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Background: Human coronaviruses can be divided based on their pathogenicity. The types with high pathogenicity including SARS-CoV, MERS-CoV, and the current novel SARS-CoV2. SARS COV2 has led to possibly the worst pandemic of this century in the form of Coronavirus disease 2019 (COVID-19). Initially recognized as a respiratory system disease, COVID-19 has been found to interact with functions of other organ systems like cardiovascular, GIT, CNS Peripheral nervous system, during the course of the disease and postcovid syndromic manifestations including Endocrinal and psychological. The acute manifestations primarily lung will be involved that leads to ARDS, in severe disease all the organs will be effected that may lead to multiorgan dysfunction (MODS), and death. AIM: Evaluation of various endocrinal manifestations secondary to endocrinal gland dysfunction, in COVID 19 peak of the pandemic causing morbidity and mortality. In this COVID 19 pandemic everywhere the mortality was very high, the researchers and all over the globe thought that this is not only viral invasion or host's immune mediated of it's not due to viral virulence and postulated the actual pathogenesis of the disease and its manifestations causing morbidity and mortality. Some patients with coronavirus disease 2019 (COVID-19) develop a life-threatening hyper-inflammatory state that is commonly referred to as cytokine storm. This is the prime cause of all the syndromes presenting in this SARS COV2. The mortality has been increasing and new biochemical parameters are increasing in moderate to severe disease. [ABSTRACT FROM AUTHOR]

Introduction: COVID-19 induced cytokine storm is a well-documented phenomena that contributes significantly in the disease's evolution and prognosis. Therefore, therapies such as therapeutic plasma exchange, constitute a mainstay of therapeutic management especially for critically-ill patients. Methods: We conducted a monocentric retrospective cohort study in the Resuscitation Department of the Mohammed VI University Hospital of Oujda-Morocco, to evaluate the efficiency of therapeutic plasma exchange on critically-ill COVID-19 patients over a 6 months period. We divided our patients into two groups: patients who received TPE (Therapeutic Plasma Exchange) sessions (TPE group) and patients who only benefited from the standard protocol treatment (non TPE group). Results: Our study included a total of 165 patients, 34.5% of which benefited from TPE sessions. We observed an improvement of oxygenation parameters (SpO2 and PaO2/FiO2 ratio) and a progressive respiratory weaning, as well as a significant decrease of biomarkers indicative of inflammation (lymphocyte count, CRP (C Reactive Protein), IL-6, Ferritin) and coagulopathy (d-dimers, fibrinogen) in the TPE group after 5 consecutive TPE sessions. In comparison with the non-TPE group, The TPE-group patients had a shorter ICU (Intensive Care Unit) length of stay, required less frequently mechanical ventilation, and we more likely to be extubated. Furthermore, the TPE group had a lower mortality rate. Discussion: Multiple studies have reported the safety and efficiency of therapeutic plasma exchange in the COVID-19 induced cytokine storm. Given the urgent character of the pandemic at the time, each center followed its own protocol in implementing plasma exchange. Conclusion: Similar to the results reported in the literature, our study reports positive results after using TPE specifically in terms of respiratory weaning and an improvement of the cytokine storm biomarkers, and more importantly a lower mortality rate. [ABSTRACT FROM AUTHOR]

Introduction: COVID-19 induced cytokine storm is a well-documented phenomena that contributes significantly in the disease's evolution and prognosis. Therefore, therapies such as therapeutic plasma exchange, constitute a mainstay of therapeutic management especially for critically-ill patients. Methods: We conducted a monocentric retrospective cohort study in the Resuscitation Department of the Mohammed VI University Hospital of Oujda-Morocco, to evaluate the efficiency of therapeutic plasma exchange on critically-ill COVID-19 patients over a 6 months period. We divided our patients into two groups: patients who received TPE (Therapeutic Plasma Exchange) sessions (TPE group) and patients who only benefited from the standard protocol treatment (non TPE group). Results: Our study included a total of 165 patients, 34.5% of which benefited from TPE sessions. We observed an improvement of oxygenation parameters (SpO2 and PaO2/FiO2 ratio) and a progressive respiratory weaning, as well as a significant decrease of biomarkers indicative of inflammation (lymphocyte count, CRP (C Reactive Protein), IL-6, Ferritin) and coagulopathy (d-dimers, fibrinogen) in the TPE group after 5 consecutive TPE sessions. In comparison with the non-TPE group, The TPE-group patients had a shorter ICU (Intensive Care Unit) length of stay, required less frequently mechanical ventilation, and we more likely to be extubated. Furthermore, the TPE group had a lower mortality rate. Discussion: Multiple studies have reported the safety and efficiency of therapeutic plasma exchange in the COVID-19 induced cytokine storm. Given the urgent character of the pandemic at the time, each center followed its own protocol in implementing plasma exchange. Conclusion: Similar to the results reported in the literature, our study reports positive results after using TPE specifically in terms of respiratory weaning and an improvement of the cytokine storm biomarkers, and more importantly a lower mortality rate. [ABSTRACT FROM AUTHOR]

