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COVID-19 patients have presented with a wide range of neurological disorders, among which stroke is the most devastating. We have reviewed current studies, case series, and case reports with a focus on COVID-19 patients complicated with stroke, and presented the current understanding of stroke in this patient population. As evidenced by increased D-dimer, fibrinogen, factor VIII and von Willebrand factor, SARS-CoV-2 infection induces coagulopathy, disrupts endothelial function, and promotes hypercoagulative state. Collectively, it predisposes patients to cerebrovascular events. Additionally, due to the unprecedented strain on the healthcare system, stroke care has been inevitably compromised. The underlying mechanism between COVID-19 and stroke warrants further study, so does the development of an effective therapeutic or preventive intervention.
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The coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has rapidly spread across the globe, causing innumerable deaths and a massive economic catastrophe. Exposure to household members with confirmed COVID-19 is the most common source of infection among children. Children are just as likely as adults to get infected with SARS-CoV-2. Most children are asymptomatic and when symptoms occur, they are usually mild. Infants <12 months old are at a higher risk for severe or critical disease. COVID-19 is diagnosed the same way in pediatric population as adults by testing specimen obtained from upper respiratory tract for nucleic acid amplification test (NAAT) using reverse transcriptase viral polymerase chain reaction (RT-PCR). The common laboratory findings in hospitalized patient include leukopenia, lymphopenia, and increased levels of inflammatory markers. Chest X-ray findings are variable and computed tomography scans of the chest may show ground glass opacities similar to adults or non-specific findings. Prevention is the primary intervention strategy. Recently the U.S. Food and Drug Administration (FDA) has provided emergency authorization of the Pfizer-BioNTech COVID-19 vaccine and many other vaccine candidates are in the investigational stage. There is limited data in children on the use of antivirals, hydroxychloroquine, azithromycin, monoclonal antibody, and convalescent plasma. Oxygen therapy is required in hypoxic children (saturation <92%). Similar to adults, other measures to maintain oxygenation such as high flow nasal cannula, CPAP, or ventilatory support may be needed. Ventilatory management strategies should include use of low tidal volumes (5-6 cc/kg), high positive expiratory pressure, adequate sedation, paralysis, and prone positioning. Recently, a new entity associated with COVID-19 called multisystem inflammatory syndrome in children (MIS-C) has emerged. Clinical, laboratory, and epidemiological criteria are the basis for this diagnosis. Management options include ICU admission, steroids, intravenous gamma globulin, aspirin, anakinra, and anticoagulants. Vasoactive-inotropic score (VIS) is used to guide vasopressor support.
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Blood pressure is controlled through a complex network of interacting peptide systems, principally involving the angiotensin, natriuretic peptide, endothelin and apelin families. The most complex and thoroughly investigated is the renin-angiotensin system (RAS) in which selective and potent inhibitors of the key biosynthetic proteolytic enzymes, renin and angiotensin-converting enzyme (ACE), have proved to be valuable drugs for the effective treatment of hypertension and heart failure, as well as other cardiovascular and renal disorders. Some of the other proteases in these pathways, e.g.neprilysin and ACE2, are also being explored as potential drug targets. © 2023 Elsevier Inc. All rights reserved.
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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused the outbreak of pneumonia which originated in Wuhan, China, at the end of 2019 has turned into a global pandemic—now termed coronavirus diseases 2019 (COVID-19). Like previously reported SARS-CoV strains, the newly discovered SARS-CoV-2 was also found to initiate the pathogenesis by binding with the angiotensin-converting enzyme 2 (ACE2), a receptor produced by various organs in the human body. Hence, COVID-19 is a viral multisystem disease which particularly infects the vascular system expressing ACE2 and reduced the ACE2 function;this further complexed by organ-specific pathogenesis related to the damage of cells expressing ACE2, such as alveolus, glomerulus, endothelium, and cardiac microvasculature. Under these conditions, it was advocated that the upregulation of ACE2 expression in predisposing individuals with aberrant renin–angiotensin system (RAS) level to advanced viral load on infection and relatively a greater number of cell death. Recently, a significant role of decreased ACE2 production and inequality between the RAS and ACE2/angiotensin-(1–7)/ MAS (mitochondrial Ang system) after the onset of SARS-CoV-2 infection was established as a key factor for multiple organ injury in SARS-CoV-2-infected individuals. Furthermore, restoration of this imbalance has been suggested as a therapeutic approach to attenuate organ injuries in SARS-CoV-2 infection. Based on available data, this chapter presents the updated mechanism of the multi-organ diseases causes by COVID-19 via ACE2 which can be further helpful in the development of specific therapeutics. © The Author(s), under exclusive licence to Springer Nature Singapore Pte Ltd. 2021.
