Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 20 de 27
Filter
1.
Infect Drug Resist ; 13: 3715-3725, 2020.
Article in English | MEDLINE | ID: covidwho-1389036

ABSTRACT

The renin-angiotensin system (RAS) is the most important regulatory system of electrolyte homeostasis and blood pressure and acts through angiotensin-converting enzyme (ACE)/angiotensin II (Ang II)/Ang II type 1 (AT1) receptor axis and angiotensin-converting enzyme 2 (ACE2)/angiotensin (1-7)/MAS receptor axis. RAS dysfunction is related to the occurrence and development of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) and causes a serious prognosis and even death. ALI/ARDS can be induced by various ways, one of which is viral infections, such as SARS-CoV, SARS-CoV-2, H5N1, H7N9, and EV71. This article reviews the specific mechanism on how RAS dysfunction affects ALI/ARDs caused by viral infections. SARS-CoV and SARS-CoV-2 enter the host cells by binding with ACE2. H5N1 and H7N9 avian influenza viruses reduce the ACE2 level in the body, and EV71 increases Ang II concentration. Treatment with angiotensin-converting enzyme inhibitor and angiotensin AT1 receptor blocker can alleviate ALI/ARDS symptoms. This review provides suggestions for the treatment of lung injury caused by viral infections.

2.
Vasc Health Risk Manag ; 17: 273-298, 2021.
Article in English | MEDLINE | ID: covidwho-1262578

ABSTRACT

COVID-19 sepsis is characterized by acute respiratory distress syndrome (ARDS) as a consequence of pulmonary tropism of the virus and endothelial heterogeneity of the host. ARDS is a phenotype among patients with multiorgan dysfunction syndrome (MODS) due to disseminated vascular microthrombotic disease (VMTD). In response to the viral septicemia, the host activates the complement system which produces terminal complement complex C5b-9 to neutralize pathogen. C5b-9 causes pore formation on the membrane of host endothelial cells (ECs) if CD59 is underexpressed. Also, viral S protein attraction to endothelial ACE2 receptor damages ECs. Both affect ECs and provoke endotheliopathy. Disseminated endotheliopathy activates two molecular pathways: inflammatory and microthrombotic. The former releases inflammatory cytokines from ECs, which lead to inflammation. The latter initiates endothelial exocytosis of unusually large von Willebrand factor (ULVWF) multimers and FVIII from Weibel-Palade bodies. If ADAMTS13 is insufficient, ULVWF multimers activate intravascular hemostasis of ULVWF path. In activated ULVWF path, ULVWF multimers anchored to damaged endothelial cells recruit circulating platelets and trigger microthrombogenesis. This process produces "microthrombi strings" composed of platelet-ULVWF complexes, leading to endotheliopathy-associated VMTD (EA-VMTD). In COVID-19, microthrombosis initially affects the lungs per tropism causing ARDS, but EA-VMTD may orchestrate more complex clinical phenotypes, including thrombotic thrombocytopenic purpura (TTP)-like syndrome, hepatic coagulopathy, MODS and combined micro-macrothrombotic syndrome. In this pandemic, ARDS and pulmonary thromboembolism (PTE) have often coexisted. The analysis based on two hemostatic theories supports ARDS caused by activated ULVWF path is EA-VMTD and PTE caused by activated ULVWF and TF paths is macrothrombosis. The thrombotic disorder of COVID-19 sepsis is consistent with the notion that ARDS is virus-induced disseminated EA-VMTD and PTE is in-hospital vascular injury-related macrothrombosis which is not directly  related to viral pathogenesis. The pathogenesis-based therapeutic approach is discussed for the treatment of EA-VMTD with antimicrothrombotic regimen and the potential need of anticoagulation therapy for coinciding macrothrombosis in comprehensive COVID-19 care.


