Steroids: A Therapeutic Option for COVID-19 Pneumonia Patients With ESRD?
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ABSTRACT:
SUBMITTER: Delafosse M
PROVIDER: S-EPMC7298510 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundWe use longitudinal chest CT images to explore the effect of steroids therapy in COVID-19 pneumonia which caused pulmonary lesion progression.Materials and methodsWe retrospectively enrolled 78 patients with severe to critical COVID-19 pneumonia, among which 25 patients (32.1%) who received steroid therapy. Patients were further divided into two groups with severe and significant-severe illness based on clinical symptoms. Serial longitudinal chest CT scans were performed for each patient. Lung tissue was segmented into the five lung lobes and mapped into the five pulmonary tissue type categories based on Hounsfield unit value. The volume changes of normal tissue and pneumonia fibrotic tissue in the entire lung and each five lung lobes were the primary outcomes. In addition, this study calculated the changing percentage of tissue volume relative to baseline value to directly demonstrate the disease progress.ResultsSteroid therapy was associated with the decrease of pneumonia fibrotic tissue (PFT) volume proportion. For example, after four CT cycles of treatment, the volume reduction percentage of PFT in the entire lung was -59.79[±12.4]% for the steroid-treated patients with severe illness, and its p-value was 0.000 compared to that (-27.54[±85.81]%) in non-steroid-treated ones. However, for the patient with a significant-severe illness, PFT reduction in steroid-treated patients was -41.92[±52.26]%, showing a 0.275 p-value compared to -37.18[±76.49]% in non-steroid-treated ones. The PFT evolution analysis in different lung lobes indicated consistent findings as well.ConclusionSteroid therapy showed a positive effect on the COVID-19 recovery, and its effect was related to the disease severity.
| S-EPMC9329540 | biostudies-literature
Project description:The 2019 novel coronavirus (officially known as severe acute respiratory syndrome coronavirus 2, SARS-CoV2) was first found in Wuhan, China. On February 11, 2020, the World Health Organization (WHO) has declared the outbreak of the disease caused by SARS-CoV2, named coronavirus disease 2019 (COVID-19), as an emergency of international concern. Based on the current epidemiological surveys, some COVID-19 patients with severe infection gradually develop impairment of the respiratory system, acute kidney injury (AKI), multiple organ failure, and ultimately, death. Currently, there is no established pharmacotherapy available for COVID-19. As seen in influenza, immune damage mediated by excessive production of inflammatory mediators contributes to high incidence of complications and poor prognosis. Thus, removal or blocking the overproduction of these mediators potentially aids in reducing the deleterious cytokine storm and improving critically ill patients' outcomes. Based on previous experience of blood purification to treat cytokine storm syndrome (CSS) in severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), here we aimed to review the current literature on extracorporeal hemoperfusion as a potential therapeutic option for CSS-associated conditions, with a focus on severe COVID-19.
| S-EPMC7587998 | biostudies-literature
Project description:With the number of Coronavirus Disease 2019 (COVID-19) cases soaring worldwide and limited vaccine availability for the general population in most countries, the monoclonal antibody (mAb) remains a viable therapeutic option to treat COVID-19 disease and its complications, especially in the elderly individuals. More than 50 monoclonal antibody-related clinical trials are being conducted in different countries around the world, with few of them nearing the completion of the third and fourth phase clinical trial. In view of recent emergency use authorization (EUA) from the FDA (Food and Drug Administration) of casirivimab and imdevimab, it is of importance that mAbs, already used to treat diseases such as Ebola and respiratory syncytial virus (RSV) infection, are discussed in scientific communities. This brief review discusses the mechanism of action and updates to clinical trials of different monoclonal antibodies used to treat COVID-19, with special attention paid to SARS-CoV-2 immune response in host cells, target viral structures, and justification of developing mAbs following the approval and administration of potential effective vaccine among vulnerable populations in different countries.