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Highly mutable influenza is successfully countered based on individual susceptibility and similar precision-like medicine approach should be effective against SARS-COV-2. Among predictive markers to bring precision medicine to COVID-19, circulating ACE2 has potential features being upregulated in both severe COVID-19 and predisposing comorbidities. Spike SARS-CoVs were shown to induce ADAM17-mediated shedding of enzymatic active ACE2, thus accounting for its increased activity that has also been suggested to induce positive feedback loops leading to COVID-19-like manifestations. For this reason, pre-existing ACE2 activity and inhibition of ACE2/ADAM17 zinc-metalloproteases through zinc chelating agents have been proposed to predict COVID-19 outcome before infection and to protect from COVID-19, respectively. Since most diagnostic laboratories are not equipped for enzymatic activity determination, other potential predictive markers of disease progression exploitable by diagnostic laboratories were explored. Concentrations of circulating albumin, zinc, ACE2 protein and its activity were investigated in healthy, diabetic (COVID-19-susceptible) and SARS-CoV-2-negative COVID-19 individuals. ACE2 both protein levels and activity significantly increased in COVID-19 and diabetic patients. Abnormal high levels of ACE2 characterised a subgroup (16–19%) of diabetics, while COVID-19 patients were characterised by significantly higher zinc/albumin ratios, pointing to a relative increase of albumin-unbound zinc species, such as ACE2-bound and free zinc ones. Data on circulating ACE2 levels are in line with the hypothesis that they can drive susceptibility to COVID-19 and elevated zinc/albumin ratios support the therapeutic use of zinc chelating inhibitors of ACE2/ADAM17 zinc-metalloproteases in a targeted therapy for COVID-19.
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Background: COVID-19 (coronavirus disease 2019) is still a major challenge worldwide. The disease is caused by binding the coronavirus to ACE2 receptors on lung cells, infecting the cells and triggering the onset of symptoms. The prevention of such a binding in which the virus is eventually unable to enter the cell could be a promising therapeutic approach.Methods: In this in silico study, 306 compounds of Lamiaceae family native in Iran (native Mints) were retrieved from several databases as 3D structures, and after that molecular docking and virtual screening, the compounds with inhibitory potential were selected in terms of free energy binding against the spike protein of the virus. The pharmacokinetic profile of selected compounds was evaluated, and by molecular dynamic simulation and MM/PBSA, four compounds were further assessed for binding affinities against the receptor-binding domain of the spike.Results: The results showed the Catechin gallate and Perovskone B from Stachys and Salvia genus generated a stronger binding affinity, and therefore could act as potential inhibitory compounds of RBD of the SARS-CoV-2 spike protein.Conclusion: This study revealed that some members of the Lamiaceae family could be employed to inhibit SARS-CoV-2 activity through interaction with spike protein and therefore could be used for further investigation in vitro and in vivo.
