ANTIPHOSPHOLIPID ANTIBODIES AND VASCULAR THROMBOSIS IN PATIENTS WITH THE MOST SEVERE FORMS OF COVID-19

BackgroundThe presence of antiphospholipid antibodies (aPL) has been observed in patients with COVID-19 (1,2), suggesting that they may be associated with deep vein thrombosis, pulmonary embolism, or stroke in severe cases (3). Antiphospholipid syndrome (APS) is a systemic autoimmune disorder and the most common form of acquired thrombophilia globally. At least one clinical criterion, vascular thrombosis (arterial, venous or microthrombosis) or pregnancy morbidity and at least one laboratory criterion- positive aPL two times at least 12 weeks apart: lupus anticoagulant (LA), anticardiolipin (aCL), anti-β2-glycoprotein 1 (anti-β2GPI) antibody, have to be met for international APS classification criteria(4). Several reports also associate anti-phosphatidylserine/prothrombin antibodies (aPS/PT) with APS.ObjectivesTo combine clinical data on arterial/venous thrombosis and pregnancy complications before and during hospitalisation with aPL laboratory findings at 4 time points (hospital admission, worsening of COVID-19, hospital discharge, and follow-up) in patients with the most severe forms of COVID-19 infection.MethodsPatients with COVID-19 pneumonia were consequetively enrolled, as they were admitted to the General hospital Pancevo. Exclusion criteria were previous diagnosis of inflammatory rheumatic disease and diagnosis of APS. Clinical data were obtained from the medical records. Laboratory results, including LA, aCL, anti-β2GPI, and aPS/PT antibodies were taken at hospital admission, worsening (defined as cytokine storm, connection of the patient to the respirator, use of the anti-IL-6 drug- Tocilizumab), at hospital discharge and at 3-months follow-up and sent to University Medical Centre Ljubljana, Slovenia for analysis. Statistics was performed by using SPSS 21.Results111 patients with COVID-19 pneumonia were recruited;7 patients died during hospitalisation (none were aPL-positive on admission and at the time of worsening), 3 due to pulmonary artery embolism. All patients were treated according to a predefined protocol which included antibiotics, corticosteroids, anticoagulation therapy and specific comorbidity drugs;patients with hypoxia were supported with oxygen. During hospitalisation, pulmonary artery thrombosis occurred in 5 patients, one was aPL-positive at all time points (was diagnosed with APS), others were negative. In addition, 9/101 patients had a history of thrombosis (5 arterial thrombosis (coronary and cerebral arteries), none of whom was aPL-positive on admission and at follow-up, and 4 venous thrombosis, one of which was aPL-positive at all time points and received an APS diagnosis). Among 9/101 patients with a history of thrombosis, 55.6% were transiently positive at the time of discharge, compared to patients without prior thrombosis, in whom 26.1% were transiently positive at the hospital release (p=0.074). Two patients had a history of pregnancy complications (both had miscarriage after 10th week of gestation), but did not have aPL positivity at any time point.ConclusionAlthough aPL was expected to be associated with vascular disease in the most severe forms of COVID-19, all patients that have died in our cohort were aPL negative. At hospital discharge, 56% of patients with a history of arterial or venous thrombosis had positive aPL that became negative at the 3-months follow-up (were transienlty positive), which should be considered when prescribing therapy after hospitalisation.References[1]Trahtemberg U, Rottapel R, Dos Santos CC, et al. Anticardiolipin and other antiphospholipid antibodies in critically ill COVID-19 positive and negative patients. Annals of the Rheumatic Diseases 2021;80:1236-1240.[2]Stelzer M, Henes J, Saur S. The Role of Antiphospholipid Antibodies in COVID-19. Curr Rheumatol Rep. 2021;23(9):72-4.[3]Xie Y, Wang X, Yang P, Zhang S. COVID-19 complicated by acute pulmonary embolism. Radiology: Cardiothoracic Imaging 2020: 2: e200067.[4]Miyakis S, Lockshin MD, Atsumi T, Branch DW, Brey RL, et al. J.Thromb.Haemost. 2006;4: 295-306.Acknowledgements:NIL.Disclosure of nterestsNone Declared.

