Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476273 (respiratory distress)
 19,632 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The newly emergent novel coronavirus disease 2019 (COVID-19) outbreak, which is caused by SARS-CoV-2 virus, has posed a serious threat to global public health and caused worldwide social and economic breakdown. Angiotensin-converting enzyme 2 (ACE2) is expressed in human vascular endothelium, respiratory epithelium, and other cell types, and is thought to be a primary mechanism of SARS-CoV-2 entry and infection. In physiological condition, ACE2 via its carboxypeptidase activity generates angiotensin fragments (Ang 1-9 and Ang 1-7), and plays an essential role in the renin-angiotensin system (RAS), which is a critical regulator of cardiovascular homeostasis. SARS-CoV-2 via its surface spike glycoprotein interacts with ACE2 and invades the host cells. Once inside the host cells, SARS-CoV-2 induces acute respiratory distress syndrome (ARDS), stimulates immune response (i.e., cytokine storm) and vascular damage. SARS-CoV-2 induced endothelial cell injury could exacerbate endothelial dysfunction, which is a hallmark of aging, hypertension, and obesity, leading to further complications. The pathophysiology of endothelial dysfunction and injury offers insights into COVID-19 associated mortality. Here we reviewed the molecular basis of SARS-CoV-2 infection, the roles of ACE2, RAS signaling, and a possible link between the pre-existing endothelial dysfunction and SARS-CoV-2 induced endothelial injury in COVID-19 associated mortality. We also surveyed the roles of cell adhesion molecules (CAMs), including CD209L/L-SIGN and CD209/DC-SIGN in SARS-CoV-2 infection and other related viruses. Understanding the molecular mechanisms of infection, the vascular damage caused by SARS-CoV-2 and pathways involved in the regulation of endothelial dysfunction could lead to new therapeutic strategies against COVID-19.
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PMID:COVID-19, Renin-Angiotensin System and Endothelial Dysfunction. 3266 65

Coronavirus disease 2019 (COVID-19) continues to pose a major global threat. Although a wide range of organ manifestations have now been described, the respiratory system remains in the forefront in terms of the course of infection. Severe pneumonia can develop and is generally prognostically relevant. The following article discusses currently known features of these pulmonary manifestations from a pathophysiological, symptomatological, and radiological perspective. With regard to pathophysiology, the complex nature of the acute pulmonary disease involving severe injury to the alveolar epithelium and pulmonary vascular endothelium resulting in severe respiratory failure in a proportion of patients is discussed. The differences from "classic" acute respiratory distress syndrome and the major effects these have on the treatment of COVID-19 are elucidated. Following a brief description of PCR-based pathogen identification and information on typical laboratory findings, imaging of COVID-19 pneumonia is described in greater details (typical findings, differential diagnoses, grading of the likelihood of COVID-19 pneumonia). This is followed by a description of symptoms, which develop in three phases. With regard to treatment, supportive and intensive care approaches are discussed, including O2 administration and (non-)invasive ventilation. The article concludes with a summary of the insights gained into pharmacological therapies: thrombosis prevention on the one hand, and specific antiviral and immunomodulatory therapies (remdesivir, tocilizumab, anakinra, dexamethasone) on the other.
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PMID:[COVID-19 pneumonia]. 3272 17

The COVID-19 pandemic is an unprecedented healthcare emergency causing mortality and illness across the world. Although primarily affecting the lungs, the SARS-CoV-2 virus also affects the cardiovascular system. In addition to cardiac effects, e.g. myocarditis, arrhythmias, and myocardial damage, the vasculature is affected in COVID-19, both directly by the SARS-CoV-2 virus, and indirectly as a result of a systemic inflammatory cytokine storm. This includes the role of the vascular endothelium in the recruitment of inflammatory leucocytes where they contribute to tissue damage and cytokine release, which are key drivers of acute respiratory distress syndrome (ARDS), in disseminated intravascular coagulation, and cardiovascular complications in COVID-19. There is also evidence linking endothelial cells (ECs) to SARS-CoV-2 infection including: (i) the expression and function of its receptor angiotensin-converting enzyme 2 (ACE2) in the vasculature; (ii) the prevalence of a Kawasaki disease-like syndrome (vasculitis) in COVID-19; and (iii) evidence of EC infection with SARS-CoV-2 in patients with fatal COVID-19. Here, the Working Group on Atherosclerosis and Vascular Biology together with the Council of Basic Cardiovascular Science of the European Society of Cardiology provide a Position Statement on the importance of the endothelium in the underlying pathophysiology behind the clinical presentation in COVID-19 and identify key questions for future research to address. We propose that endothelial biomarkers and tests of function (e.g. flow-mediated dilatation) should be evaluated for their usefulness in the risk stratification of COVID-19 patients. A better understanding of the effects of SARS-CoV-2 on endothelial biology in both the micro- and macrovasculature is required, and endothelial function testing should be considered in the follow-up of convalescent COVID-19 patients for early detection of long-term cardiovascular complications.
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PMID:Endothelial dysfunction in COVID-19: a position paper of the ESC Working Group for Atherosclerosis and Vascular Biology, and the ESC Council of Basic Cardiovascular Science. 3275 Jan 8

The potential for a rapid increase in severity is among the most frightening aspects of severe acute respiratory syndrome coronavirus 2 infection. Evidence increasingly suggests that the symptoms of coronavirus disease-2019 (COVID-19)-related acute respiratory distress syndrome (ARDS) differ from those of classic ARDS. Recently, the severity of COVID-19 has been attributed to a systemic, thrombotic, and inflammatory disease that damages not only the lungs but also multiple organs, including the heart, brain, toes, and liver. This systemic form of COVID-19 may be due to inflammation and vascular endothelial cell injury. The vascular endothelial glycocalyx comprises glycoproteins and plays an important role in systemic capillary homeostasis maintenance. The glycocalyx covers the entire vascular endothelium, and its thickness varies among organs. The endothelial glycocalyx is very thin in the pulmonary capillaries, where it is affected by gaseous exchange with the alveoli and the low intravascular pressure in the pulmonary circulation. Despite the clearly important roles of the glycocalyx in vascular endothelial injury, thrombosis, vasculitis, and inflammation, the link between this structure and vascular endothelial cell dysfunction in COVID-19 remains unclear. In this prospective review, we summarize the importance of the glycocalyx and its potential as a therapeutic target in cases of systemic COVID-19.
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PMID:Vascular endothelial injury exacerbates coronavirus disease 2019: The role of endothelial glycocalyx protection. 3279 68

Coronavirus disease (COVID-19) is a systemic disease which can cause multiple organ failure and death primarly due to vascular endothelium injury. Severe acute respiratory distress syndrome (ARDS) is the main cause of death: its management and treatment should be tailored to the individual COVID-19 patient's phenotype. Early diagnosis of COVID-19 is paramount for disease treatment and infection control. Naso-pharyngeal (NP) swab is commonly used as screening and diagnostic tool for COVID-19, but in some cases it can be resulted negative even in presence of clinical and epidemiological criteria, and typical radiological and laboratory findings of COVID-19, as we have observed. Here we report our experience in the first month of the Italian epidemic. We strongly recommend clinicians to maintain a high index of suspicion for COVID-19, regardless of the persistence negativity of NP swabs, and not to delay the initiation of therapy in presence of typical clinical, radiological and laboratory findings of COVID-19.
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PMID:Negative nasopharyngeal swabs in COVID-19 pneumonia: the experience of an Italian Emergengy Department (Piacenza) during the first month of the Italian epidemic. 3292 20


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