Subject(s)
COVID-19/epidemiology , Endothelial Cells/metabolism , Fibrinolytic Agents/therapeutic use , Hemostasis/physiology , SARS-CoV-2 , Sepsis/complications , Thrombosis/etiology , COVID-19/complications , Humans , Pandemics , Phenotype , Sepsis/metabolism , Thrombosis/drug therapy , Thrombosis/metabolism
3.
Cureus ; 13(4): e14280, 2021 Apr 03.
Article in English | MEDLINE | ID: covidwho-1212081

ABSTRACT

Coronavirus disease 2019 (COVID-19) is known to be primarily a viral infection affecting the pulmonary system leading to severe pneumonia and acute respiratory distress syndrome. COVID-19 has also been found to affect the neurological system causing various nerve palsies. While some studies have suggested these neurological manifestations may indicate severe disease, cranial nerve palsies in the setting of COVID-19 infection have been linked to improved patient outcomes and mild viral symptoms. We present a case of a 55-year-old male with confirmed COVID-19 infection presenting with third cranial nerve palsy. Since his hospital course remained unremarkable, he was treated supportively for his COVID-19 infection and remained stable on room air during his hospitalization. No causative factors other than COVID-19 were identified as a cause for his cranial three nerve palsy which resolved spontaneously during outpatient follow-up. Although different cranial nerve palsies associated with COVID-19 infection have been identified in the literature, the pathogenesis and prognosis of cranial nerve palsy is still unclear. This case emphasizes the need for continued symptom monitoring and identification in patients diagnosed with COVID-19.

4.
Curr Mol Med ; 22(4): 312-324, 2022.
Article in English | MEDLINE | ID: covidwho-1172905

ABSTRACT

A novel coronavirus SARS-CoV-2, which initially originated in China, has outstretched to all nations and turned out to be an intense global concern for both the governments and the public. In addition to the health concerns, the COVID-19 pandemic has caused a tremendous impact on the economic and political conditions of every nation. Ever since the start of the pandemic, the physicians were constrained to rely on the management strategies due to a lack of clear understanding of the disease pathogenesis caused by SARS-CoV-2 infection. Scientists are working tirelessly to gather maximum information about the deadly virus and come up with various strategies, which can be used against COVID-19 infection in terms of therapeutics and vaccine development. It is quite evident that the virus infection leads to acute respiratory distress syndrome (ARDS), and most of the deaths occur due to respiratory failure. As the virus spreads through respiratory droplets, the strenuous exercise of preventive measures and diagnosis at a large scale has been in practice across the globe to prevent transmission. This review amalgamates the various updates and acts as an umbrella to provide insights on SARS-CoV-2 mediated ARDS pathogenesis, the impact of co-morbidities, diagnostics, current progress in vaccine development, and promising therapeutics and immuno-modulatory strategies, highlighting various concerns and gaps that need to be addressed to fight current and future pandemics effectively.


Subject(s)
COVID-19 , Respiratory Distress Syndrome , China/epidemiology , Humans , Pandemics/prevention & control , Respiratory Distress Syndrome/etiology , Respiratory Distress Syndrome/prevention & control , SARS-CoV-2
5.
ACS Omega ; 6(11): 7754-7760, 2021 Mar 23.
Article in English | MEDLINE | ID: covidwho-1155693

ABSTRACT

COVID-19 is a deadly pandemic and has resulted in a huge loss of money and life in the past few months. It is well known that the SARS-CoV-2 gene mutates relatively slowly as compared to other viruses but still may create hurdles in developing vaccines. Therefore, there is a need to develop alternative routes for its management and treatment of COVID-19. Based on the severity of viral infection in COVID-19 patients, critically ill patients (∼5%, with old age, and comorbidities) are at high risk of morbidities. The reason for this severity in such patients is attributed to "misleading cytokine storm", which produces ARDS and results in the deaths of critically ill patients. In this connection, ethyl pyruvate (EP) controls these cytokines/chemokines, is an anti-inflammatory agent, and possesses a protective effect on the lungs, brain, heart, and mitochondria against various injuries. Considering these facts, we propose that the site-selective EP formulations (especially aerosols) could be the ultimate adjuvant therapy for the regulation of misleading cytokine storm in severely affected COVID-19 patients and could reduce the mortalities.