Binge drinking alcohol and circadian misalignment in night shift nurses is associated with decreased resiliency to COVID-19 infection

Background: Nurses and other first responders are at high risk of exposure to the SARS-CoV2 virus, and many have developed severe COVID-19 infection. A better understanding of the factors that increase the risk of infection after exposure to the virus could help to address this. Although several risk factors such as obesity, diabetes, and hypertension have been associated with an increased risk of infection, many first responders develop severe COVID-19 without established risk factors. As inflammation and cytokine storm are the primary mechanisms in severe COVID-19, other factors that promote an inflammatory state could increase the risk of COVID-19 in exposed individuals. Alcohol misuse and shift work with subsequent misaligned circadian rhythms are known to promote a pro-inflammatory state and thus could increase susceptibility to COVID-19. To test this hypothesis, we conducted a prospective, cross-sectional observational survey-based study in nurses using the American Nursing Association network. Method(s): We used validated structured questionnaires to assess alcohol consumption (the Alcohol Use Disorders Identification Test) and circadian typology or chronotype (the Munich Chronotype Questionnaire Shift -MCTQ-Shift). Result(s): By latent class analysis (LCA), high-risk features of alcohol misuse were associated with a later chronotype, and binge drinking was greater in night shift workers. The night shift was associated with more than double the odds of COVID-19 infection of the standard shift (OR 2.67, 95% CI: 1.18 to 6.07). Binge drinkers had twice the odds of COVID-19 infection of those with low-risk features by LCA (OR: 2.08, 95% CI: 0.75 to 5.79). Conclusion(s): Working night shifts or binge drinking may be risk factors for COVID-19 infection among nurses. Understanding the mechanisms underlying these risk factors could help to mitigate the impact of COVID-19 on our at-risk healthcare workforce.Copyright © 2023 The Authors. Alcohol: Clinical and Experimental Research published by Wiley Periodicals LLC on behalf of Research Society on Alcohol.

Relationship between COVID-19 and liver diseases: The role of hepatologists in clinical practice.

COVID-19 due to severe acute respiratory syndrome coronavirus 2, which has become a global pandemic, produces elevated liver enzymes, especially in severe cases. The mechanism suggests involvement of an administrated drug, cytokine storm, or hypoxia, etc., as opposed to virus-induced direct damage. If liver enzymes are elevated in COVID-19, we should evaluate for the presence of other liver diseases, and strictly follow-up liver enzyme values. In patients with COVID-19 complicated by chronic liver disease, we will use telemedicine/visits by phone, so as not to interrupt the treatment of the underlying disease, avoid unnecessary outpatient visits, and strive to halt the spread of the infection. Metabolism-associated fatty liver disease, which is often related to obesity, diabetes, and hypertension, may be a risk factor for COVID-19 severity. International academic societies have recommended guidance outlining the evidence to date regarding the management of patients with COVID-19 and liver disorders, and chronic liver disease under the COVID-19 pandemic.Copyright 2020 The Japan Society of Hepatology.

The Role of Inflammation in the Development of Complications Caused by Covid-19: A Review Study

Background and Aim: It is important to understand how inflammation caused by COVID-19 affects patients and leads to more complications and diseases. According to the importance of controlling COVID-19 related complications, the current study was designed to evaluate the inflammation caused by COVID-19 and its related complications. Materials and Methods: The present study is a review study. Studies were retrieved from PubMed, Web of science, Scopus and Google scholar databases. Finally, according to the purpose of the study, the relevant resources were selected by the researchers and a summary of their results was presented in this study. Results: The present study showed that SARS-CoV-2 viruses enter their genome into the host cell after entering to the cell by the spike protein (S) and the important receptor of coronavirus, angiotensin converting enzyme 2 (ACE - 2), and causes the onset of cytokine storms and consequently increase of primary cytokines involved in inflammation. IL-6, IL-8, TNF-α and IL-1 cytokines are key factors;These factors in turn activate macrophages, dendritic cells (DC) and other immune cells. Studies revealed that the inflammation caused by SARS-CoV-2 in the liver by inducing IL-6 activates the JAKs/STAT3 pathway, whose receptor is only found in the liver and immune cells, and causes cytokine release syndrome. Cytokines also cause the release of reactive oxygen species (ROS), superoxide anion, and nitric oxide, so that all of them can damage myocardial cells and cause insulin resistance and diabetes. In addition, the increase of inflammatory cytokines such as IL4, IL10 and IL6 and immune cells lead to cardiac disorders such as arrhythmia. The entry of the virus into the digestive system reduces the bacteria secreting butyrate (with anti-inflammatory effects) and leads to the induction of severe inflammation. Also, corona virus causes obsessive compulsive disorder, depression and other neurological disorders by increasing pro-inflammatory cytokines and increasing the activity of indoleamine 2,3 dioxygenase (IDO). Conclusion: Studies have shown that the inflammation caused by COVID-19 plays an important role in the development of the related complications such as disorders in the digestive, hepatic, cardiac, neurologic, pancreas systems and other organs. Therefore, targeting cytokines can potentially improve survival and reduce mortality. © 2022 the Authors. Published by Tehran University of Medical Sciences.

