View clinical trials related to Pneumonia.
Filter by:Randomized, open, single-center, controlled clinical trial, with 2 treatment arms that seeks to demonstrate the effectiveness of tocilizumab against systemic corticosteroids, both treatments added to supportive treatment in patients admitted for COVID-19 with bilateral pneumonia and poor evolution
The COVID-19 pandemic is caused by the severe acute respiratory syndrome coronavirus 2 (SARS CoV-2), an emerging coronavirus, which has already infected 192 million people with a case fatality rate close to 2%. About 5% of patients infected with SARS CoV-2 have a critical form with organ failure. Among critical patients admitted to intensive care, about 70% of them will require ventilatory assistance by invasive mechanical ventilation (MV) with a mortality rate of 35% and a median MV duration of 12 days. The most severe lung damage resulting from SARS CoV-2 infection is the acute respiratory distress syndrome (ARDS). The virus infects alveolar epithelial cells and capillary endothelial cells leading to an activation of endothelium, hypercoagulability and thrombosis of pulmonary capillaries. This results in abnormal ventilation / perfusion ratios and profound hypoxemia. To date, the therapeutic management of severe SARS CoV-2 pneumonia lay on the early use of corticosteroids and Interleukin-6 (IL-6) receptor antagonist, which both reduce the need of MV and mortality. The risk factors of death in Intensive Care Unit (ICU) are: advanced age, severe obesity, coronary heart disease, active cancer, severe hypoxemia, and hepatic and renal failure on admission. Among MV patients, the death rate is doubled in those with both reduced thoracopulmonary compliance and elevated D-dimer levels. Patients with severe alveolar damage are at risk of progressing towards irreversible pulmonary fibrosis, the incidence of which still remain unknown. The diagnosis of pulmonary fibrosis is based on histology but there are some non-invasive alternative methods (serum or bronchoalveolar biomarkers, chest CT scan). We aim to assess the incidence of pulmonary fibrosis in patients with severe SARS CoV-2 related pneumonia. We will investigate the prognostic impact of fibrosis on mortality and the number of days alive free from MV at Day 90. Finally, we aim to identify risk factors of fibrosis.
The aim of the joint project PROVID is to contribute to better outcome prediction for COVID-19 patients, to better clinical management, and to the development of new therapies. To this end, the investigators will collect detailed data on the course of COVID-19 patients and deeply characterize them at the molecular level. The investigators also aim to identify compounds with the potential to improve outcome. The PROVID-PROGRESS study is being carried out as a prospective, longitudinal, multicenter observational study (case cohort study) with material asservation for genomic, transcriptomic and proteomic analyzes on adult patients with COVID-19.
The purpose of this research is to provide baseline surveillance of pneumonia in young children in Malaysia before and during the implementation of the pneumococcal conjugate vaccine (PCV). Pneumonia is a respiratory infection that can cause mild to life-threatening disease among all age groups but is the leading infectious cause of death among children globally. The most common cause of pneumonia is infection with a bacteria called Streptococcus pneumoniae, also known as pneumococcus. Hence, immunisation with a pneumococcal vaccine is an effective way to prevent pneumonia. In Malaysia, pneumococcal vaccination under the National Immunisation Programme (NIP) for children has since commenced in December 2020, comprising of 3 doses at four, six and 15 months. The routine use of PCV in children will contribute to reducing the burden of pneumococcal infections in the country, especially severe infections. The ongoing COVID-19 pandemic may also have implications on the pneumococcal serotype and clinical presentation of infections in the community.
Prospective study in a group of patients with COVID-19 pneumonia.