6.
Hong Kong Med J ; 2021 Mar 10.
Article in English | MEDLINE | ID: covidwho-1145707

ABSTRACT

The novel coronavirus disease (COVID-19) may result in acute respiratory distress syndrome and respiratory failure, necessitating mechanical respiratory support. Healthcare professionals are exposed to a particularly high risk of contracting the virus while providing resuscitation and respiratory support, which may in turn result in grave consequences and even death. Although COVID-19 has been shown to cause milder disease in children, paediatricians and intensivists who provide care for children must be prepared to provide optimal respiratory support without putting themselves or other medical, nursing, and paramedical staff at undue risk. We propose an airway management approach that is especially relevant in the current COVID-19 pandemic and provides instructions for: (1) Elective intubation for respiratory failure; and (2) Emergency intubation during cardiopulmonary resuscitation. To minimise risk, intubation methods must be kept as straightforward as possible and should include the provision of appropriate personal protection and equipment to healthcare workers. We identify two key considerations: that bag-mask ventilation should be avoided if possible and that bacterial and viral filters should be placed in the respiratory circuit. Our novel approach provides a framework for airway management that could benefit paediatric critical care practitioners who provide care for any children with a novel viral illness, with a focus on infection prevention during high-risk airway management procedures.

7.
Nat Commun ; 12(1): 1325, 2021 02 26.
Article in English | MEDLINE | ID: covidwho-1104490

ABSTRACT

The coronavirus disease 2019 (COVID-19) can result in a hyperinflammatory state, leading to acute respiratory distress syndrome (ARDS), myocardial injury, and thrombotic complications, among other sequelae. Statins, which are known to have anti-inflammatory and antithrombotic properties, have been studied in the setting of other viral infections, but their benefit has not been assessed in COVID-19. This is a retrospective analysis of patients admitted with COVID-19 from February 1st through May 12th, 2020 with study period ending on June 11th, 2020. Antecedent statin use was assessed using medication information available in the electronic medical record. We constructed a multivariable logistic regression model to predict the propensity of receiving statins, adjusting for baseline sociodemographic and clinical characteristics, and outpatient medications. The primary endpoint includes in-hospital mortality within 30 days. A total of 2626 patients were admitted during the study period, of whom 951 (36.2%) were antecedent statin users. Among 1296 patients (648 statin users, 648 non-statin users) identified with 1:1 propensity-score matching, statin use is significantly associated with lower odds of the primary endpoint in the propensity-matched cohort (OR 0.47, 95% CI 0.36-0.62, p < 0.001). We conclude that antecedent statin use in patients hospitalized with COVID-19 is associated with lower inpatient mortality.


Subject(s)
COVID-19/drug therapy , COVID-19/mortality , Hydroxymethylglutaryl-CoA Reductase Inhibitors/administration & dosage , Aged , Female , Hospital Mortality , Hospitalization , Humans , Logistic Models , Male , Middle Aged , New York City/epidemiology , Propensity Score , Retrospective Studies , SARS-CoV-2/isolation & purification
8.
Front Med (Lausanne) ; 7: 559811, 2020.
Article in English | MEDLINE | ID: covidwho-1063325

ABSTRACT

In numerous animal studies, vitamin C has prevented and alleviated viral and bacterial infections. In a few dozen placebo-controlled trials with humans, vitamin C has shortened infections caused by respiratory viruses, which indicates that the vitamin can also influence viral infections in humans. In critically ill patients, plasma vitamin C levels are commonly very low. Gram doses of vitamin C are needed to increase the plasma vitamin C levels of critically ill patients to the levels of ordinary healthy people. A meta-analysis of 12 trials with 1,766 patients calculated that vitamin C reduced the length of ICU stay on average by 8%. Another meta-analysis found that vitamin C shortened the duration of mechanical ventilation in ICU patients. Two randomized placebo-controlled trials found statistically significant reduction in the mortality of sepsis patients. The effects of vitamin C on acute respiratory distress syndrome (ARDS) frequently complicating COVID-19 pneumonia should be considered. Vitamin C is a safe and inexpensive essential nutrient.

9.
Front Immunol ; 11: 604944, 2020.
Article in English | MEDLINE | ID: covidwho-1058416

ABSTRACT

Hypoxia and inflammation often coincide in pathogenic conditions such as acute respiratory distress syndrome (ARDS) and chronic lung diseases, which are significant contributors to morbidity and mortality for the general population. For example, the recent global outbreak of Coronavirus disease 2019 (COVID-19) has placed viral infection-induced ARDS under the spotlight. Moreover, chronic lung disease ranks the third leading cause of death in the United States. Hypoxia signaling plays a diverse role in both acute and chronic lung inflammation, which could partially be explained by the divergent function of downstream target pathways such as adenosine signaling. Particularly, hypoxia signaling activates adenosine signaling to inhibit the inflammatory response in ARDS, while in chronic lung diseases, it promotes inflammation and tissue injury. In this review, we discuss the role of adenosine at the interphase of hypoxia and inflammation in ARDS and chronic lung diseases, as well as the current strategy for therapeutic targeting of the adenosine signaling pathway.