Mastocytosis and COVID19 infection and vaccination: A pediatric series

Introduction: Mastocytosis encompasses a heterogeneous group of diseases characterized by an accumulation of clonal mast cells (MC) in the skin and/or internal organs, and symptoms of MC activation. This MC activation can be elucidated by several factors, including infections or vaccination. Objective(s): We present our experience with COVID infection and vaccination in a series of 133 patients with pediatric mastocytosis. Method(s): Between January 1998 and December 2022, 133 pediatric patients have been referred to our hospital owing to clinically suspected MC disorder, mainly with mastocytosis in the skin. The final diagnoses of mastocytosis were established by the presence of typical skin lesions together with an increase of MC numbers in a biopsy from lesional skin or activating KIT mutations in lesional skin tissue. Serum baseline tryptase and total immunoglobulin E levels were measured, and patients underwent a comprehensive allergy workup to confirm atopic status and history of anaphylaxis. Regarding vaccination, REMA's (Spanish Network on Mastocytosis) protocol was followed. Result(s): 13 patients with COVID infection were identified, of which 25 (56,8%) were female and 0% had symptoms of MC activation. All of them had an asymptomatic or mild course of COVID infection. None of the patients experimented MC activation symptoms during viral illness. Regarding COVID vaccination, all patients received premedication with antihistamine 60 minutes prior vaccination. No one experimented immediate reactions and only one patient (0,75%) referred worsening of MC activation symptoms (baseline pruritus, urtication and brain fog) only after the first doses, recovering without changes in his treatment (oral cromoglycate and antihistamine) in two months. Discussion(s): Although MC have been implicated in the pathogenesis of cytokine storm in COVID19, there is no clinical evidence of SARSCoV- 2-induced MC activation, perhaps related to the fact that bone marrow MC lack angiotensin-converting enzyme 2 receptors.

Hemophagocytosis in the Red Bone Marrow of Patients with Covid-19 with Sars-Cov-2 Infection

Red bone marrow samples investigation in deceased COVID-19 patients enabled to identify the phenomena of secondary hemophagocytosis. Analysis of the data showed that phagocytic reactions during infection of patients with SARS-CoV-2 are manifested both in relation to erythrocytes and leukocytes. The data obtained make it possible to expand the strategy of therapeutic measures, taking into account the new data on the mechanisms of the pathogenesis of COVID-19 in severe viral infection based on morphological findings and additional information on the involvement of young erythrocytes and lymphocytes in the structure of the red bone marrow in the cascade of pathological reactions. The results obtained confirm a wide range of aggressive damaging effects of SARS-CoV-2 in the development of multiple organ failure against the background of COVID-19 and the involvement of the red bone marrow in the pathological process. The authors supplemented information about the mechanisms of hypoxia in COVID-19, which is not only a consequence of damage to the respiratory epithelium, but also the result of damage to erythrocyte differons both at the level of red bone marrow and in peripheral blood. This fact must be taken into account in the development of a treatment strategy and in the creation of new drugs for the treatment of infected patients with various strains of SARS-CoV-2.

