ABSTRACT
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.
ABSTRACT
The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) caused a new coronavirus disease (COVID-19), which is highly contagious and its pathogenesis has not been fully elucidated. In COVID-19, the inflammation and blood coagulation systems are excessively activated. SARS-CoV-2 damages endothelial cells and pneumocytes, which leads to disruption of hemostasis in SARS. Thromboembolism is the main cause of mortality in patients with COVID-19. Clots, including pulmonary embolism (PE) and deep vein thrombosis (DVT), ranging from minor to fatal complications of the SARS-CoV-2 infection are known. Individuals with pre-existing diseases are more susceptible to the development of blood clots and poor outcomes. High levels of circulating cytokines and D-dimer (DD) are influential biomarkers of poor outcomes in COVID-19. The latter occurs as a result of hyperfibrinolysis and hypercoagulation. Plasmin is a key player in fibrinolysis and is involved in the cleavage of many viral envelope proteins, including SARS-CoV. Due to this function penetration of viruses into the host cell occurs. In addition, plasmin is involved in the pathophysiology of acute respiratory distress syndrome (ARDS) in SARS and promotes the secretion of cytokines, such as IL-6 and TNF, from activated macrophages. The focus of existing treatment to alleviate fibrinolysis in patients with COVID-19 is the use of systemic fibrinolytic therapy given thrombotic pathology in severe forms of COVID-19 which may lead to death. However, fibrinolytic therapy may be harmful in the advanced stages of COVID-19, when the status of disseminated intravascular coagulation (DIC) changes from suppressed fibrinolysis to its enhancement during the progression of the disease. This narrative review aims to elucidate the pathogenesis of COVID-19, which will further help in precise diagnosis and treatment. Take-home message: The COVID-19 virus disrupts haemostasis and thromboembolism by over activating the inflammation and blood coagulation systems. High levels of cytokines and D-dimer are indicators of pre-existing diseases and blood clots. Systemic fibrinolytic treatment can reduce severe fibrinolysis in COVID-19, which is caused by plasmin. In the late stages of DIC, when fibrinolysis increases, it may be dangerous. To improve therapy and results, understanding COVID-19 pathogenicity is critical. © 2023 by the authors.
ABSTRACT
Introduction: Infection with SARS-CoV-2 is particularly hazardous in patients with cardiovascular pathology, diabetes or chronic lung disease. Arginine vasopressin (AVP), an antidiuretic hormone secreted in response to hemodynamic and osmotic disturbances plays a crucial role in maintenance of cardiovascular homeostasis. Copeptin has shown promising results regarding its utility in prediction of morbidity and mortality of COVID-19. Therefore, we conducted a meta-analysis to evaluate the role of copeptin in risk stratification in COVID-19. Methods: This study was designed as a systematic review and meta-analysis. We systematically searched the following databases: Scopus, Web of Science, PubMed, EMBASE, Cochrane Library through September 10th, 2022. Methodological quality was assessed using the Cochrane risk-of-bias tool. Results: Pooled analysis of four trials showed that mean copeptin plasma concentrations were higher in patients with severe course of COVID-19 than in patients with non-severe course of the disease (26.64 ± 13.59 vs. 16.75 ± 6.13, respectively;MD=9.39;95%CI: 1.38 to 17.40;I2=99%;p=0.02). Furthermore, higher copeptin concentrations in COVID-19 patients who died than in those who survived (13.25 ± 3.23 vs. 44.65 ± 26.92, respectively;MD=-31.40;95%CI:-42.93 to-19.87;p<0.001). Discussion: Results from the present meta-analysis revealed that increased copeptin plasma concentrations found in COVID-19 patients are associated with the severity of the disease. Copeptin may assist in early identification of COVID-19 progression and possibly in prediction of adverse outcomes, thus its use in risk stratification could be beneficial. Take-home message: Copeptin may assist in early identification of COVID-19 progression and possibly in prediction of adverse outcomes, thus its use in risk stratification could be beneficial. © 2022 by the authors.
ABSTRACT
Introduction: This systematic review and meta-analysis aimed to determine the correlation between IL-4 concentrations and COVID-19 severity. Methods: This study was designed as a systematic review and meta-analysis and was performed in accordance to the PRISMA statement. Titles, abstracts, and full texts of articles were independently reviewed by at least 2 authors. Continuous variables were compared by the mean difference (MD) with 95% confidence interval (CI). Results: Thirty-three studies reported IL-4 levels among severe versus non-severe COVID-19 patients. Pooled analysis showed that levels of IL-4 among those groups varied and amounted to 2.72 ± 3.76 pg/mL vs 3.08 ± 4.14 pg/mL (MD =-0.26;95%CI:-0.43 to-0.10;p = 0.002. In addition, eight studies reported levels of IL-4 among COVID-19 patients who survived vs deceased and was 2.61 ± 0.49 pg/mL vs (3.44 ± 16.4 pg/mL, respectively (MD = 0.22;95%CI: 0.08 to 0.37;p = 0.002). Discussion: This detailed systematic review and meta-analysis revealed that the plasma concentration of IL-4 is a potential risk factor for COVID-19 severity and mortality. Specifically, old age and male gender were associated with high IL-4 levels. Lung damage could result from the change in IL-4 concentration, thus making critical and severe COVID-19 cases at a very high risk of dying, thereby reducing their quality of life. Therefore, strategies such as using monoclonal antibodies to inhibit Th2 cytokines could be explored in developing an effective treatment regimen for COVID-19 patients. Take-home message: An independent risk factor for the severity and fatality of COVID-19 is the plasma levels of IL-4. High IL-4 levels are specifically related to old age and male gender. Lung damage may be a result of the change in IL-4 concentration, placing COVID-19 critically and severely ill at a high risk of dying. © 2022 by the authors.