The pathophysiological processes involved in COVID-19 pneumonia are not fully understood. Specific alterations of the airways, lung parenchyma and pulmonary vascular tree could explain a severe ventilation/perfusion heterogeneity resulting in severe hypoxemia during the active phase of the disease. Additional skeletal muscle impairment related to systemic inflammation may also explain persisting symptoms in the follow-up phase. The first aim of the present project is to explore these different processes by evaluating the impact of the COVID-19 pneumonia on exercise capacity, pulmonary function and perfusion by a physiological and radiologic study. An ambulatory pulmonary rehabilitation will also be studied to assess its impact on the physiological parameter mentioned and the health-related quality of life questionnaire as a potential long-term treatment. The investigators propose a single center randomized controlled study at the University Hospitals of Geneva. 60 adult patients having suffered a hypoxemic COVID-19 pneumonia with persistent symptoms at 3-months after hospital discharge will be included. A functional and physiological study will be performed, including a six-minute walk test, pulmonary function testing, diffusing capacity for carbon monoxide, maximal inspiratory pressure and sniff nasal inspiratory pressure. Those with at least one abnormal value will be invited to fill the Saint Georges Respiratory Questionnaire, the Short Form 36 and the Hospital Anxiety and Depression Scale and will undergo a chest dual energy computed tomography (DECT), a cardiopulmonary exercise testing with non-invasive cardiac output and stroke volume evaluation and an evaluation of the pulmonary shunt by hyperoxia (100% oxygen breathing) at rest and during light effort. Then patients will be randomized on a 1:1 basis for pulmonary rehabilitation program or usual care. All work-up except DECT will be repeated at 6 and 12 months after hospital discharge. The investigators hypothesize that our study will allow a better understanding of pathophysiological mechanisms involved in COVID-19. This will potentially determine therapeutic target for patients with persisting symptoms and functional decay after COVID-19. The investigators also expect to see an improvement of exercise capacity and physiological parameters in the pulmonary rehabilitation group, as compared to the control group, suggesting pulmonary rehabilitation as a possible long-term treatment of this condition.
The antifibrotic agents, namely pirfenidone and nintedanib have been found to be effective in the treatment of idiopathic pulmonary fibrosis (IPF). Nintedanib has also been found to be effective in treating systemic sclerosis-related interstitial lung disease (ILD) and non-IPF progressive fibrosing ILDs. Pirfenidone has also been found beneficial unclassifiable ILDs. Whether these drugs would be effective in treating post-COVID lung fibrosis also is unknown. As the final pathway of lung fibrosis appears to be common among different diffuse parenchymal lung diseases (DPLDs), it is hoped that these antifibrotic agents might be helpful in post-COVID fibrosis. There are no randomized studies that have assessed the role of pirfenidone or nintedanib in post COVID fibrosis. In the current study, we aim to assess the efficacy and safety of pirfenidone and compare it with nintedanib in the treatment of post-COVID lung fibrosis.
Chest computed tomography of patients having coronavirus disease (COVID-19) will be analyzed with regards to vascular abnormalities (pulmonary embolism and vascular thickening), and their association with lung inflammation. The prevalence, severity, distribution, and prognostic value of chest CT findings will be assessed. Patients with vascular abnormalities will be compared to patients without, which is supposed to provide insights into the prognostic role of such abnormalities, and the potential impact on treatment strategy.
PREV-HAP study is part of a larger project entitled 'Host-targeted Approaches for the Prevention and the treatment of Hospital-Acquired Pneumonia' (HAP2), funded by the European Union's H2020 research and innovation programme under grant agreement N°847782. HAP2 aims to develop stratified host-directed drugs and biomarkers to enhance the prevention and the treatment of HAP and develop precision medicine in infectious diseases. Its ambition is to revolutionize the management of HAP: capitalising on the novel concept of critical-illness related immunosuppression altering the host-pathogens interactions, the aim is to propose a complete reappraisal of the physiopathology of HAP based on the concept of respiratory dysbiosis. The main hypothesis of the PREV-HAP study is that human recombinant Interferon gamma 1b (rHuIFN-γ, Imukin) treatment can restore immunity in critically ill patients and prevent Hospital-Acquired Pneumonia. The hypothesesis is that the in vivo investigations of the host-pathogens interactions can be used for the stratification of patients into high/low risk and responders/non-responders to host-targeted prevention of hospital-acquired infections. The involvement of a state of critical-illness related immunosuppression in the susceptibility to hospital-acquired pneumonia is widely accepted, and an emerging trend is that the development of drugs for the treatment of this acquired immunosuppression will prevent infection and enhance outcomes of hospitalized patients. It has been demonstrated that the productions of IFN-γ by immune cells are decreased in critically ill patients, and that these defects are associated with the susceptibility to HAP. rHuIFN-γ has neither been tested nor is recommended as adjunctive treatment of patients with HAP. Based on these specific factors identified in the host response, it is proposed in this study to use rHuIFN-γ as novel preventive approach for HAP.
The purpose of this study is to evaluate the safety and efficacy of omadacycline as compared to moxifloxacin in the treatment of adults with community-acquired bacterial pneumonia.