The effectiveness of Tocilizumab in severe covid 19 pneumonia among critically ill patients

Background: Tocilizumab, an interleukin-6 (IL-6) antagonist, is being evaluated for the management of covid-19 pneumonia. The objective of this study was to assess the effectiveness of Tocilizumab in severe covid-19 pneumonia. Method(s): This was a retrospective, observational, single centre study performed in 121 patients diagnosed with severe covid-19 pneumonia. 83 patients received standard of care treatment whereas 38 patients received tocilizumab along with standard of care. Tocilizumab was administered intravenously at 8mg/kg (upto a maximum of 800mg). The second dose of Tocilizumab was given 12 to 24 hours apart. The primary outcome measure was ICU related and hospital related mortality. The secondary outcome measures were change in clinical status of patients measured by WHO (World Health Organisation) 7 category ordinary scale, changes in interleukin-6 (IL-6) levels, secondary infections and duration of ICU stay. Result(s): Tocilizumab was administered between 3-27 days after the patient reported symptoms ( a median of 10.9 days ) and between the 1st to 3rd day of ICU admission (median of 2.1 days) . In Tocilizumab group, 16(42.1%) of 38 patients died in ICU whereas in standard of care group, 27(32.53%) of 83 patients died. The difference in clinical status assessed using WHO (World Health Organisation) 7 category ordinary scale at 28 days between Tocilizumab group and standard of care group was not statistically significant (odds ratio 1.35, 95% confidence interval 0.61 to 2.97, p = 0.44). Conclusion(s): Tocilizumab plus standard care was not superior to standard care alone in reducing mortality and improving clinical outcomes at day 28.Copyright © RJPT All right reserved.

INFLAMMATORY RESPONSE AND ITS CORRECTION IN FORMING A HOST RESPONSE TO EXPOSURE TO ADVERSE ENVIRONMENTAL FACTORS

This study systematically review knowledge about the mechanisms of formation of an inflammatory reaction under the influence of biological, physical, and chemical factors, their similarities and differences, and possible methods of pharmacological correction of pathological conditions associated with excessive activation. The effect of adverse environmental factors, such as biological, physical, and chemical factors, causes a systemic response, which is aimed at maintaining homeostasis and is caused, among other things, by a coordinated reaction of the immune system. Phlogogenic agents result in the activation and regulation of the inflammatory response, which is formed by cellular and humoral components of innate immunity. The activation of innate immunity is characterized by a rapid host response, which diminishes following the elimination of "foreign” invaders, endogenous killer cells, and neogenesis. Depending on the nature of the active factors (biopathogens, allergens, toxins, ionizing radiation, etc.), the mechanisms of immune response arousal have unique features mainly originating from the differences in the recognition of specific molecular patterns and "danger signals” by different receptors. However, inflammatory mediators and inflammatory response patterns at the systemic level are largely similar even under widely different triggers. Inflammation, having evolved as an adaptive reaction directed at the immune response, can lead to the development of chronic inflammation and autoimmune diseases due to a mismatch in mechanisms of its control. A "failure” in the regulation of the inflammatory process is the excessive activation of the immune system, which leads to the cytokine release syndrome (hypercytokinemia, or "cytokine storm”) and can cause self-damage (destruction) of tissues, multiple-organ failure, sepsis, and even death. Modern advances in the study of the pathogenetic bases of the inflammatory response are suggested, such as pharmacological correction using pattern recognition receptor antagonists, pro-inflammatory cytokine inhibitors, or blocking of key control genes or signaling pathways. All rights reserved © Eco-Vector, 2022.

Boosting the Immune System with Vitamin D: Special Focus on Prevention of COVID-19 and Complications

In addition to the classical functions of the musculoskeletal system and calcium homeostasis, the function of vitamin D as an immune modulator is well established. The vitamin D receptors and enzymes that metabolize vitamin D are ubiquitously expressed in most cells in the body, including T and B lymphocytes, antigen-presenting cells, monocytes, macrophages and natural killer cells that trigger immune and antimicrobial responses. Many in vitro and in vivo studies revealed that vitamin D promotes tolerogenic immunological action and immune modulation. Vitamin D adequacy positively influences the expression and release of antimicrobial peptides, such as cathelicidin, defensin, and anti-inflammatory cytokines, and reduces the expression of proinflammatory cytokines. Evidence suggestss that vitamin D's protective immunogenic actions reduce the risk, complications, and death from COVID-19. On the contrary, vitamin D deficiency worsened the clinical outcomes of viral respiratory diseases and the COVID-19-related cytokine storm, acute respiratory distress syndrome, and death. The study revealed the need for more preclinical studies and focused on well-designed clinical trials with adequate sizes to understand the role of vitamin D on the pathophysiology of immune disorders and mechanisms of subduing microbial infections, including COVID-19.Copyright © 2023 Bentham Science Publishers.