ABSTRACT
Emerging Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-Cov-2) variants continue to be a threat to tackling the pandemic and a challenge to scientists as they continue to find solutions to the evolving complexities of the pandemic. This rapid literature scan aims to synthesize evidence related to the existence of the new variants, their epidemiology, and data related to vaccine efficacy. Previous variants, such as Alpha, Beta, Gamma, Delta, and Omicron were identified as “Variants of Concern” (VOCs), whereas Lambda and Mu were classified as “Variants of Interest” (VOIs). The risk of hospitalization largely differs among all these variants and the research landscape is still evolving. According to the collective evidence, Gamma variant had the highest hospitalization risk (adjusted hazard ratio, aHR 3.20, 95% CI: 2.40 to 4.26) followed by Beta (aHR 2.85, 95% CI: 1.56 to 5.23), Delta (aHR 2.28, 95% CI: 1.56 to 3.34), Alpha (aHR 1.64, 95% CI: 1.29 to 2.07), and Omicron (aHR 0.92, 95% CI: 0.56 to 1.52) as compared to the original Wuhan strain. It was also found that vaccination decreased the risk of hospitalization following infections with more virulent strains, such as Alpha, Beta, Gamma, and Delta. The risk of hospitalization was the lowest following Omicron infection among vaccinated individuals. Deltacron, a new hybrid strain (AY.4/BA.1) is believed to result from the previous co-circulation of SARS-CoV-2 Delta and Omicron during November 2021-February 2022. This hybrid virus may have been formed in the body of a person who was exposed to both viruses at the same time. Existing evidence suggested no change in epidemiology and severity of infections resulting from this hybrid strain. The COVID-19 pandemic continues to be insidious and treacherous in every form and variant. Vaccination offers a pragmatic solution to fight against the pandemic and in reducing the risk of hospitalizations. Further research and epidemiological surveillance will be needed to determine the evolving complexities of the variants and the pandemic, especially as the pandemic changes its course towards endemicity. The development of efficacious therapeutic interventions and increased vaccine uptake could reduce the morbidity and mortality associated with the SARS-CoV-2 variants. Take-home message: The SARS-CoV-2 virus and its variants are going to appear as the part of typical evolution cycle. This review emphasizes the need for performing continuous genomic surveillance at all levels (local, national, and global) to monitor variant trajectories and outcomes. © 2022 by the authors.
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INTRODUCTION: This study was designed to assess the levels of human serum amyloid A (SAA) among COVID-19 patients. MATERIAL AND METHODS: A systematic review and meta-analysis were conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis. A comprehensive literature search was performed (PubMed, Web of Science, Scopus, and Cochrane network), and studies comparing SSA levels in: (A) with non-severe vs severe COVID-19;(B) severe vs critical COVID-19 condition;(C) survived vs died due to COVID-19 in-hospital treatment period - were included. Random-effects meta-analyses were performed to obtain pooled estimates. RESULTS: Thirty studies met the criteria and were included in the meta-analysis. Pooled analysis showed that SAA levels were statistically significantly lover in non-severe group 58.7 ± 53.9 mg/L compared to 154.5 ± 169.6 mg/L for patients with severe condition (MD = -120.29;95% CI: -135.35 to -105.22;p < 0.001). SAA levels among patients with critical condition were 89.5 ± 90.4 mg/L compared to 195.3 ± 206.2 mg/L (MD = -56.66;95% CI: -101.81 to -11.51;p = 0.01). SAA levels in patient who survived were 108.7 ± 157.3 mg/L, and 206.8 ± 58.8 mg/L for patients who not survived (MD = -85.04;95% CI: -145.78 to -24.29;p = 0.006). CONCLUSIONS: In conclusion, this updated meta-analysis suggests that SAA concentrations are positively correlated with the severity of the COVID-19. Therefore, SAA can be considered a biomarker for predicting the severity and prognosis of COVID-19. Measurement of this parameter might assist clinicians in monitoring and evaluating the severity and prognosis of COVID-19. Copyright © 2022 Via Medica.