Subject(s)
Adenosine/metabolism , Hypoxia/metabolism , Inflammation/metabolism , Acute Lung Injury/etiology , Acute Lung Injury/metabolism , Acute Lung Injury/pathology , Acute Lung Injury/therapy , Disease Management , Disease Susceptibility , Humans , Hypoxia-Inducible Factor 1/metabolism , Inflammation/etiology , Molecular Targeted Therapy , Receptors, Purinergic P1/metabolism , Respiratory Distress Syndrome/etiology , Respiratory Distress Syndrome/metabolism , Respiratory Distress Syndrome/pathology , Respiratory Distress Syndrome/therapy , Signal Transduction
10.
Front Bioeng Biotechnol ; 8: 619980, 2020.
Article in English | MEDLINE | ID: covidwho-1058408

ABSTRACT

The COVID-19 pandemic has become a priority in the health systems of all nations worldwide. In fact, there are currently no specific drugs or preventive treatments such as vaccines. The numerous therapies available today aim to counteract the symptoms caused by the viral infection that in some subjects can evolve causing acute respiratory distress syndromes (ARDS) with consequent admission to intensive care unit. The exacerbated response of the immune system, through cytokine storm, causes extensive damage to the lung tissue, with the formation of edema, fibrotic tissues and susceptibility to opportunistic infections. The inflammatory picture is also aggravated by disseminated intravascular coagulation which worsens the damage not only to the respiratory system, but also to other organs. In this context, perinatal cells represent a valid strategy thanks to their strong immunomodulatory potential, their safety profile, the ability to reduce fibrosis and stimulate reparative processes. Furthermore, perinatal cells exert antibacterial and antiviral actions. This review therefore provides an overview of the characteristics of perinatal cells with a particular focus on the beneficial effects that they could have in patients with COVID-19, and more specifically for their potential use in the treatment of ARDS and sepsis.

11.
J Fungi (Basel) ; 7(2)2021 Jan 27.
Article in English | MEDLINE | ID: covidwho-1050620

ABSTRACT

Viral infections can cause acute respiratory distress syndrome (ARDS), consequently leading to susceptibility for secondary pulmonary infections. Over the past few weeks, a number of studies have reported on secondary pulmonary aspergillosis complicating severe COVID-19. We report the case of a 53-year old male patient with secondary acute myeloid leukemia (AML) who suffered from COVID-19 ARDS and was diagnosed postmortem with mucormycosis.

12.
Eur Arch Otorhinolaryngol ; 277(7): 2133-2135, 2020 Jul.
Article in English | MEDLINE | ID: covidwho-1049646

ABSTRACT

PURPOSE: The role of tracheostomy in COVID-19-related ARDS is unknown. Nowadays, there is no clear indication regarding the timing of tracheostomy in these patients. METHODS: We describe our synergic experience between ENT and ICU Departments at University Hospital of Modena underlining some controversial aspects that would be worth discussing tracheostomies in these patients. During the last 2 weeks, we performed 28 tracheostomies on patients with ARDS due to COVID-19 infection who were treated with IMV. RESULTS: No differences between percutaneous and surgical tracheostomy in terms of timing and no case of team virus infection. CONCLUSION: In our experience, tracheostomy should be performed only in selected patients within 7- and 14-day orotracheal intubation.