Should Young Covid-19 Patients be Suplemented with Vitamin D?

It is well known that vitamin D's general immunomodulatory actions are helpful in viral infections and that a shortage is linked to a more serious prognosis for Covid-19. In this sistematic review, we examined the existing literature on evidence as to whether there is also link between vitamin D range levels in pediatric population and the outcome of the Covid-19 infection. We looked for studies that measured vitamin D blood concentrations and examined the effects of vitamin D supplementation in young infected patients. Vitamin D may decrease the risk of respiratory infections in a number of ways through its interactions with numerous cells, including by decreasing viral survival and replication, reducing the cytokine storm, raising angiotensin-converting enzyme 2 concentrations (ACE2) while not damaging the endothelial integrity. The incidence or severity of Covid-19 is linked with blood 25-hydroxyvitamin D concentrations, according to many observational studies. However experimental verification is still needed. Given their safety and broad therapeutic window, vitamin D supplements seem to be an effective way for individuals and doctors to prevent or treat Covid-19. Nonetheless, the outcomes of significant vitamin D randomized controlled trials are further needed.Copyright © 2022 Maria Nicolae et al., published by Sciendo.

SARS-CoV-2 Variants Impact on Key Signaling Pathways Metamorphoses into Severity

The Severe Acute Respiratory Syndrome Coronavirus-2 causes a dreadful Coronavirus Disease namely COVID-19. Respiratory system is the primary target of the virus. It also impairs other major organs such as kidney, heart, liver, brain etc. Multiple novel variants of SARS-CoV-2 have appeared since the SARS-CoV-2 pandemic occurred which are linked to increased virulence, disease transmission and severity. The virus attacks the host signalling pathways to maintain a favourable environment for its spread. The present study focuses on the comprehensive analysis of major signaling pathways affected due to several variants of SARS-CoV-2 leading to abnormalities in cell growth and differentiation. The information was curated from the weblinks of several platforms like WHO, CDC, PANGO, Nextstrain clade and GISAID clade. The data on signaling pathways and comorbidities was generated by screening of different research and review articles. SARS-CoV-2 consolidates the cytoskeleton of the host for effective cell invasion and modulates the transcription processes to enable the translation of viral protein(s). These events lead to significant increase and prolonged hyper inflammation. Further, a decreased interferon (IFN) response along with increased interleukin production leading to cytokine storm is observed. Deregulation of interleukin pathways, TNF-alpha signalling through JAK/STAT-3 signalling, MAPK1, mTOR, PI3K are few other signalling pathways that are affected on SARS-CoV-2 infection. This review represents a comprehensive analysis of the vigorous life cycle of SARS CoV-2, its different variants affecting host signalling pathways which eventually cause dysfunctioning of several organs and development of comorbidities.

CARDIOVASCULAR COMPLICATIONS IN PATIENTS AFTER CORONAVIRUS DISEASE-2019

The data of the modern literature describing the long-term consequences of infection of the body with SARSCoV-2 on the cardiovascular system in the framework of postcovid syndrome are analyzed. To date, postcovid syndrome refers to a condition in which symptoms continue to persist for more than 12 weeks from the moment of diagnosis of COVID-19. Various complaints of patients after undergoing a new coronavirus infection are described, the distinguishing feature of which is their versatility, where cardiovascular manifestations are assigned one of the leading roles. Postural orthostatic tachycardia syndrome, cardiac arrhythmia and conduction disorders are considered. The role of SARS-CoV-2 in the formation of de novo and decompensation of pre-existing cardiovascular diseases has been demonstrated. The possibility of developing heart failure in patients with COVID-19 as an outcome of inflammation of the heart muscle is shown. Particular attention is paid to the analysis of the incidence of myocarditis after 3 months or more from the diagnosis of COVID-19, as well as thrombotic complications, in the genesis of which the main role belongs to the formation of endothelial dysfunction resulting from the interaction of SARS-CoV-2 with vascular endothelial cells. The autoimmune component of the pathogenesis of damage to the cardiovascular system as a result of the formation of endothelial dysfunction in COVID-19 is also considered. The authors present a laboratory-instrumental algorithm for determining cardiovascular complications in people who have undergone COVID-19, including the determination of the N-terminal fragment of the brain natriuretic peptide B-type prohormone, the level of anticardial antibodies, electrocardiography, echocardiography, as well as magnetic resonance imaging of the heart with contrast. All rights reserved © Eco-Vector, 2022.