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Intro: The spike protein of the SARS-CoV-2 virus targets the human cell receptor of angiotensin-converting enzyme (ACE2), including the myocardium and heart's conduction system. Patients diagnosed with COVID-19 have also been found to exhibit cardiac arrhythmia. Here, a whole-genome sequencing analysis using long-read sequencing was proposed to evaluate the virus genome in a patient who presented with AVNRT as a main presentation of COVID-19. Method(s): The sample was recovered from nasopharyngeal and oropharyngeal swab specimens of a 46-year-old female with no comorbidities who presented with palpitation, and ECG showed typical AVNRT features. The RT-qPCR of SARS- CoV-2 was confirmed positive with a CT-value of 15.82. The total RNAs were extracted and proceeded for RT-qPCR and proceeded with Oxford Nanopore Flongle sequencing. The genomics data of the virus was deposited in GISAID (EPI_ISL_3241561) and further analysed using online bioinformatics tools such as Nextclade CLI 2.3.0. Ethical approval (IREC 2021-080) for the study was obtained from IIUM Research Ethics Committee. Finding(s): Here, we reported a total of 29,775 bp near-complete whole-genome belonging to clade 21J (Delta) of AY.79 lineage (also known as B.1.617.2.79), which formed a dominant variant in Malaysia during the time of sampling. Discussion(s): While a previous study showed an association between Delta variant infection with fulminant myocarditis, the present study reported the benign AVNRT as the main presentation of SARS-CoV-2 infection. Furthermore, we observed the presence of the C3037T mutation previously described in the endomyocardial biopsy of a patient with persistent arrhythmia. Conclusion(s): Even though SARS-CoV-2 targets the respiratory tract, the present study supports the evidence that the ACE2 receptors are present in the heart. In addition, COVID19 is causing more and more damage to heart tissue, and viral transcription has been confirmed on cardiomyocytes. Further functional studies are needed to explore the associated mutations and their relation to cardiac manifestation.Copyright © 2023
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Background: Hepatocellular carcinoma (HCC) is the second leading cause of malignancy-related mortality and the fifth most common worldwide. Immuno-cancer microenvironment (ICME) was highlighted recently because scientists want to unlock the detailed mechanism in carcinogenesis pathway and find the novel interactions in ICME. Besides, single cell analysis could mitigate the interrupted signals between cells and tissues. On the other hand, COVID-19 angiotensin I converting enzyme (ACE) previously was reported associated with cancer. However, the robust association between COVID-19 and HCC ICME is still unaddressed. Aim(s): We plan to investigate the COVID-19 ACE relevant genes to HCC ICME regarding survival. Method(s): We used Reactome for COVID-19 ACE gene pathway mapping and explored the positive relevant gene expression. DISCO website was applied for single cell analyses using the above-collected genes from Reactome. Finally, we implanted the biomedical informatics into TIMER 2.0 for ICME survival analyses. Result(s): In Fig. 1, the gene-gene interaction mapping was shown. We collected 13 genes (CPB2, ACE2, AGT, MME, ANPEP, CPA3, ENPEP, GZMH, CTSZ, CTSD, CES1, ATP6AP2, and AOPEP) for further single cell relevant analyses, in Table 1, with detailed expression level (TPM). Among the above 13 genes, AGT, GZMH, CTSZ, CTSD, CES1, and ATP6AP2 were strongly expressed in liver tissue. We then applied the initial 13 genes to TIMER 2.0 for HCC ICME 2-year survival analyses. CPA3 and GZMH low expressions with high macrophage infiltration in HCC ICME showed significantly worse 2-year cumulative survival [hazard ratio (HR):CPA3 2.21, p-value 0.018;GZMH 2.07, p-value 0.0341]. ACE2, CPB2, AGT, MME, ANPEP, ENPEP, CTSZ, CTSD, CES1, and ATP6AP2 high expressions with high macrophage infiltration in HCC ICME revealed significantly worse 2-year cumulative survival. Conclusion(s): We demonstrate that ACE2 was strongly associated with HCC clinical survival with macrophage infiltration. However, the bidirectional translational roles about ACE2 relevant genes in HCC should be documented.
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Both diabetes and Corona Virus Disease 2019 (COVID-19) are seriously harmful to human health, and they are closely related. It is of great significance to find drugs that can simultaneously treat diabetes and COVID-19. Based on the theory of traditional Chinese medicine for treating COVID-19, this study first sorted out the compounds of Guizhou Miao medicine with "return to the lung channel” and "clear heat and detoxify” effects in China. The active components against COVID-19 were screened by molecular docking with SARS-CoV-2 PLpro and angiotensin-converting enzyme II as targets. Furthermore, the common target dipeptidyl peptidase 4 (DPP4) of diabetes and COVID-19 was used as a screening protein, and molecular docking was used to obtain potential components for the treatment of diabetes and COVID-19. Finally, the mechanism of potential ingredients in the treatment of diabetes and COVID-19 was explored with bioinformatics. More than 80 kinds of Miao medicine were obtained, and 584 compounds were obtained. Further, 110 compounds against COVID-19 were screened, and top 6 potential ingredients for the treatment of diabetes and COVID-19 were screened, including 3-O-β-D-Xylopyranosyl-(1-6)-β-D-glucopyranosyl-(1-6)-β-D-glucopyranosyl oleanolic acid 28-O-β-D-glucopyranosyl ester, Glycyrrhizic acid, Sequoiaflavone, 2-O-Caffeoyl maslinic acid, Pholidotin, and Ambewelamide A. Bioinformatics analysis found that their mechanism of action in treating diabetes and COVID-19 may be related to regulating the expression of DPP4, angiotensin II type 1 receptor, vitamin D receptor, plasminogen, chemokine C-C-motif receptor 6, and interleukin 2. We believe that Guizhou Miao medicine is rich in potential ingredients for the treatment of diabetes and COVID-19.