The discovery of zinc fingers and homeoboxes (ZHX) transcriptional factors and the upregulation of hyposialylated angiopoietin-like 4 (ANGPTL4) in podocytes have been crucial in explaining the cardinal manifestations of human minimal change nephrotic syndrome (MCNS). Recently, uncovered genomic defects upstream of ZHX2 induce a ZHX2 hypomorph state that makes podocytes inherently susceptible to mild cytokine storms resulting from a common cold. In ZHX2 hypomorph podocytes, ZHX proteins are redistributed away from normal transmembrane partners like aminopeptidase A (APA) toward alternative binding partners like IL-4Rα. During disease relapse, high plasma soluble IL-4Rα (sIL-4Rα) associated with chronic atopy complements the cytokine milieu of a common cold to displace ZHX1 from podocyte transmembrane IL-4Rα toward the podocyte nucleus. Nuclear ZHX1 induces severe upregulation of ANGPTL4, resulting in incomplete sialylation of part of the ANGPTL4 protein, secretion of hyposialylated ANGPTL4, and hyposialylation-related injury in the glomerulus. This pattern of injury induces many of the classic manifestations of human minimal change disease (MCD), including massive and selective proteinuria, podocyte foot process effacement, and loss of glomerular basement membrane charge. Administration of glucocorticoids reduces ANGPTL4 upregulation, which reduces hyposialylation injury to improve the clinical phenotype. Improving sialylation of podocyte-secreted ANGPTL4 also reduces proteinuria and improves experimental MCD. Neutralizing circulating TNF-α, IL-6, or sIL-4Rα after the induction of the cytokine storm in Zhx2 hypomorph mice reduces albuminuria, suggesting potential new therapeutic targets for clinical trials to prevent MCD relapse. These studies collectively lay to rest prior suggestions of a role of single cytokines or soluble proteins in triggering MCD relapse. [ABSTRACT FROM AUTHOR]

Introduction: COVID-19 induced cytokine storm is a well-documented phenomena that contributes significantly in the disease's evolution and prognosis. Therefore, therapies such as therapeutic plasma exchange, constitute a mainstay of therapeutic management especially for critically-ill patients. Methods: We conducted a monocentric retrospective cohort study in the Resuscitation Department of the Mohammed VI University Hospital of Oujda-Morocco, to evaluate the efficiency of therapeutic plasma exchange on critically-ill COVID-19 patients over a 6 months period. We divided our patients into two groups: patients who received TPE (Therapeutic Plasma Exchange) sessions (TPE group) and patients who only benefited from the standard protocol treatment (non TPE group). Results: Our study included a total of 165 patients, 34.5% of which benefited from TPE sessions. We observed an improvement of oxygenation parameters (SpO2 and PaO2/FiO2 ratio) and a progressive respiratory weaning, as well as a significant decrease of biomarkers indicative of inflammation (lymphocyte count, CRP (C Reactive Protein), IL-6, Ferritin) and coagulopathy (d-dimers, fibrinogen) in the TPE group after 5 consecutive TPE sessions. In comparison with the non-TPE group, The TPE-group patients had a shorter ICU (Intensive Care Unit) length of stay, required less frequently mechanical ventilation, and we more likely to be extubated. Furthermore, the TPE group had a lower mortality rate. Discussion: Multiple studies have reported the safety and efficiency of therapeutic plasma exchange in the COVID-19 induced cytokine storm. Given the urgent character of the pandemic at the time, each center followed its own protocol in implementing plasma exchange. Conclusion: Similar to the results reported in the literature, our study reports positive results after using TPE specifically in terms of respiratory weaning and an improvement of the cytokine storm biomarkers, and more importantly a lower mortality rate. [ABSTRACT FROM AUTHOR]