Subject(s)
Coronavirus Infections/diagnosis , Intubation, Intratracheal , Minimally Invasive Surgical Procedures/methods , Pneumonia, Viral/diagnosis , Respiratory Distress Syndrome/therapy , Tracheostomy/methods , Adult , Betacoronavirus , COVID-19 , Coronavirus Infections/epidemiology , Humans , Intensive Care Units , Male , Middle Aged , Pandemics/prevention & control , Patient Care Team , Pneumonia, Viral/epidemiology , Respiratory Distress Syndrome/etiology , SARS-CoV-2 , Treatment Outcome
13.
Cytokine Growth Factor Rev ; 58: 114-133, 2021 04.
Article in English | MEDLINE | ID: covidwho-1007960

ABSTRACT

The devastating global impact of the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has prompted scientists to develop novel strategies to fight Coronavirus Disease of 2019 (COVID-19), including the examination of pre-existing treatments for other viral infections in COVID-19 patients. This review provides a reasoned discussion of the possible use of Mesenchymal Stromal Cells (MSC) or their products as a treatment in SARS-CoV-2-infected patients. The main benefits and concerns of using this cellular therapy, guided by preclinical and clinical data obtained from similar pathologies will be reviewed. MSC represent a highly immunomodulatory cell population and their use may be safe according to clinical studies developed in other pathologies. Notably, four clinical trials and four case reports that have already been performed in COVID-19 patients obtained promising results. The clinical application of MSC in COVID-19 is very preliminary and further investigational studies are required to determine the efficacy of the MSC therapy. Nevertheless, these preliminary studies were important to understand the therapeutic potential of MSC in COVID-19. Based on these encouraging results, the United States Food and Drug Administration (FDA) authorized the compassionate use of MSC, but only in patients with Acute Respiratory Distress Syndrome (ARDS) and a poor prognosis. In fact, patients with severe SARS-CoV-2 can present infection and tissue damage in different organs, such as lung, heart, liver, kidney, gut and brain, affecting their function. MSC may have pleiotropic activities in COVID-19, with the capacity to fight inflammation and repair lesions in several organs.


Subject(s)
COVID-19/therapy , Mesenchymal Stem Cell Transplantation , Mesenchymal Stem Cells/physiology , COVID-19/epidemiology , Cell- and Tissue-Based Therapy/methods , Cell- and Tissue-Based Therapy/trends , Humans , Mesenchymal Stem Cell Transplantation/methods , Mesenchymal Stem Cell Transplantation/trends , Multiple Organ Failure/prevention & control , Multiple Organ Failure/therapy , SARS-CoV-2/pathogenicity
14.
Expert Rev Clin Immunol ; 16(12): 1185-1204, 2020 12.
Article in English | MEDLINE | ID: covidwho-965246

ABSTRACT

Introduction: The mortality of coronavirus disease 2019 (COVID-19) is frequently driven by an injurious immune response characterized by the development of acute respiratory distress syndrome (ARDS), endotheliitis, coagulopathy, and multi-organ failure. This spectrum of hyperinflammation in COVID-19 is commonly referred to as cytokine storm syndrome (CSS). Areas covered: Medline and Google Scholar were searched up until 15th of August 2020 for relevant literature. Evidence supports a role of dysregulated immune responses in the immunopathogenesis of severe COVID-19. CSS associated with SARS-CoV-2 shows similarities to the exuberant cytokine production in some patients with viral infection (e.g.SARS-CoV-1) and may be confused with other syndromes of hyperinflammation like the cytokine release syndrome (CRS) in CAR-T cell therapy. Interleukin (IL)-6, IL-8, and tumor necrosis factor-alpha have emerged as predictors of COVID-19 severity and in-hospital mortality. Expert opinion: Despite similarities, COVID-19-CSS appears to be distinct from HLH, MAS, and CRS, and the application of HLH diagnostic scores and criteria to COVID-19 is not supported by emerging data. While immunosuppressive therapy with glucocorticoids has shown a mortality benefit, cytokine inhibitors may hold promise as 'rescue therapies' in severe COVID-19. Given the arguably limited benefit in advanced disease, strategies to prevent the development of COVID-19-CSS are needed.