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Severe pneumonia is a condition with a high risk of death and mandatory hospitalization in the intensive care unit. The incidence of severe pneumonia has increased dramatically during the pandemic of new coronavirus infection. Timely diagnosis and early initiation of adequate treatment of severe pneumonia are crucial for improving survival of critically ill patients. The aim of this review was to analyze published scientific research on molecular markers that allow to objectively assess the severity of pneumonia and to determine treatment tactics based on the predicted outcome upon admission to the hospital. A systematic search was conducted in the electronic databases PubMed, Medline, Web of Science for the period 2019 – 2022. Conclusion. The review focuses on the prognostic role of a number of markers of immune response, vascular transformation, as well as angiotensin II and angiotensin converting enzyme-2. Further prospective studies of potential predictors of severe pneumonia will enable using marker molecules in a comprehensive clinical and laboratory diagnosis for early prediction of the hospitalized patient's condition and expected outcome. © Volchkova E.V. et al., 2023.
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Neurological complications of COVID-19 contribute significantly to mortality in the intensive care unit (ICU). Preventive therapy, though discussed in literature, is limited for COVID-19 neurological manifestations and treatment algorithms continue to rely on evidence from previous pandemics. Thus, in this chapter we evaluate current in vitro, in vitro, histopathological studies to ascertain the most likely mechanisms of SARS-CoV-2 central nervous system entry. From this understanding, we determine probable mechanisms for neurological compilations observed in COVID-19 as relevant to the clinician. SARS-CoV-2 infection of nasal epithelium and the respiratory tract may allow for a systemic inflammatory response that results in neuroinflammation. While most neurological complications are inflammatory in etiology, rarely, SARS-CoV-2 may enter into the central nervous system and mediate neuronal damage. © The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland AG 2022.
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Context: The coronavirus disease 2019 (COVID-19) pandemic is still a cause of worldwide health concern. Diabetes and its associated comorbidities are risk factors for mortality and morbidity in COVID-19. Selecting the right antidiabetic drug to achieve optimal glycemic control might mitigate some of the negative impacts of diabetes. Metformin continues to be the most widely administered antidiabetic agent. There is evidence of its beneficial outcome in COVID-19 independent of its glucose-lowering effect. Evidence Acquisition: A thorough literature search was conducted in PubMed, Google Scholar, Scopus, and Web of Science to identify studies investigating metformin in COVID-19. Result(s): Several overlapping mechanisms have been proposed to explain its antiviral properties. It could bring about conformational changes in the angiotensin-converting enzyme-2 receptor and decrease viral entry. The effects on the mammalian target of the rapamycin pathway and cellular pH have been proposed to reduce viral protein synthesis and replication. The immunomodulatory effects of metformin might counter the detrimental effects of hyperinflammation associated with COVID-19. Conclusion(s): These findings call for broader metformin usage to manage hyperglycemia in COVID-19.Copyright © 2023, International Journal of Endocrinology and Metabolism.
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One of the symptoms of a new coronavirus infection (COVID-19) is a complete or partial violation of the sense of smell. The aim of the work is to analyze the published results of scientific research on the mechanisms of olfactory impairment in COVID-19. Material and methods. Research was conducted for publications in Pubmed on the problem of olfactory impairment in COVID-19 using terms indexed by MeSH. The systematic review was compiled in accordance with the checklist Preferred Reporting Items for Systematic Reviews and Meta-Analyses Statement (PRISMA). Results. Publication's analysis has shown that the existing ideas about conductive anosmia are insufficient to explain the causes of olfactory impairment caused by SARS-CoV-2. It has been established that ACE2 and TMPRSS2 receptors located on the surface of target cells are necessary for the penetration of a new coronavirus. It is known that these receptors are mainly located on the cells of the olfactory epithelium. The main hypothesis of olfactory impairment in COVID-19 is that anosmia/hyposmia is caused by damage not to neuronal cells (as previously assumed), but to the olfactory epithelium. There is no confirmation of the point of view about the damage of SARS-CoV-2 olfactory bulbs and olfactory neurons, since they do not express receptor proteins for the virus on their surface.Copyright © 2022 by the authors.
