View clinical trials related to Covid19.
Filter by:The COVID-19 pandemic has been spreading continuously, and in Brazil, until August 18, 2020, there have been more than 3,359,000 cases with more than 108,536 deaths, with daily increases. The present study proposes to evaluate the efficacy and safety of using convalescent plasma for treating patients with COVID-19 pneumonia without indication of ventilatory support.
Time to recover of Anosmia and / or ageusia and early corticosteroid use
COVID-19 is associated with acute pulmonary and cardiac injury. To better understand the degree and severity of cardiopulmonary injury as well as short and long-term sequelae of COVID-19 infection, this study will perform longitudinal study in patients who had recent known diagnosis of COVID-19.
This study is an open-label, single-arm study to evaluate the safety and efficacy of Astrostem-V, allogenic adipose tissue derived mesenchymal stem cells (AdMSC), in patients with COVID-19 pneumonia. After each subject completes 12-Weeks visit (Visit 12) and the data management team confirms all individual data have no issue, the individual database will be locked and the blinding will be open for the statistical analysis.
People living with HIV could have different susceptibility and outcome to the SARS CoV-2 infection. The risk of SARS CoV-2 infection in this population could be no related to HIV infection, immunodepression or antiretroviral therapy, but to the different susceptibility as measured by ACE2 or CD26 receptors. Also, patients with HIV-1 infection could have different cytokine profile and cellular immune response after SARS-CoV-2 infection, leading to a differential outcome,
This project covers several research aims. In a cohort study, the investigators aim to compare confirmed COVID-19 patients with non-COVID-19 patients who undergo surgical treatment and study factors associated with good or bad outcomes.
Considering the potential of mesenchymal stromal cells (MSCs) in the treatment of lung injuries by COVID-19, this pilot clinical trial evaluates the safety and potential efficacy of the cell therapy, administered intravenously, in patients with pneumonia associated with COVID-19-associated acute respiratory distress syndrome.
Morphine is used in the treatment of dyspnea and polypnea with a proven benefit on the improvement of these symptoms, both etiologically and symptomatically. This medication is used in particular in palliative care for this type of symptom. The Sars CoV2 viral pneumonia table can lead to respiratory distress. In patients with moderate to severe impairment without goal of resuscitation (level of care 3 and 4), the introduction of morphine may sometimes be necessary to relieve respiratory symptoms. These also lead to major exhaustion which can worsen the clinical picture. However, the prescription of morphine is not systematic in front of a respiratory distress table. The investigators hypothesized that early treatment with morphine lead to a better management of dyspnea, quality of live and survival in COVID-19 positive participants patients when there is not resuscitation objective management (level of care 3 and 4). The objective is to measure the efficacy of morphine in the early management of dyspnea, quality of life and survival in COVID-19 positive participants patients treated in the Hospices Civils of Lyon during COVID-19 pandemic.
Coronaviruses are enveloped viruses with an RNA genome. Carrageenans are sulfate polysaccharides synthesized by red algae. Studies conducted in adults and children with the common cold showed the effectiveness of the use of Carrageenan in nasal spray. For decades, the antiviral action of Carrageenans has been described in numerous studies with different viruses that infect humans: herpes viruses types 1 and 2, human immunodeficiency virus, human papillomavirus, H1N1 influenza virus, dengue virus, rhinovirus, hepatitis A virus, and enteroviruses. Studies on the dynamics of COVID-19 disease show an intense and rapid pharyngeal multiplication in the first 3-5 days of the onset of symptoms, prior to the onset of pulmonary disease. Finally, this molecule has shown a viricidal effect against SARS-Cov2 in vitro. All this underscores the potential value of a therapy that inhibits the virus in the rhinopharynx.
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.