Subject(s)
COVID-19 , Cytokine Release Syndrome , Cytokines/blood , SARS-CoV-2/metabolism , Therapies, Investigational , COVID-19/blood , COVID-19/mortality , COVID-19/prevention & control , COVID-19/therapy , Cytokine Release Syndrome/blood , Cytokine Release Syndrome/mortality , Cytokine Release Syndrome/prevention & control , Cytokine Release Syndrome/therapy , Humans
15.
Cytotherapy ; 23(6): 471-482, 2021 06.
Article in English | MEDLINE | ID: covidwho-952449

ABSTRACT

The end of 2019 saw the beginning of the coronavirus disease 2019 (COVID-19) pandemic that soared in 2020, affecting 215 countries worldwide, with no signs of abating. In an effort to contain the spread of the disease and treat the infected, researchers are racing against several odds to find an effective solution. The unavailability of timely and affordable or definitive treatment has caused significant morbidity and mortality. Acute respiratory distress syndrome (ARDS) caused by an unregulated host inflammatory response toward the viral infection, followed by multi-organ dysfunction or failure, is one of the primary causes of death in severe cases of COVID-19 infection. Currently, empirical management of respiratory and hematological manifestations along with anti-viral agents is being used to treat the infection. The quest is on for both a vaccine and a more definitive management protocol to curtail the spread. Researchers and clinicians are also exploring the possibility of using cell therapy for severe cases of COVID-19 with ARDS. Mesenchymal stromal cells are known to have immunomodulatory properties and have previously been used to treat viral infections. This review explores the potential of mesenchymal stromal cells as cell therapy for ARDS.


Subject(s)
COVID-19/epidemiology , COVID-19/surgery , Mesenchymal Stem Cell Transplantation/methods , Pandemics , Respiratory Distress Syndrome/epidemiology , Respiratory Distress Syndrome/surgery , SARS-CoV-2 , Animals , COVID-19/virology , Clinical Trials as Topic , Comorbidity , Humans , Immunomodulation , Mesenchymal Stem Cells/immunology , Respiratory Distress Syndrome/virology , Treatment Outcome
16.
Neurol India ; 68(5): 989-993, 2020.
Article in English | MEDLINE | ID: covidwho-895444

ABSTRACT

BACKGROUND: A terrible pandemic, Covid-19, has captivated scientists to investigate if SARS-CoV-2 virus infects the central nervous system (CNS). A crucial question is if acute respiratory distress syndrome (ARDS), the main cause of death in this pandemic, and often refractory to treatments, can be explained by respiratory center dysfunction. OBJECTIVE: To discuss that ARDS can be caused by SARS-CoV-2 infection of the respiratory center in the brainstem. MATERIALS AND METHODS: I reviewed literature about SARS-CoV-2 mechanisms to infect the respiratory center in the brainstem. RESULTS AND CONCLUSIONS: An increasing amount of reports demonstrates that neurotropism is a common feature of coronavirus, which have been found in the brains of patients and experimental models, where the brainstem was severely infested. Recent studies have provided tremendous indication of the incidence of acute respiratory failure due to SARS-CoV-2 infection of the brainstem. SARS-CoV-2 might infect the CNS through the olfactory bulb, spreading from the olfactory nerves to the rhinencephalon, and finally reaching the brainstem. Hence, the virus infection causes respiratory center dysfunctions, leading to ARDS in COVID-19 patients. I conclude that acute ARDS in Covid-19 can be caused by SARS-CoV-2 invasion of brainstem respiratory center, suggesting the needs of more specific and aggressive treatments, with the direct participation of neurologists and neurointensivists.


Subject(s)
Coronavirus Infections/physiopathology , Pneumonia, Viral/physiopathology , Respiratory Center/physiopathology , Respiratory Distress Syndrome/physiopathology , Betacoronavirus , Brain Stem/physiopathology , Brain Stem/virology , COVID-19 , Humans , Hypoxia/physiopathology , Pandemics , Respiratory Center/virology , SARS-CoV-2 , Viral Tropism
17.
Nutrition ; 81: 110989, 2021 01.
Article in English | MEDLINE | ID: covidwho-857038

ABSTRACT

Coronavirus disease 2019 (COVID-19) is a global pandemic causing one of the biggest challenges for critical care medicine. Mortality from COVID-19 is much greater in elderly men, many of whom succumb to acute respiratory distress syndrome (ARDS) triggered by the viral infection. Because there is no specific antiviral treatment against COVID-19, new strategies are urgently needed. Selenium is an essential trace element with antioxidant and immunomodulatory effects. Poor nutritional status increases the pathogenicity of viruses and low selenium in particular can be a determinant of viral virulence. In the past decade, selenium pharmaconutrition studies have demonstrated some reduction in overall mortality, including how reduced incidence of ventilator-associated pneumonia and infectious complications such as ARDS in the critically ill. Consequently, we postulate that intravenous selenium therapy, could be part of the therapeutic fight against COVID-19 in intensive care unit patients with ARDS and that outcomes could be affected by age, sex, and body weight. Our working hypothesis addresses the question: Could high-dose selenite pharmaconutrition, as an early pharmacologic intervention, be effective at reducing the incidence and the progression from type 1 respiratory failure (non-ARDS) to severe ARDS, multiorgan failure, and new infectious complications in patients with COVID-19 patients?