| S-EPMC7872849 | biostudies-literature
Project description:Background: Outcomes in patients with severe SARS-CoV-2 infection (COVID-19) are conditioned by viral control and regulation of inflammation. Variants in IFIH1, a gene coding the cytoplasmatic RNA sensor MDA5, regulate the response to viral infections. Methods: Patients admitted to an intensive care unit (ICU) with documented COVID-19 were prospectively included and IFIH1 rs1990760 genotypes determined. Peripheral blood gene expression, cell populations and immune mediators were measured during the first day after ICU admission before steroid therapy. Peripheral blood mononuclear cells from healthy volunteers were exposed ex-vivo to an MDA5 agonist and dexamethasone, and changes in gene expression assessed. ICU discharge and hospital death were modelled using rs1990760 variants and dexamethasone therapy as factors. Findings: 237 patients were studied. Patients with the IFIH1 rs1990760 TT variant showed a decrease in expression of inflammation-related pathways, an anti-inflammatory cell profile and a decrease in pro-inflammatory mediators. Cells with TT variant exposed to an MDA5 agonist ex-vivo showed an increase in FOXO3 and IL6 when dexamethasone was added. All patients with the TT variant not treated with steroids (n=14) survived their ICU stay (HR 2.49 95% confidence interval 1.29 – 4.79). Dexamethasone therapy in this subgroup (N=50) delayed ICU discharge and increased hospital mortality (HR 2.19, 95% confidence interval 1.01 – 4.87) and serum IL-6 concentrations. Interpretation: COVID-19 ICU patients with the IFIH1 rs1990760 TT variant show an ameliorated inflammatory response that results in better outcomes than CC/CT variants. Dexamethasone can reverse this anti-inflammatory phenotype, worsening the outcome. Funding: Instituto de Salud Carlos III.
2021-07-03 | GSE177025 | GEO
Project description:Coronavirus disease 2019 (COVID-19) is a pandemic viral disease originated in Wuhan, China, in December 2019, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The severe form of the disease is often associated with acute respiratory distress syndrome (ARDS), and most critically ill patients require mechanical ventilation and support in intensive care units. A significant portion of COVID-19 patients also develop complications of the cardiovascular system, primarily acute myocardial injury, arrhythmia, or heart failure. To date, no specific antiviral therapy is available for patients with SARS-CoV-2 infection. Exosomes derived from mesenchymal stem cells (MSCs) are being explored for the management of a number of diseases that currently have limited or no therapeutic options, thanks to their anti-inflammatory, immunomodulatory, and pro-angiogenic properties. Here, we briefly introduce the pathogenesis of SARS-CoV-2 and its implications in the heart and lungs. Next, we describe some of the most significant clinical evidence of the successful use of MSC-derived exosomes in animal models of lung and heart injuries, which might strengthen our hypothesis in terms of their utility for also treating critically ill COVID-19 patients.
| S-EPMC7565764 | biostudies-literature
Project description:The rapid spread of SARS-CoV-2 and the resulting pandemic has led to a spasmodic search for approaches able to limit the diffusion of the disease. The epigenetic machinery has aroused considerable interest in the last decades, and much evidence has demonstrated that this type of modification could regulate the early stages of viral infection. Recently it was reported that N6-methyladenosine (m6A) influences SARS-CoV-2 replication, although its role remains to be further investigated. The knockdown of enzymes involved in the m6A pathway could represent an optimal strategy to deepen the epigenetic mechanism. In the present study, we blocked the catalytic activity of the fat mass and obesity-associated protein (FTO) by using the selective inhibitor rhein. We observed a strong broad-spectrum reduction of infectivity caused by various coronaviruses, including SARS-CoV-2. This effect could be due to the modulation of m6A levels and could allow identification of this modification as a new therapeutic target to treat SARS-CoV-2 infection.