Paraguay is currently facing a new outbreak of Chikungunya virus. This report summarizes two severe cases of Chikungunya (CHIKV) infection, confirmed by real-time reverse transcription polymerase chain reaction. We present the cases of patients with acute CHIKV infection and multisystem involvement, with fever, rash, abdominal pain, vomiting, myocarditis, and coronary artery anomalies, very similar to the cases described in MIS-C related to SARS-CoV-2 during the COVID-19 Pandemic. Both patients received IVIG and methylprednisolone, with good clinical response. In this setting of cytokine storm in Chikungunya, can we call it "Multisystem inflammatory syndrome associated with Chikungunya"?. [ABSTRACT FROM AUTHOR]

Patients with hematological malignancies who experience severe infections are at risk of developing dangerous complications due to excessive inflammatory cytokines. To improve the prognosis, it is crucial to identify better ways to manage the systemic inflammatory storm after infection. In this study, we evaluated four patients with hematological malignancies who developed severe bloodstream infections during the agranulocytosis phase. Despite receiving antibiotics, all four patients presented elevated serum IL-6 levels as well as persistent hypotension or organ injury. Adjuvant therapy with tocilizumab, an IL-6-receptor antibody, was administered, and three of the four patients showed significant improvement. Unfortunately, the fourth patient died due to multiple organ failure caused by antibiotic resistance. Our preliminary experience suggests that tocilizumab, as an adjuvant therapy, may help alleviate systemic inflammation and reduce risk of organ injury in patients with elevated IL-6 levels and severe infection. Further randomized controlled trials are needed to confirm the effectiveness of this IL-6 targeting approach. [ABSTRACT FROM AUTHOR]

Objective: Cytokine storm syndrome is a fatal condition related to infectious and autoimmune diseases. Here, we aim to investigate the regulatory mechanisms of Blimp-1 on multiple cytokine production. Methods: The Blimp1 shRNA was transfected into RAW264.7 macrophages, followed by Toll-like receptor (TLR) ligand stimulation. The mRNA and protein levels of cytokines were detected by real-time PCR and flow cytometric bead array. The nuclear translocation of AP-1 and NF-κB p65 was measured by immunofluorescence staining. The transcriptional activity was detected by luciferase reporter assay with 5 × NF-κB reporter or with IL6 promoter reporter. Results: Blimp-1 significantly inhibited the expression and secretion of IL-1β, IL-6, and IL-18 in macrophages during stimulation with a variety of TLR ligands. The immunofluorescence staining results showed that Blimp-1 strictly controlled the nuclear translocation of NF-κB p65 in LPS-challenged macrophages. Furthermore, Blimp-1 directly inhibited the transcriptional activity of NF-κB and the transcription of IL6 gene. Conclusion: Blimp-1 represses the production of multiple pro-inflammatory cytokines by directly binding the genomic region and restricting the nuclear translocation and transcriptional activity of NF-κB. This finding may provide potential therapeutic strategies for the cytokine storm-related diseases. [ABSTRACT FROM AUTHOR]

• Treatment of adults with severe COVID-19 and cytokine storm were compared. • In all, 102/463 patients received tocilizumab, and 361 of 463 received baricitinib. • At 28 days, there was no difference in all-cause mortality between subgroups. • No differences regarding side effects were observed between groups. Our aim was to compare outcomes of hospitalized adults with severe COVID-19 and cytokine storm treated with tocilizumab or baricitinib. A prospective, investigational, real-world study was performed from April 2020 to April 2021 at our center. COVID-19 severity was classified by World Health Organization criteria, and cytokine storm was documented along predefined criteria. Eligible patients were enrolled at diagnosis if they fulfilled a priori inclusion criteria and received standard-of-care plus tocilizumab or baricitinib for >48 hours. Patients were followed per protocol for 28 days post-diagnosis. The primary outcome was all-cause mortality; secondary outcomes were invasive mechanical ventilation and major infectious complications. Of 463 patients, 102/463 (22.1%) received tocilizumab, and 361/463 (77.9%) baricitinib. Baseline characteristics were balanced. At 28 days, there was no difference in all-cause mortality (22/102, 21.6% vs 64/361, 17.7%; P -value = 0.38). Requirement for invasive mechanical ventilation was more frequent after tocilizumab (52/102, 50.9% vs 96/361, 26.6%; P <0.01), rate of major infectious complications was similar (32/102, 31.4% vs 96/361, 26.6%; P -value = 0.34). In logistic regression, the immunomodulatory drug was not retained as a predictor of all-cause mortality. Kaplan–Meier analysis revealed statistically similar survival distributions. All-cause mortality was similar between adults treated with baricitinib or tocilizumab for severe COVID-19 with cytokine storm. [ABSTRACT FROM AUTHOR]

