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Background: Presepsin (PSN) is a soluble CD14 subtype that has lately been presented as a novel biomarker in patients with sepsis. The aim of the current study was to detect the relation of PSN to COVID‑19 as well as its relation to other biomarkers. Materials and Methods: A total of 125 severe/critical COVID‑19 patients were involved in this work as well as 60 persons enrolled as a control group. Between February 2022 and July 2022, these patients were admitted to Marjan Medical City and Al‑Sadiq hospital. Patients were determined as severe cases according to the guidelines released by National Health World depending on SpO2 percentage. The inflammatory cytokine (PSN) was detected by the ELISA technique. Results: PSN revealed statistically significant differences between patients 261 pg/ml (244–324) and control groups 193 pg/ml (172–218) (P < 0.0001). Correlations between PSN and lymphocytes (LYM), as well as platelets (PLT), were nonsignificant (P > 0.05), while significant negative correlation was found between PSN and both white blood cell (WBC) (r = −0.21, P = 0.01) and granulocytes (GRA) (r = −0.25, P = 0.004). No significant differences between males 273.55 pg/ml and females 284.90 pg/ml regarding presepsin titer mean were detected (P = 0.67). Conclusion: This work adds to the mounting evidence that pro‑inflammatory cytokines directly influence COVID‑19 progression. The management of a cytokine storm that affects COVID‑19 patients and is mostly brought on by pro‑inflammatory cytokines may depend on the early detection and treatment of PSN. [ABSTRACT FROM AUTHOR]

COVID-19 is a viral disease that commonly presents with mild symptoms with predominant respiratory system involvement. However, it can cause serious complications such as acute respiratory disease, multi-organ dysfunction, especially in patients with comorbidities. As it is a new disease, the full picture of the disease and its complications are not yet fully understood. Moreover, the patients at risk of complications are not well identified, and the data about the biphasic pattern of cytokine storm syndrome are limited. Here, we report the case of a 64-year-old male having diabetes mellitus, hypertension, ischemic heart disease with triple-vessel coronary artery disease tested positive for severe acute respiratory syndrome coronavirus 2, then complicated with acute respiratory distress syndrome and two waves of cytokine storm in 28 days. [ABSTRACT FROM AUTHOR]

Aim and objective Fever and lymphocyte count to start the interventions and not wait for the upregulation of IL-6 and down regulation of SpO2 levels amongst the patients. Background In SARS-CoV-2 host immune response play a critical role in disease pathogenesis. The coronavirus not only activates antiviral immune responses, but it can also cause uncontrolled inflammatory responses categorized by marked proinflammatory cytokine release in patients with severe COVID-19, leading to lymphopenia. In this present article we have studied the basic parameters of COVID-19 that includes fever and lymphocyte count and their deep association with markers of disease prognosis and cytokine storm such as IL-6, HRCT score and SpO2 levels. With this basic routine clinical and laboratory parameters we can consider recurrent/prolonged fever and low count of lymphocytes are the earliest biomarkers of the upcoming cytokine storm. Method We conducted a hospital-based case-control study of patients who visited to the tertiary healthcare centre in Amravati (Maharashtra), India with a positive SARS-CoV-2 polymerase chain reaction (PCR) assay, from August 01, 2020 to July 03, 2021. Upon hospital visit, all patients underwent a HRCT chest score, complete blood count (CBCs), renal and liver panel, IL-6. Patients with fever and other symptoms which were not responsive to the treatment were admitted to the hospital. Patients who tested positive and admitted to the hospital were not discharged until they had 2 negative RTPCR tests 24 hours apart. Patient details including demographics, history of comorbidities associated with every patient, the records of the vital signs, symptoms and all the reports of radiological and blood assays were obtained from computerized medical records of the hospital. Results We screened total 1324 patients admitted to Tertiary health care center Amravati (Maharashtra), India, from 01 August 2020 to 03 July 2021. From these study, total 156 patients are excluded because of the number of patients, i.e. 106/156 patients founded with no prolonged fever but having same common symptoms. And remaining 50 patients excluded because of they were found with no short duration of fever and asymptomatic. Data was collected from the remaining 1168 (88.21%) as a cohort control group. The cases with recurrent/prolonged fever and short duration had median age [52 (21-83) v/s 52 (17-92) p=0.42] it shows that age is not statistically significant. On the other hand, the cases with recurrent/prolonged fever were more likely to have hypoxia were SpO2 level [90 (50-98)] v/s in short duration of fever were observed.[95 (45-98) p=0.02] shows statistically associated. Similarly, the HRCT chest score in recurrent/prolonged fever were found to be around [8 (0-24)] v/s [6 (0-22) p=0.027] it represents the significant difference. Conclusion Fever and lymphocyte count and their deep association with markers of disease prognosis and cytokine storm such as IL-6, HRCT score and SpO2 level. With this basic routine clinical and labortory parameters we can consider recurrent/prolonged fever and low count of lymphocytes are the earliest biomarkers of the upcoming cytokine storm. Therefore, study recommends the use of fever and lymphocyte count to start the interventions and not wait for the upregulation of IL-6 and down regulation of SpO2 which occurs in late stage. [ABSTRACT FROM AUTHOR]