| S-EPMC8625908 | biostudies-literature
Project description:IntroductionCoronavirus disease (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2. Although most patients with COVID-19 develop asymptomatic or mild disease, some patients develop severe disease. The effectiveness of various therapeutic agents, including antiviral drugs, steroids, and anti-inflammatories for COVID-19, have been being confirmed. The effect of administering steroids in early disease is unclear. This study therefore aimed to evaluate the effectiveness and risk of exacerbation of steroids administered preceding antiviral drugs in patients with COVID-19 pneumonia.MethodsThis retrospective, single-center, observational study included consecutive patients with COVID-19 between March 2020 and March 2021. Patients were divided into a steroids-first group and antiviral-drugs-first group. Mortality, duration of hospitalization, incidence rate and duration of intensive care unit (ICU) admission, intubation, and extracorporeal membrane oxygenation (ECMO) induction of the two groups were compared.ResultsA total of 258 patients were admitted during the study period. After excluding patients who received symptomatic treatment only, who were taking immunosuppressive drugs, or who were administered antiviral drugs only, 68 patients were included in the analysis, 16 in the steroids-first group and 52 in the antiviral-drugs-first group. The rate of intubation, ICU admission and ECMO induction were significantly higher in the steroids-first group than in the antiviral-drugs-first group (81.3% vs. 33.3, p<0.001, 75.0% vs. 29.4%, p = 0.001, and 31.3% vs. 7.8%, p = 0.017, respectively). Furthermore, patients who received steroids within ten days after starting antiviral drugs had significantly lower rates of ICU admission, intubation, and ECMO induction. (81.3% vs. 42.9% p = 0.011, 75.0% vs. 37.1% p = 0.012, and 31.3% vs. 8.6% p = 0.039, respectively).ConclusionsAdministering steroids prior to antiviral drugs soon after symptom onset can aggravate disease severity. When administration of steroids is considered soon after symptom onset, it may be safer to initiate antiviral drugs first.
| S-EPMC8412353 | biostudies-literature
Project description:Anthraquinone derivatives are identified for their immune-boosting, anti-inflammatory, and anti-viral efficacy. Hence, the present study aimed to investigate the reported anthraquinone derivatives as immune booster molecules in COVID-19 infection and evaluate their binding affinity with three reported targets of novel coronavirus i.e. 3C-like protease, papain-like protease, and spike protein. The reported anthraquinone derivatives were retrieved from an open-source database and filtered based on a positive druglikeness score. Compounds with positive druglikeness scores were predicted for their targets using DIGEP-Pred and the interaction among modulated proteins was evaluated using STRING. Further, the associated pathways were recorded concerning the Kyoto Encyclopedia of Genes and Genomes pathway database. Finally, the docking was performed using autodock4 to identify the binding efficacy of anthraquinone derivatives with 3C-like protease, papain-like protease, and spike protein. After docking the pose of ligand scoring minimum binding energy was chosen to visualize the ligand-protein interaction. Among 101 bioactives, 36 scored positive druglikeness score and regulated multiple pathways concerned with immune modulation and (non-) infectious diseases. Similarly, docking study revealed torososide B to possess the highest binding affinity with papain-like protease and 3C-like protease and 1,3,6-trihydroxy-2-methyl-9,10-anthraquinone-3-O-(6'-O-acetyl)-?-D-xylopyranosyl-(1?? 2)-?-D-glucopyranoside with spike protein.
| S-EPMC7414902 | biostudies-literature
Project description:IntroductionCOVID 19 pneumonia can lead to an inappropriate inflammatory response, and can be complicated by acute respiratory distress syndrome, multivisceral failure with a high mortality rate.ObjectiveTo observe the effect of therapeutic plasma exchange on the excessive inflammatory response.Materials and methodsIn this study, we included 7 confirmed cases of COVID-19 in the intensive care unit (ICU) department of the university hospital of Oujda. COVID-19 cases were confirmed by RT PCR (reverse transcription-polymerase chain) and CT (computerized tomography) imaging according to WHO guidelines. Therapeutic plasma exchange was performed decrease cytokine storm-induced ARDS (Acute respiratory distress syndrome). Inflammation marker assays were performed before and after therapeutic plasma exchange to assess its efficacy.ResultsLevels of inflammatory cytokines (IL-6) and acute phase response proteins, including ferritin and CRP, were elevated before therapeutic plasma exchange.After therapeutic plasma exchange, levels of acute phase reactants, inflammatory mediators, were significantly reduced (p < 0.05).ConclusionOur data suggest that therapeutic plasma exchange reduces the inflammatory response in patients with severe COVID-19 not undergoing mechanical ventilation. Further studies are needed to explore the efficacy of therapeutic plasma exchange in patients with COVID-19.
| S-EPMC8495054 | biostudies-literature
Project description: Not available
| S-BSST416 | biostudies-other