A comprehensive review and meta-analysis of the relationships between interleukin-7 levels and COVID-19 severity

Introduction: As the major mechanism for coronavirus disease 2019, cytokine storm-mediated organ harm continues to dominate current understanding. Despite the first hyper-inflammatory phase, emerging data show that virus-induced poor host immunity may be the true cause of mortality in many individuals. Interleukin 7 (IL-7) is an interleukin that participates in the COVID-19 cytokine storm and regulates the immune system. Its role in COVID-19 cytokine storms is thought to be related to its ability to stimulate the formation and activation of immune cells such as T cells and B cells. This meta-analysis aims to determine the relationship, if any, between interleukin-7 and COVID-19 severity. Methods: This study was planned as a systematic review and meta-analysis and followed the PRISMA guidelines. Four main electronic databases (Web of Science, PubMed, Scopus, and the Cochrane Central Register of Controlled Trials) were searched from January 1st, 2020 to September 2nd, 2022, to find papers investigating the prognostic significance of interleukin-7 in COVID-19-hospitalized adults. Google Scholar was used in addition to the online database search. A random effects model was used to calculate mean differences and 95% confidence interval (CIs) as well as the I2 statistics for heterogeneity analysis. Results: Seven papers were chosen for meta-analysis findings synthesis. All six trials reported interleukin-7 levels among severe and non-severe COVID-19 patients. Pooled analysis showed that IL-7 levels in the severe group were 62.79±81.03 pg/mL, compared to 33.39±56.54 pg/mL for the non-severe group (SMD =-0.17;95%CI:-0.93 to 0.60;p=0.67). Discussion: Available evidence suggests that elevated levels of IL-7 were not associated with the disease severity of COVID-19. While IL-7 levels alone may not have a substantial impact on COVID-19 severity, the interaction between IL-7 and other cytokines, immune cells, and variables such as viral load and genetics should be investigated further. Take-home message: This meta-analysis found that there was no strong link between levels of interleukin-7 and the severity of COVID-19. However, further research is needed to explore the interaction between IL-7 and other factors such as cytokines, immune cells, viral load, and genetics in order to better understand the role of IL-7 in COVID-19 pathogenesis. © 2023 by the authors.

Nutrition Strategies Pre-infection, during, and Post-infection with Coronavirus Disease

Coronavirus disease is a serious viral infection that is characterized by severe inflammation and lymphopenia. The virus attacks many organs causing acute respiratory distress and malfunctioning of the organs leading to death. Through strengthening of the innate immune system, a balanced diet plays a critical role in defense against bacterial and viral diseases. A healthy diet before, during and after an infection can lessen the severity of the symptoms and speed up the recovery of damaged cells. Due to the Mediterranean diet's high concentration of bioactive polyphenols, which have antioxidant, anti-inflammatory, and antithrombic properties, numerous studies have suggested that it is a preventative dietary strategy against many diseases including coronavirus disease. Nutrition and herbal plants play a key role to enhance the immunity of people to protect and fight against coronavirus. Diet rich in antioxidants and phytochemicals represents perfect barrier to the virus through elevation of the innate immunity of the body. In addition, gut microbiota including prebiotics, probiotics, and synbiotics were found to enhance immunity to reduce the symptoms of the disease during infection. Protein-rich foods and honey bee products reported significant role during and post-coronavirus infection. This review presents updated information from original pre-clinical and clinical researches, and review articles as well to expose the nutritive strategies including breastfeeding benefits to infants pre-infection, during, and post-infection with coronavirus.Copyright © 2023, Scientific Foundation SPIROSKI. All rights reserved.