COVID-19 has caused significant morbidity and mortality around the world. Recent reports point toward the "cytokine storm" as core of pathogenesis in SAR-CoV-2-induced acute lung injury, acute respiratory distress syndrome (ARDS), coagulopathy, and multiorgan failure. We have presented clinical data here wherein cytokine levels in COVID-19 patients do not match typical cytokine storm seen in ARDS. Interestingly, COVID-19 patients in early disease present with hypoxemia with no significant respiratory dysfunction. In addition, it is reported that hospitalized COVID-19 patients have a high incidence of thrombotic complications, especially involving the pulmonary vasculature. We hypothesized that core to pathogenesis of COVID-19 is the dysregulation of neutrophils, which culminates in excessive release of neutrophil extracellular traps (NETs). Recently, an increasing amount of NETs have been seen in sera of severe COVID-19 patients. We have discussed here mechanisms involved which lead to thrombogenesis and vasculitis because of excessive release of NETs. [ABSTRACT FROM AUTHOR]

Introduction: Immunosuppressive agents are theorized to target the cytokine storm syndrome in COVID-19. However, the downstream effects regarding susceptibilities to secondary infection risk remains unknown. This study seeks to determine risk differences for secondary infections among COVID-19 patients who did and did not receive tocilizumab. Methods: We conducted a matched retrospective cohort study from two large, acute care hospitals in Western Connecticut from March 1, to May 31, 2020. We collected variables using manual medical record abstraction. The primary exposure variable was any dose of tocilizumab. The primary outcome was any healthcare-associated bacterial or fungal infection as defined by the National Healthcare Safety Network. We performed a Kaplan–Meier analysis to assess the crude difference in cumulative probability of healthcare-associated infection (HAI) across exposure groups. We also performed a multivariable Cox regression analysis to determine the hazard ratio for HAI by exposure group while controlling for potential confounders. Results: The Kaplan–Meier analysis demonstrated no difference in the cumulative probability of HAI across groups. The adjusted hazard of HAI for patients given tocilizumab was 0.85 times that of patients not given tocilizumab (95% confidence interval = 0.29, 2.52, P = 0.780) after controlling for relevant confounders. Conclusions: Tocilizumab did not increase the incidence of secondary infection among COVID-19 patients. Larger, randomized trials should evaluate infection as a secondary outcome to validate this finding. [ABSTRACT FROM AUTHOR]