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Worldwide, up to 8.8 million excess deaths/year have been attributed to air pollution, mainly due to the exposure to fine particulate matter (PM). Traffic-related noise is an additional contributor to global mortality and morbidity. Both health risk factors substantially contribute to cardiovascular, metabolic and neuropsychiatric sequelae. Studies on the combined exposure are rare and urgently needed because of frequent co-occurrence of both risk factors in urban and industrial settings. To study the synergistic effects of PM and noise, we used an exposure system equipped with aerosol generator and loud-speakers, where C57BL/6 mice were acutely exposed for 3d to either ambient PM (NIST particles) and/or noise (aircraft landing and take-off events). The combination of both stressors caused endothelial dysfunction, increased blood pressure, oxidative stress and inflammation. An additive impairment of endothelial function was observed in isolated aortic rings and even more pronounced in cerebral and retinal arterioles. The increase in oxidative stress and inflammation markers together with RNA sequencing data indicate that noise particularly affects the brain and PM particularly affects the lungs. Noise also increased levels of circulating stress hormones adrenaline and noradrenaline, while PM increased levels of circulating cytokines CD68 and MCP-1. The combination of both stressors has additive adverse effects on the cardiovascular system that are based on PM-induced systemic inflammation and noise-triggered stress hormone signaling. We demonstrate an additive upregulation of ACE-2 in the lung, suggesting that there may be an increased vulnerability to COVID-19 infection. The data warrant further mechanistic studies to characterize the propagation of primary target tissue damage (lung, brain) to remote organs such as aorta and heart by combined noise and PM exposure.Copyright © 2023
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Introduction: Multiple meta-analyses have shown that over 15% patients with COVID-19 have at least one gastrointestinal complaint, most commonly diarrhea. The effects on the gastrointestinal system are thought to be mediated by the high expression of angiotensin-converting enzyme 2 (ACE2) and cellular serine proteases (TMPRSS2) in enterocytes, which cause altered intestinal permeability. The purpose of this study was to determine the incidence of diarrhea as it relates to COVID-19 infection and to determine if having concomitant diarrhea had a significant impact on disease course. Method(s): A retrospective chart review of 164,730 patients in a hospital system who were older than 18 years of age and had a positive SARS-CoV-2 test from March 2020 to February 2022 was completed. Diarrhea was determined using ICD code or patient's symptoms. Patients with confounding variables such as IBD, IBS, Celiac, Clostridium difficile, and pancreatic insufficiency were excluded. Demographic clinical characteristics and outcomes, including inpatient admission and mortality, were compared in patients with and without diarrhea. The Mann-Whitney test and Fisher's exact or Chi-square test was used for continuous and categorical variables respectively and multivariate logistic regression was used to evaluate for significant differences in disease outcome between the two groups. (Table) Results: Of the 164,730 patients included, 14,648 (8.89%) had diarrhea at the time of SARS-CoV-2. 6,748/33,464 (20.16%) of inpatient admissions were associated with diarrhea. On multivariate analysis, diarrhea was an independent risk factor for inpatient hospitalization (OR 2.39, CI 95% 2.28-2.51, P, 0.001) and inpatient mortality (OR 1.15, CI 96% 1.06-1.26, P= 0.001) after controlling for age, gender, race, comorbidities that could impact patient outcome, use of immunomodulators and outpatient antibiotics. Conclusion(s): These findings show that, even with controlling for comorbidities with COVID-19, diarrhea was an independent factor for predicting inpatient mortality and inpatient admission in general. Patients who had diarrhea and COVID-19 were sicker, having more comorbid conditions than those without diarrhea in our cohort. Attention should be given to not only respiratory complaints of COVID-19, but also gastrointestinal complaints, as they are an indicator of poor prognosis and mortality.
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In elderly patients with COVID-19 cognitive functions decline;it has been suggested that SARS-CoV-2 infection may lead to the development of Alzheimer's disease (AD) and other long-term neurological consequences. We review several parallels between AD and COVID-19 in terms of pathogenetic mechanisms and risk factors. Possible mechanisms through which COVID-19 can initiate AD are discussed. These include systemic inflammation, hyperactivation of the renin-angiotensin system, innate immune activation, oxidative stress, and direct viral damage. It has been shown that increased expression of angiotensin-renin receptors (ACE2) may be a risk factor for COVID-19 in patients with AD. When entering the central nervous system, the SARS-CoV-2 virus can directly activate glial cell-mediated immune responses, which in turn can lead to the accumulation of beta-amyloid and the subsequent onset or progression of current AD. The involvement of inflammatory biomarkers, including interleukins (IL): IL6, IL1, as well as galectin-3, as a link between COVID-19 and AD is discussed. The rationale for the use of memantine (akatinol memantine) in patients with COVID-19 in order to prevent the development of cognitive deficits is discussed. Memantine has been shown to have a positive effect on neuroinflammatory processes in the onset or exacerbation of cognitive deficits, in reducing cerebral vasospasm and endothelial dysfunction in viral infections. Memantine therapy may improve everyday activity and reduce the risk of severe SARS-CoV-2 infection.Copyright © 2022 Ima-Press Publishing House. All rights reserved.
