Active clinical trials for "COVID-19"

The prevalence and clinical relevance of viremia in patients with COVID-19 have not been well investigated. Seeking to understand the need for dentistry to perform bloody procedures in critically ill patients with COVID-19 admitted to the ICU, the quantification of the magnitude of viral replication may play a fundamental role in this scenario. For this, it is necessary to study the viremia kinetics of SARS-CoV-2, seeking to assess whether there is any characteristic pattern that may be associated with a worse clinical outcome of the patient with COVID-19 after undergoing bloody dental procedures, therefore, the objective of this research will be to investigate the occurrence of viral kinetics produced by dental procedures in patients with SARS-CoV-2 in Intensive Care Units, where, in addition to analyzing the oral health condition, the viral kinetics of SARS-CoV-2 will also be investigated by means of reverse transcription polymerase chain reaction (RT-PCR) examination of blood samples from patients with COVID-19 undergoing bloody dental treatment. This research is expected to identify risks and consequences regarding the possibility of performing bloody dental treatment in patients with COVID-19 in serious condition, in addition to verifying the association of the impact of oral infection foci on this profile of patients.

Patients with post-Covid-19 syndrome are at high risk of developing cardiovascular diseases 12 months after acute infection of COVID-19. We recently revealed that these patients have elevated muscular sympathetic nerve activity (MSNA), vascular dysfunction, impaired cardiac diastolic function, and reduced functional capacity. Considering that these outcomes are independent predictors of cardiovascular mortality, it is urgent to restore the cardiovascular health of these patients. High resistance inspiratory muscle strength training (IMST) at 75% of pressure inspiratory (PImax) performed at home (5 min/session, 5-7 times/week per 6 weeks) reduces the MSNA, improves the endothelial function and lowers blood pressure in different populations. Based on these findings, IMST (75% PImax) is an excellent therapeutic option for patients with post-COVID-19 syndrome. Therefore, the aim of the present proposal is to test whether IMST (75% PImax) reduces sympathetic activity, improves vascular function, and restores cardiac function, evoking an increase in functional capacity in patients with post-COVID-19 syndrome. To test these hypotheses we will conduct a randomized, double-blind, sham-controlled clinical trial to test these hypotheses.

Cognitive impairment is increasingly recognised as a major component of long Covid, and is estimated to be present in 25-75% of affected individuals. This impairment impacts quality of life and the loss of functional ability has major consequences for affected people, their families and the wider economy given people's difficulty in returning to work. This study will focus on helping people recover from cognitive Covid. This will involve use of rehabilitation strategies aimed at improving function in those cognitive functions identified in Stage 1 as being most affected, and assessing the benefit of rehabilitation on quality of life and people's ability to return to everyday function. These strategies will be co-produced in collaboration with a group of people living with cognitive Covid. At the end of Stage 2 we will produce a freely available "Covid-19 Cognitive Recovery Guide" for affected people, their close contacts and clinicians. In conclusion, cognitive impairment is frequently observed in long Covid but at present little is understood about its nature, or how it can be treated. The sheer scale of the CV19 pandemic makes this a top priority unmet need for healthcare worldwide. The aim of this study is to meet this need and to deliver a treatment plan for affected people which will help them return to normal life and working ability.

The main aim is to determine whether vitamin C can reduce 28-day all-cause mortality or persistent organ dysfunction compared with placebo in patients with severe and critical ill COVID-19 patients. Participants will randomly receive HIVC or placebo for 4 days once enrolled. The primary outcome is a composite of death or persistent organ dysfunction (defined as dependency on vasopressors, mechanical ventilation, or CRRT) at day 28 after randomization.