The world is fighting the onslaught of COVID 19 for the last 10 months, ever since the first case was reported in December 2019 in Wuhan, China. Now, it has spread to over 200 countries. COVID 19-associated respiratory syndrome is causing a lot of mortality and morbidity. There are reports suggesting that the complications and ARDS associated with COVID 19 is an immune response reaction. The cytokine storm associated with severe cases of COVID 19 acts as a cause of death in many sick patients. It has been shown that COVID 19 is associated with a peculiar immune profile: Decrease in CD3, CD4, CD8, natural killer cell and B-cells; Rise in interleukin (IL)-4, IL-6 and tumor necrosis factor (TNF) alpha; Decrease in IL-10; Decrease in interferon-gamma. Low-dose radiotherapy (LDRT) immunosuppressive features resulting from M2 macrophage phenotype activation, increase in IL-10, transforming growth factor beta, a decrease in IL-6, TNF alpha and an increase in CD3, CD4, and CD8 T cell counts may negate the harmful effects of cytokine release syndrome. Literature review shows that radiation was previously used to treat viral pneumonia with a good success rate. This practice was discontinued in view of the availability of effective antibiotics and antivirals. As there are no scientifically proven treatment for severe COVID 19-associated respiratory distress today, it is prudent that we understand the benefits of LDRT at this critical juncture and take rational decisions to treat the same. This article provides an radioimmunological rationale for the treatment of immune crisis mediated complications in severe cases of COVID 19. [ABSTRACT FROM AUTHOR]

Since the beginning of the COVID-19 pandemic, many therapeutic strategies have been tried, with mixed results, to prevent and treat adult multisystem inflammatory syndrome in COVID-19 (AMIS-COVID-19). The reason behind this may the complex web of highly intertwined pathophysiologic mechanisms involved in the SARS-CoV-2 infection and the corresponding human systemic response, leading to end-organ damage, disability, and death. Colchicine, high-dose aspirin, and montelukast are being investigated currently as potential modulators of AMIS-COVID-19 in patients who fail to improve with traditional therapeutic approaches. Here, we present a patient who presented with high fevers, extreme fatigue and dyspnea, and ongoing deterioration. As part of our clinical approach, we used the simultaneous combination of the three agents listed above, capitalizing on their different respective mechanisms of action against AMIS-COVID-19. Following the initiation of therapy, the patient showed symptomatic improvement within 24 h, with the ability to return to daily activities after 72 h of continued triple-agent approach. Based on this experience, we have reviewed the immunomodulatory basis of this regimen, including potential avenues in which it may prevent the development of cytokine release syndrome (CRS) and its clinical manifestation, AMIS-COVID-19. By blocking the early stages of an inflammatory response, via diverse mechanistic pathways, the regimen in question may prove effective in halting the escalation of CRS and AMIS-COVID-19 in acutely symptomatic, nonimproving COVID-19 patients. [ABSTRACT FROM AUTHOR]

Although many potent drugs have been used for cytokine storm, mortality is high for patients with coronavirus disease-2019 (COVID-19), which is followed up in the intensive care unit. Interferons (IFNs) are the major cytokines of the antiviral defense system released from many cell types. However, IFN-γ plays a key role in both primary and secondary cytokine storms. If the cytokine storm is not treated urgently, it will be fatal; therefore, it should be treated immediately. Anakinra, an interleukin-1 (IL-1) antagonist, tocilizumab, an IL-6 antagonist, and Janus kinase (JAK) inhibitors are successfully used in cytokine storm caused by COVID-19. However, sometimes, despite these treatments, the patient's clinical course does not improve. Emapalumab (Eb) is the human immunoglobulin G1 monoclonal antibody and is a potent and noncompetitive antagonist of IFN-γ. Eb can be life saving for cytokine storm caused by COVID-19, which is resistant to anakinra, tocilizumab, and JAK inhibitors. [ABSTRACT FROM AUTHOR]

A 32-year-old man with a clear and compact graft following a penetrating keratoplasty 6 years back, developed an episode of acute graft rejection, coinciding with the COVID-19 disease. Subsequent to the infection with the novel coronavirus, he developed symptoms of acute graft rejection concurrent with the development of respiratory distress and peak systemic symptoms. This was the phase of cytokine storm as evidenced by the raised inflammatory markers in his blood tests. Such a case of acute corneal graft rejection coinciding with SARS-CoV-2 infection has been reported only once in the literature and this unique association needs to be researched further. [ABSTRACT FROM AUTHOR]