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Aim To explore the active compound of Maxingganshi decoction in treatment of novel coronavirus pneumonia(COVID-19). Methods With the help of TCMSP database, the chemical components and action targets of ephedra, almond, licorice, and gypsum in Maxingganshi decoction were searched, and then a C-T network, protein interaction analysis, GO functional enrichment analysis, and KEGG pathway enrichment were constructed. Analysis was performed to predict its mechanism of action. Results A total of 120 compounds in Maxingganshi decoction corresponded to 222 targets. PTGS2, ESR1, PPARG, AR, NOS2, NCOA2 acted on PI3K-Akt signaling pathway, TNF signaling pathway, IL-17 signaling pathway, T cell receptor signaling pathways, etc. The results of molecular docking showed that the affinity of quercetin, kaempferol, glabridin and other core compounds was similar to recommended drugs in treatment of COVID-19. Conclusions The active compounds of Maxingganshi decoction can target multiple pathways to achieve the therapeutic effect of COVID-19.Copyright © 2020 Publication Centre of Anhui Medical University. All rights reserved.
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Risk factors for severe COVID-19 are also associated with periodontitis. They are smoking, older age, obesity, diabetes mellitus, hypertension and cardiovascular diseases. The aim of the study was to select and analyze publications that consider a possible relationship between inflammatory periodontal diseases and the severity of COVID-19. Material and methods. The search for publications by the key words was conducted using the electronic databases: Cochrane Library;MEDLINE, eLIBRARY for systematic review. We selected 94 publications, the systematic review included 10 scientific articles presenting the results of randomized trials. Results. The results of the analysis showed the connection between COVID-19 severity and inflammatory periodontal diseases presence. In the patients with severe COVID-19 on the background of periodontitis it was established a high risk for artificial lung ventilation prescription. The course of COVID-19 is possibly depending on high expression of ACE2 receptors in oral mucosal cells and aspiration of pathogenic bacteria from periodontal tissues with saliva on the background of SARS-CoV-2 viral infection. The bacterial etiology of periodontitis plays important role of an immunological trigger that causes hyperreaction of humoral and cellular immunity, NETosis activation and NLRP3 inflammation. Conclusion. The presence of periodontitis in patients with overweight and obesity, DM or hypertension may be associated with severe COVID-19 course, possible development of complications and pneumonia.Copyright © Eco-Vector, 2023. All rights reserved.
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Patients infected by the SARS-CoV-2 virus are commonly diagnosed with threatening liver conditions associated with drug-induced therapies and systemic viral action. RNA-Seq data from cells in bronchoalveolar lavage fluid from COVID-19 patients have pointed out dysregulation of kallikrein-kinin and renin-angiotensin systems as a possible mechanism that triggers multi-organ damage away from the leading site of virus infection. Therefore, we measured the plasma concentration of biologically active peptides from the kallikrein-kinin system, bradykinin and des-Arg9-bradykinin, and liver expression of its proinflammatory axis, bradykinin 1 receptor (B1R). We measured the plasma concentration of bradykinin and des-Arg9-bradykinin of 20 virologically confirmed COVID-19 patients using a liquid chromatography-tandem mass spectrometry-based methodology. The expression of B1R was evaluated by immunohistochemistry from post-mortem liver specimens of 27 COVID-19 individuals. We found a significantly higher blood level of des-Arg9-bradykinin and a lower bradykinin concentration in patients with COVID-19 compared to a healthy, uninfected control group. We also observed increased B1R expression levels in hepatic tissues of patients with COVID-19 under all hepatic injuries analyzed (liver congestion, portal vein dilation, steatosis, and ischemic necrosis). Our data indicate that des-Arg9-bradykinin/B1R is associated with the acute hepatic dysfunction induced by the SARS-CoV-2 virus infection in the pathogenesis of COVID-19.