Possibilities of low-dose radiation therapy in the treatment of intrapulmonary injuries caused by COVID-19 infection.

This paper examines the relevance of the use of a single irradiation of lungs in treatment of pneumonia caused by a new coronavirus infection. Clinical observations are presented that demonstrate perspectives in the treatment of this disease. Patients with severe pneumonia who were prescribed LD-RT (low-dose radiation therapy) at a dose of 0.5-1.5 Gy showed shorter recovery times and no complications. This method of treatment has shown its effectiveness in a number of studies from different countries, predicting success and economic benefits in its further use and study. A literature search containing information on relevant studies was carried out in PubMed, EMBASE, Web of Science and Google Scholar systems. Attention was focused on full-text articles given their general availability in a pandemic.Copyright © 2021 VIDAR Publishing House. All right reserved.

Features of the Immune Response in COVID-19

BACKGROUND This review is devoted to the analysis of the features of the immune response in COVID-19. The review indicates the clinical manifestations of COVID-19, modern data on the immunopathogenesis of the disease and its complications are considered. AIM OF STUDY To clarify some pathogenetic mechanisms of the immune response in COVID-19, which can help in creating an algorithm for examining patients for early prognosis and prevention of severe course and complications of the disease. MATERIAL AND METHODS To achieve this goal, the results of domestic and foreign scientific studies on the pathogenesis, diagnosis and treatment of COVID-19 were analyzed. The literature search was carried out in electronic search engines Scopus and PubMed. For the analysis, scientific articles published in the period from 2019 to 2021 were selected;88% of analyzed works are not older than 5 years. CONCLUSION The late production of type I IFN, an increase in the level of pro-inflammatory monocytes, a decrease in the expression of HLA-DR on monocytes, violation of the presentation of the virus and the formation of specific lymphocytes, the death of T-lymphocytes and profound immunosuppression are of greatest importance for the development of a severe form of COVID-19. © 2023 Sklifosovsky Research Institute for Emergency Medicine. All rights reserved.

COVID-19 cardiac injury: is there a common approach to nosological classification?.

The literature review showed the main scenarios of SARS-CoV-2-associated myocardial injury. On the basis of the analysis of literature it can be concluded that myocardial lesion is multi-factor at COVID-19. Possible scenarios include direct damage to myocardium, development of acute systemic inflammatory response and cytokine storm, effects of acute respiratory distress syndrome, coagulopathy and electrolyte imbalance associated with COVID-19, as well as the toxic effects of drugs used in SARS-CoV-2 treatment schemes. At the same time, a rather vague concept - <<acute damage of myocardium>> - is often used to describe symptoms and laboratory changes in literature. Given the multifactor of myocardial lesions in COVID-19, the clinician often faces a difficult situation - the need for a nosological interpretation of the clinical status of the patient. Knowledge and correct verification of the leading pathogenetic variant of a heart injury can simplify this task, narrow the scope of diagnostic monitoring and organize a personalized approach to therapy.Copyright © 2022 Sinergia Press. All rights reserved.

Non-steroidal anti-inflammatory drugs amid COVID-19 pandemic: An ally or an enemy?

As the current global pandemic of the novel coronavirus diseases 2019 (COVID-19) continues to rage, the scientific and medical worlds are working to establish an effective therapy against the illness. Recently questions regarding non-steroidal anti-inflammatory drugs (NSAIDs) as a potential therapeutic option for COVID-19 have surfaced. While some studies hint towards the possible benefit of NSAIDs against SARS-CoV-2 infection, the current body of evidence also sheds light on the potential risk of using NSAIDs in COVID-19 patients. Thus, the available literature does not provide conclusive evidence for or against the use of NSAIDs for treating COVID-19 patients. Given the limited data available, we suggest cautionary approaches for the public to avoid possible harm until further evidence emerges. NSAIDs should not be used as the first-line agents for COVID-19 unlessunder medical supervision. Moreover, patients with chronic inflammatory conditions should continue the NSAIDs as per their regular prescriptions.