Therapeutic Strategies for Treatment of COVID-19

2022 ◽  
pp. 55-72
Author(s):  
Lahcen Tamegart ◽  
Mjid Oukhrib ◽  
Hafida El Ghachi ◽  
Abdelali Ben Maloui ◽  
Abdelaati El Khiat ◽  
...  
Keyword(s):  
Infectious Disease ◽  
Immune Response ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Virus Entry ◽  
Therapeutic Strategies ◽  
Strong Immune Response ◽  
Immunomodulatory Agents

Coronavirus disease 2019 (COVID-19) is an emerging infectious disease caused by a dangerous virus named SARS-CoV-2. The most important symptoms are fever, cough, fatigue, and breathing problems. In the most serious forms of the disease, the appearance of an acute respiratory distress syndrome caused by the virus can be deadly, especially when people are fragile due to their age or in case of comorbidities. The exacerbated innate immune response could be another deadly complication. Different strategies of treatments are proposed for COVID-19 such as inhibition of virus entry by blocking ACE2 receptor used by COVID-19, inhibition of virus replication by using replication inhibitors, immunomodulatory agents to stimulate a strong immune response against COVID-19, and by using vaccines as an effective method for a long-term strategy for prevention of COVID-19.

Long term veno-venous extracorporeal life support without intravenous anticoagulation for diffuse alveolar hemorrhage

Perfusion ◽  
2019 ◽  
Vol 34 (6) ◽  
pp. 523-525 ◽  
Author(s):  
Samuel M Galvagno ◽  
Nirav G Shah ◽  
Christopher R Cornachione ◽  
Kristopher B Deatrick ◽  
Michael A Mazzeffi ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Life Support ◽  
Extracorporeal Life Support ◽  
Diffuse Alveolar Hemorrhage ◽  
Alveolar Hemorrhage ◽  
Systemic Anticoagulation

Introduction: Diffuse alveolar damage is the histologic hallmark for the acute phase of acute respiratory distress syndrome and can occasionally present as diffuse alveolar hemorrhage. Case report: We report a patient with diffuse alveolar hemorrhage and acute respiratory distress syndrome requiring veno-venous extracorporeal life support for 210 days, who was successfully treated for a period of 130 consecutive days without intravenous anticoagulation. Discussion: Although there are a few brief reports detailing long extracorporeal life support runs, the literature is largely devoid of data regarding long-term extracorporeal life support without full systemic anticoagulation. Regular inspection of the extracorporeal membrane oxygenation circuit is critical because externally visible thrombi may predict internal thrombus generation with the potential for systemic embolization or abrupt oxygenator failure. In our case, multiple circuit and oxygenators changes were required. Conclusion: We have demonstrated that a patient with a contraindication for systemic anticoagulation can safely have veno-venous extracorporeal life support for prolonged periods without catastrophic thrombotic complications.

scholarly journals Long-Term Pulmonary Function and Quality of Life in Children After Acute Respiratory Distress Syndrome

2017 ◽  
Vol 18 (1) ◽  
pp. e48-e55 ◽  
Author(s):  
Shan L. Ward ◽  
Autumn Turpin ◽  
Aaron C. Spicer ◽  
Marsha J. Treadwell ◽  
Gwynne D. Church ◽  
...  
Keyword(s):  
Quality Of Life ◽  
Acute Respiratory Distress Syndrome ◽  
Pulmonary Function ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome

Healthcare costs and long-term outcomes after acute respiratory distress syndrome: A phase III trial of inhaled nitric oxide*

2006 ◽  
Vol 34 (12) ◽  
pp. 2883-2890 ◽  
Author(s):  
Derek C. Angus ◽  
Gilles Clermont ◽  
Walter T. Linde-Zwirble ◽  
Amjad A. Musthafa ◽  
Tony T. Dremsizov ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Healthcare Costs ◽  
Distress Syndrome ◽  
Phase Iii ◽  
Long Term Outcomes ◽  
Phase Iii Trial

scholarly journals Early Upregulation of Acute Respiratory Distress Syndrome-Associated Cytokines Promotes Lethal Disease in an Aged-Mouse Model of Severe Acute Respiratory Syndrome Coronavirus Infection

2009 ◽  
Vol 83 (14) ◽  
pp. 7062-7074 ◽  
Author(s):  
Barry Rockx ◽  
Tracey Baas ◽  
Gregory A. Zornetzer ◽  
Bart Haagmans ◽  
Timothy Sheahan ◽  
...  
Keyword(s):  
Immune Response ◽  
Acute Respiratory Distress Syndrome ◽  
Severe Acute Respiratory Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Host Response ◽  
Molecular Mechanisms ◽  
Distress Syndrome ◽  
Aged Mice ◽  
Young Mice

ABSTRACT Several respiratory viruses, including influenza virus and severe acute respiratory syndrome coronavirus (SARS-CoV), produce more severe disease in the elderly, yet the molecular mechanisms governing age-related susceptibility remain poorly studied. Advanced age was significantly associated with increased SARS-related deaths, primarily due to the onset of early- and late-stage acute respiratory distress syndrome (ARDS) and pulmonary fibrosis. Infection of aged, but not young, mice with recombinant viruses bearing spike glycoproteins derived from early human or palm civet isolates resulted in death accompanied by pathological changes associated with ARDS. In aged mice, a greater number of differentially expressed genes were observed than in young mice, whose responses were significantly delayed. Differences between lethal and nonlethal virus phenotypes in aged mice could be attributed to differences in host response kinetics rather than virus kinetics. SARS-CoV infection induced a range of interferon, cytokine, and pulmonary wound-healing genes, as well as several genes associated with the onset of ARDS. Mice that died also showed unique transcriptional profiles of immune response, apoptosis, cell cycle control, and stress. Cytokines associated with ARDS were significantly upregulated in animals experiencing lung pathology and lethal disease, while the same animals experienced downregulation of the ACE2 receptor. These data suggest that the magnitude and kinetics of a disproportionately strong host innate immune response contributed to severe respiratory stress and lethality. Although the molecular mechanisms governing ARDS pathophysiology remain unknown in aged animals, these studies reveal a strategy for dissecting the genetic pathways by which SARS-CoV infection induces changes in the host response, leading to death.

Sign in / Sign up

Export Citation Format

Share Document