Subject(s)
COVID-19/diet therapy , Selenium/therapeutic use , COVID-19/complications , COVID-19/epidemiology , Critical Illness , Female , Host Microbial Interactions , Humans , Inflammation/etiology , Male , Micronutrients/administration & dosage , Micronutrients/pharmacokinetics , Micronutrients/therapeutic use , Models, Biological , Nutritional Physiological Phenomena , Obesity/complications , Pandemics , Practice Guidelines as Topic , SARS-CoV-2/pathogenicity , Selenium/administration & dosage , Selenium/pharmacokinetics
18.
Cochrane Database Syst Rev ; 9: CD013708, 2020 09 01.
Article in English | MEDLINE | ID: covidwho-737854

ABSTRACT

BACKGROUND: Supplemental oxygen is frequently administered to patients with acute respiratory distress syndrome (ARDS), including ARDS secondary to viral illness such as coronavirus disease 19 (COVID-19). An up-to-date understanding of how best to target this therapy (e.g. arterial partial pressure of oxygen (PaO2) or peripheral oxygen saturation (SpO2) aim) in these patients is urgently required. OBJECTIVES: To address how oxygen therapy should be targeted in adults with ARDS (particularly ARDS secondary to COVID-19 or other respiratory viruses) and requiring mechanical ventilation in an intensive care unit, and the impact oxygen therapy has on mortality, days ventilated, days of catecholamine use, requirement for renal replacement therapy, and quality of life. SEARCH METHODS: We searched the Cochrane COVID-19 Study Register, CENTRAL, MEDLINE, and Embase from inception to 15 May 2020 for ongoing or completed randomized controlled trials (RCTs). SELECTION CRITERIA: Two review authors independently assessed all records in accordance with standard Cochrane methodology for study selection. We included RCTs comparing supplemental oxygen administration (i.e. different target PaO2 or SpO2 ranges) in adults with ARDS and receiving mechanical ventilation in an intensive care setting. We excluded studies exploring oxygen administration in patients with different underlying diagnoses or those receiving non-invasive ventilation, high-flow nasal oxygen, or oxygen via facemask. DATA COLLECTION AND ANALYSIS: One review author performed data extraction, which a second review author checked. We assessed risk of bias in included studies using the Cochrane 'Risk of bias' tool. We used the GRADE approach to judge the certainty of the evidence for the following outcomes; mortality at longest follow-up, days ventilated, days of catecholamine use, and requirement for renal replacement therapy. MAIN RESULTS: We identified one completed RCT evaluating oxygen targets in patients with ARDS receiving mechanical ventilation in an intensive care setting. The study randomized 205 mechanically ventilated patients with ARDS to either conservative (PaO2 55 to 70 mmHg, or SpO2 88% to 92%) or liberal (PaO2 90 to 105 mmHg, or SpO2 ≥ 96%) oxygen therapy for seven days. Overall risk of bias was high (due to lack of blinding, small numbers of participants, and the trial stopping prematurely), and we assessed the certainty of the evidence as very low. The available data suggested that mortality at 90 days may be higher in those participants receiving a lower oxygen target (odds ratio (OR) 1.83, 95% confidence interval (CI) 1.03 to 3.27). There was no evidence of a difference between the lower and higher target groups in mean number of days ventilated (14.0, 95% CI 10.0 to 18.0 versus 14.5, 95% CI 11.8 to 17.1); number of days of catecholamine use (8.0, 95% CI 5.5 to 10.5 versus 7.2, 95% CI 5.9 to 8.4); or participants receiving renal replacement therapy (13.7%, 95% CI 5.8% to 21.6% versus 12.0%, 95% CI 5.0% to 19.1%). Quality of life was not reported. AUTHORS' CONCLUSIONS: We are very uncertain as to whether a higher or lower oxygen target is more beneficial in patients with ARDS and receiving mechanical ventilation in an intensive care setting. We identified only one RCT with a total of 205 participants exploring this question, and rated the risk of bias as high and the certainty of the findings as very low. Further well-conducted studies are urgently needed to increase the certainty of the findings reported here. This review should be updated when more evidence is available.