At least 17 million people die from acute myocardial infarction (AMI) every year, ranking it first among causes of death of human beings, and its incidence is gradually increasing. Typical characteristics of AMI include acute onset and poor prognosis. At present, there is no satisfactory treatment, but development of coronary collateral circulation (CCC) can be key to improving prognosis. Recent research indicates that the levels of cytokines, including those related to promoting inflammatory responses and angiogenesis, increase after the onset of AMI. In the early phase of AMI, cytokines play a vital role in inducing development of collateral circulation. However, when myocardial infarction is decompensated, cytokine secretion increases greatly, which may induce a cytokine storm and worsen prognosis. Cytokines can regulate the activation of a variety of signal pathways and form a complex network, which may promote or inhibit the establishment of collateral circulation. We searched for published articles in PubMed and Google Scholar, employing the keyword "acute myocardial infarction", "coronary collateral circulation" and "cytokine storm", to clarify the relationship between AMI and a cytokine storm, and how a cytokine storm affects the growth of collateral circulation after AMI, so as to explore treatment methods based on cytokine agents or inhibitors used to improve prognosis of AMI. [ABSTRACT FROM AUTHOR]

Cytokine release syndromes represent a severe turn in certain disease states, which may be caused by several infections, including those with the virus SARS‐CoV‐2. This inefficient, even harmful, immune response has been associated with a broad release of chemokines. Although a cellular (type I) immune reaction is efficacious against viral infections, we noted a type I deficit in the cytokine patterns produced by cytokine storms of all reported etiologies. Agents including lipopolysaccharide (LPS, bacterial), anti‐CD3 (antibody) and a version of the prominent SARS‐CoV‐2 viral surface molecule, Spike Glycoprotein, were individually sufficient to induce IL‐6 and multiple chemokines in mice. They failed to upregulate the TH1 inducer cytokine Osteopontin, and the pathophysiologic triggers actually suppressed the PMA‐induced Osteopontin secretion from monocytic cells. Osteopontin administration partially reversed the chemokine elevation, more effectively so in a mouse strain with TH1 bias. Corroboration was obtained from the inverse correlation in the levels of IL‐6 and Osteopontin in plasma samples from acute COVID‐19 patients. We hypothesize that the inhibition of Osteopontin by SARS‐CoV‐2 Spike Glycoprotein or LPS represents an immune evasion mechanism employed by the pathogens of origin. The ensuing dysfunctional inflammatory response promotes a vicious cycle of amplification, resulting in a cytokine storm. [ABSTRACT FROM AUTHOR]

The pandemic of coronavirus disease 2019 (COVID-19), for which there does not appear to be an approved cure, the primary treatment options consist of non-pharmacological preventive measures and supportive treatment that are aimed at halting the progression of the disease. Nuclear factor kappa B (NFκB) presents a promising therapeutic opportunity to mitigate COVID-19-induced cytokine storm and reduce the risk of severe morbidity and mortality resulting from the disease. However, the effective clinical application of NFκB modulators in COVID-19 is hampered by a number of factors that must be taken into consideration. This paper therefore explored the modulation of the NFB pathway as a potential strategy to mitigate the severe morbidity and mortality caused by COVID-19. The paper also discusses the factors that form the barrier, and it offers potential solutions to the various limitations that may impede the clinical use of NFκB modulators against COVID-19. This paper revealed and identified three key potential solutions for the future clinical use of NFκB modulators against COVID-19. These solutions are pulmonary tissue-specific NFκB blockade, agents that target common regulatory proteins of both canonical and non-canonical NFκB pathways, and monitoring clinical indicators of hyper inflammation and cytokine storm in COVID-19 prior to using NFκB modulators. [ABSTRACT FROM AUTHOR]

