and/or thrombosis. Our hypothesis is based on various observations. Firstly, there is a substantial similarity with a reasonably related condition such as sepsis, for which there is a validated theory stating that thrombophilic mutations affect patients' clinical response. Secondly, racial and ethnic genetic differences are responsible for significant dissimilar thrombotic risks among various nations. Thirdly, an increase in stroke incidence has been reported in young patients with COVID-19, without essential thrombosis risk factors, favoring the idea that a genetic predisposition could contribute to increase the thrombotic and thromboembolic risk. Fourthly, the plasminogen activator inhibitor (PAI)-1 4G/5G inherited mutation was found to be responsible for a thrombotic state causing post-SARS osteonecrosis.
Description: The difference of prothrombotic genotypes frequency between the three groups
Measure: Number of patients with thrombophilic profile alterations Time: One yearDescription: The differences of RAAS components levels between the three groups
Measure: Number of patients with RAAS components alterations Time: One yearAlphabetical listing of all HPO terms. Navigate: Correlations Clinical Trials
Data processed on September 26, 2020.
An HTML report was created for each of the unique drugs, MeSH, and HPO terms associated with COVID-19 clinical trials. Each report contains a list of either the drug, the MeSH terms, or the HPO terms. All of the terms in a category are displayed on the left-hand side of the report to enable easy navigation, and the reports contain a list of correlated drugs, MeSH, and HPO terms. Further, all reports contain the details of the clinical trials in which the term is referenced. Every clinical trial report shows the mapped HPO and MeSH terms, which are also hyperlinked. Related HPO terms, with their associated genes, protein mutations, and SNPs are also referenced in the report.
Drug Reports MeSH Reports HPO Reports