Aspirin-exacerbated respiratory disease (AERD) is characterized by the presence of asthma, chronic rhinosinusitis with nasal polyposis (CRwNP), and acute respiratory reactions induced by aspirin and other cyclooxygenase-1 inhibitors. One of the well-established therapeutic options is aspirin desensitization followed by daily aspirin therapy. The potential mechanisms underlying the clinical benefit of this approach include the downregulation of CysLT1 receptor, inhibition of PGD2 and interleukin IL-4 via the signal transducer and activator of transcription 6, global (blood, urine) activation of type 2 (T2) inflammation as well as local (sputum) reduction of T2 asthma inflammation. Indeed, among current aspirin-treated patients with AERD (n=37), no one had severe acute respiratory syndrome coronavirus clade 2 (SARS CoV-2) infection and most importantly, none of them developed COVID19 during pandemic. WHY? Notably, patients with AERD did not have asthma and nasal polyps exacerbation on aspirin, which is in line with other studies. Respiratory infections, such as the current COVID-19 pandemic, target epithelial cells in the respiratory tract. SARS-CoV-2 spike (S) protein binds angiotensin-converting enzyme 2 (ACE2), and in concert with host proteases, principally transmembrane serine protease 2 (TMPRSS2), promotes cellular entry. Nasal and bronchial epithelium play a key role in the early phases of an immune response to respiratory viruses. Induced sputum (IS) and nasal lavage (NL) cells are likely the first immune cells to encounter SARS CoV-2 during an infection, and their reaction to the virus will have a profound impact on the outcome of the infection. Interferons (IFNs) are antiviral cytokines and among the first mediators produced upon viral infection. IFNs are divided into three groups based on their receptor usage; type I IFNs (IFN-α and IFN-β), type II IFN (IFN-γ), and type III IFNs (IFN-λ1 and 2). Both production of IFN and cellular response to IFN are critical steps for the restriction of viral dissemination. An interferon-stimulated gene (ISG) is a gene whose expression is stimulated by interferon. Specifically, type I and type III interferons are antiviral cytokines, triggering ISGs that combat viral infections. The type II interferon class only has one cytokine (IFN-γ), which has some antiviral activity. To conclude, the assessment of gene expression for interferon α1 (IFNA1), interferon β1 (IFNB1), interferon γ (IFNG), interferon λ1 and λ2 (IFNL1 and IFNL2) as well as for ACE2 and TMPRSS2 in sputum and nasal cells may shed new light on the course of this infection in patient with AERD during long term aspirin therapy.

The primary objectives of this study are to establish exercise training as a novel intervention to treat Long COVID and characterize the cardiorespiratory and autonomic physiology in these patients to precisely characterize mechanisms contributing to this syndrome.

The purpose of this research is to study if post-Covid patients using a wearable brain sensing wellness device (Muse-S) to learn meditation practice during a time where they are experiencing lengthy Covid symptoms will help in decreasing stress and anxiety.

This pilot open-label randomized controlled trial aims to assess if treatment with sulodexide may improve the endothelial status and inflammatory response in post-COVID-19 patients. Survived inpatients with severe-to-critical COVID-19 within 14 days after discharge are randomized to receive sulodexide 250 LSU 1 oral capsule twice daily or no treatment for 8 weeks. Biomarkers of endothelial dysfunction, inflammation, and prothrombotic changes are assessed at 0, 4, and 8 weeks. The hypothesis is that affected endothelial function, pro-inflammatory, and pro-thrombotic changes could be improved with sulodexide treatment in convalescent COVID-19 patients who suffered a severe-to-critical clinical presentation and have chronic comorbidities of high risk for endothelial dysfunction.

Long COVID is a common but highly debilitating illness which develops after infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2 or COVID-19). It is thought to affect as many as 1 in 7 people following COVID-19 infection. It can produce a vast array of symptoms including fatigue, breathlessness, fast heart rate, blood pressure disturbance, temperature disturbance, and dry mouth. Many of these symptoms could be explained by the nervous system being predominantly in a stress or 'fight or flight' response, also known as dysautonomia. One way of assessing whether this is the case is by measuring heart rate variability (HRV). This is the time variation between heart beats and is a marker of how stressed the nervous system is or how strong is the 'fight or flight' response. Heart rate variability can be measured using devices which are worn round the wrist or attach to the chest. An increased variability in heart rate corresponds with a more relaxed nervous system and decreased variability with a more stressed nervous system. Monitoring HRV in real-time and implementing interventions such as a breathing regime to maximise HRV is known as HRV biofeedback. The body can be trained out of the fight or flight response and into the 'rest and digest' mode response of the nervous system in this way and potentially significantly improve symptoms. We propose that for people with Long COVID, a programme of structured breathing exercises over 4 weeks whilst tracking HRV can demonstrate an improvement in HRV and consequently improve Long COVID symptoms.

This is an open-label run-in followed by a randomized, double-blind drug treatment study of COVID-19 infected patients requiring inpatient hospital admission.