Developed by Shray Alag, The Harker School
Sections: Correlations,
Clinical Trials, and HPO
Navigate: Clinical Trials and HPO
| Name (Synonyms) | Correlation | |
|---|---|---|
| drug1219 | Dietary counselling on Food Groups according to IYC Feeding practices, WHO Wiki | 1.00 |
| Name (Synonyms) | Correlation | |
|---|---|---|
| D060085 | Coinfection NIH | 0.50 |
| D045169 | Severe Acute Respiratory Syndrome NIH | 0.04 |
| D018352 | Coronavirus Infections NIH | 0.04 |
| Name (Synonyms) | Correlation |
|---|
Navigate: Correlations HPO
There is one clinical trial.
In light of the rapidly emerging pandemic of SARS-CoV-2 infections, the global population and health care systems are facing unprecedented challenges through the combination of transmission and the potential for severe disease. Acute respiratory distress syndrome (ARDS) has been found with unusual clinical features dominated by substantial alveolar fluid load. It is unknown whether this is primarily caused by endothelial dysfunction leading to capillary leakage or direct virus induced damage. This knowledge gap is significant because the initial balance between fluid management and circulatory support appear to be decisive. On progression of the disease, bacterial superinfection facilitated by inflammation and virus related damage, has been identified as the main factor for patient outcome, but the role of the host versus the environment microbiome remains unclear. The overarching aim of the present research proposal is to improve therapeutic strategies in critically ill patients with ARDS due to SARS-CoV-2 infection by advancing the pathophysiological understanding of this novel disease. This research thus focuses on inflammation, microcirculatory dysfunction and superinfection, aiming to elucidate risk factors (RF) for the development of severe ARDS in SARS-CoV-2 infected patients and contribute to the rationale for therapeutic strategies. The hypotheses are that (I) the primary damage to the lung in SARS-CoV-2 ARDS is mediated through an exaggerated pro-inflammatory response causing primary endothelial dysfunction, and subsequently acting two-fold on the degradation of the lung parenchyma - through the primary cytokine response, and through recruitment of the inflammatory-monocyte-lymphocyte-neutrophil axis. The pronounced inflammation and primary damage to the lung disrupts the pulmonary microbiome, leading secondarily to pulmonary superinfections. (II) Pulmonary bacterial superinfections are a significant cause of morbidity and mortality in COVID-19 patients. Pathogen colonization main Risk Factor for lower respiratory tract infections. To establish colonization, pathogens have to interact with the local microbiota (a.k.a. microbiome) and certain microbiome profiles will be more resistant to pathogen invasion. Finally, (III) Handheld devices used in clinical routine are a potential reservoir and carrier of both, SARS-CoV-2, as well as bacteria causing nosocomial pneumonia.
Description: Daily recorded Vitals and Inflammatory Response will be analyzed by means of multivariable mixed effect models analysis and generalized linear models, with corrections for time and randomness. To account for the different units of measure we will standardize all values to an absolute measure by means of the z-score. The following variables will be considered: Respiratory values, Vital signs, Haemodynamic monitoring, Microcirculation, Inflammatory values, Hematology: T-cells CD3, 4 and 6 Chemistry: Inflammatory Cytokines and Biomarkers:CRP, PCT, MR-ProADM, IFN-1, IFN-γ, TNF-α/β, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12, MIG, RANTES, MCP-1, IP-10, PD1, PD-L1 Lipid-pannel3: LDL, HDL, Cholesterol, Triglyceride Other: HLA DR/DQ TBS, Swabs, sublingual nonnvasive microscopy
Measure: Change of pro-inflammatory response over the ICU stay as a causative for primary endothelial dysfunction Time: Admission, on day 0, day 1, day 2 , day 3, day 5, every 5 days up to 1 yearDescription: COX proportional hazards model and generalized mixed effect models assessing the effect of positive bacterial infection on mortality. Correction for time and randomness (multiple sampling). Super infection will be defined as a positive bacterial/ fungal sample (Bood cultures, BAL, TBS, Swabs, Urine)
Measure: Time-to-event "pulmonary bacterial superinfection or death" Time: Through study completion, an average of 30 daysDescription: Mobile devices will be swabed for bacterial and viral contamination, simultaneously adherence of the user to disinfection protocols will be assessed.
Measure: Positive bacteria and/ or SARS-CoV-2 cultures on handheld devices used in clinical routine and correlation to the adherence to disinfection protocols Time: Through study completion, an average of 30 daysDescription: SF 36 questionnaire
Measure: Life Quality after COVID-19 Infection Time: follow up 30 + 90 days and 1 year after dischargeAlphabetical 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