Subject(s)
Betacoronavirus , Coronavirus Infections/complications , Intensive Care Units , Oxygen/administration & dosage , Pneumonia, Viral/complications , Respiration, Artificial , Respiratory Distress Syndrome/therapy , Bias , COVID-19 , Catecholamines/therapeutic use , Conservative Treatment , Humans , Odds Ratio , Pandemics , Renal Replacement Therapy/statistics & numerical data , Respiration, Artificial/statistics & numerical data , Respiratory Distress Syndrome/mortality , Respiratory Distress Syndrome/virology , SARS-CoV-2 , Self Concept , Time Factors
19.
J Biomol Struct Dyn ; 39(17): 6842-6851, 2021 10.
Article in English | MEDLINE | ID: covidwho-697054

ABSTRACT

Acute Respiratory Distress Syndrome (ARDS) is a form of respiratory failure in human. The number of deaths caused by SARS-CoV-2 infection inducing this severe pneumonia (ARDS) is relatively high. In fact, COVID-19 might get worsen in ARDS and provoke respiratory failure. A better understood of ARDS key features and the pathophysiological injuries of the pulmonary parenchyma are linked to lessons learned from previous severe diseases associated previous coronaviruses outbreaks (especially SARS-CoV and MERS-CoV) and more the ongoing SARS-CoV-2. The ARDS mechanism includes a diffuse alveolar damage associated disruption of alveolar capillary membrane, pulmonary edema, damaged endothelium and increased permeability. A diffuse inflammation, with acute onset, on the lung tissue accompanied by release of biochemical signal and inflammatory mediators (TNFα, IL-1 and IL-6) leading to hypoxemia, low PaO2/FiO2 ratio and the chest radiological expression of bilateral infiltrates in ARDS. The ongoing outbreak could lead to a better understood of ARDS pathophysiology and prognostic. An overview is also highlighted about the seven coronaviruses proved to infect human especially those having ability to cause severe disease SARS-CoV, MERS-CoV and SARS-CoV-2. In this review, we focused on the major pathological mechanisms leading to the ARDS development as a result of viral infection, severe COVID-19 worsening. Communicated by Ramaswamy H. Sarma.


Subject(s)
COVID-19 , Respiratory Distress Syndrome , Humans , Inflammation , SARS-CoV-2
20.
Cannabis Cannabinoid Res ; 5(3): 197-201, 2020.
Article in English | MEDLINE | ID: covidwho-638503

ABSTRACT

Introduction: In the absence of effective antivirals and vaccination, the pandemic of COVID-19 remains the most significant challenge to our health care system in decades. There is an urgent need for definitive therapeutic intervention. Clinical reports indicate that the cytokine storm associated with acute respiratory distress syndrome (ARDS) is the leading cause of mortality in severe cases of some respiratory viral infections, including COVID-19. In recent years, cannabinoids have been investigated extensively due to their potential effects on the human body. Among all cannabinoids, cannabidiol (CBD) has demonstrated potent anti-inflammatory effects in a variety of pathological conditions. Therefore, it is logical to explore whether CBD can reduce the cytokine storm and treat ARDS. Materials and Methods: In this study, we show that intranasal application of Poly(I:C), a synthetic analogue of viral double-stranded RNA, simulated symptoms of severe viral infections inducing signs of ARDS and cytokine storm. Discussion: The administration of CBD downregulated the level of proinflammatory cytokines and ameliorated the clinical symptoms of Poly I:C-induced ARDS. Conclusion: Our results suggest a potential protective role for CBD during ARDS that may extend CBD as part of the treatment of COVID-19 by reducing the cytokine storm, protecting pulmonary tissues, and re-establishing inflammatory homeostasis.

SELECTION OF CITATIONS
SEARCH DETAIL