During the coronavirus disease 2019 (COVID-19) pandemic, cognitive impairment of varying degrees of severity began to be observed in a significant percentage of patients. The present study discussed the impact of immunological processes on structural and functional changes in the central nervous system and the related cognitive disorders. The purpose of the present review was to analyse and discuss available information from the scientific literature considering the possible relationship between severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viral infection and cognitive impairment, including NeuroCOVID, frontal syndrome and cytokine storm. A systematic literature review was conducted using: Google Scholar, Elsevier and the PubMed database. When searching for materials, the following keywords were used: 'cognitive dysfunctions', 'SARS-CoV-2', 'COVID-19', 'Neuro-SARS2', 'NeuroCOVID', 'frontal syndrome', 'cytokine storm', 'Long COVID-19'. A total of 96 articles were included in the study. The analysis focused on the characteristics of each study's materials, methods, results and conclusions. SARS-CoV-2 infection may induce or influence existing cognitive disorders of various nature and severity. The influence of immunological factors related to the response against SARS-CoV-2 on the disturbance of cerebral perfusion, the functioning of nerve cells and the neuroprotective effect has been demonstrated. Particular importance is attached to the cytokine storm and the related difference between pro- and anti-inflammatory effects, oxidative stress, disturbances in the regulation of the hypothalamic-pituitary-adrenal axis and the stress response of the body. [ABSTRACT FROM AUTHOR]

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) represent a significant global burden of morbidity and mortality, with lung injury being the primary cause of death in affected patients. The pathogenesis of lung injury, however, remains a complex issue. In recent years, the role of the immune system in lung injury has attracted extensive attention worldwide. Despite advancements in our understanding of various lung injury subtypes, significant limitations persist in both prevention and treatment. This review investigates the immunopathogenesis of ALI/ARDS, aiming to elucidate the pathological processes of lung injury mediated by dendritic cells (DCs), natural killer (NK) cells, phagocytes, and neutrophils. Furthermore, the article expounds on the critical contributions of gut microbiota, inflammatory pathways, and cytokine storms in the development of ALI/ARDS. [Display omitted] • Damage to lung tissue caused by immune cell dysfunction. • The ecological stability of intestinal flora is important in protecting lung tissue. • The inflammatory pathway plays a crucial role in regulating and mediating lung injury. • The impact of cytokine storm on lung injury is severe. [ABSTRACT FROM AUTHOR]

Objectives: Patients who develop cytokine storm while they have coronavirus disease 2019 (COVID-19) experience more severe symptoms. This article aims to evaluate the effect of biochemical parameters on the clinical course of the disease in patients treated with tocilizumab (TCZ) due to cytokine storm.Methods: Medical documents of patients with COVID-19 were searched retrospectively. Patients who entered cytokine storm were classified as group 1 and divided into two subgroups as patients who were followed up in the ward and in the intensive care unit (ICU). Less severe COVID-19 patients who did not enter cytokine storm were included in the control group as group 2.Results: A total of 522 patients with COVID-19 infection were included in the study. The mean age was 62.0 ± 15.6 years, and the majority were male (64.4%). Hypertension and diabetes mellitus were the two most common diseases, seen in 50.8% and 29.9%, respectively. There were 392 patients with TCZ application (group 1) and 130 patients without TCZ (group 2). Significantly higher serum glucose, magnesium, and sodium and lower calcium levels were present in group 1 than in group 2 (<0.001). Hypocalcemia, hypernatremia, hypermagnesemia, and hyperkalemia were more frequently detected in the ICU compared with the patients treated in the wards (P = 0.001, P < 0.001, P = 0.039, and P < 0.001, respectively).Conclusions: Following up closely electrolyte disturbances may support patient survival and decrease the probability of ICU necessity. This approach should be taken before the development of important disorders to be effective in the treatment process of the main disease. [ABSTRACT FROM AUTHOR]

Background: Coronavirus disease‐2019 (COVID‐19)‐related organ failure is partly related to a sepsis‐like syndrome and extreme pro‐inflammatory cytokine release, named cytokine storm. Therapeutic strategies that prevent the production of or remove the pro‐inflammatory cytokines could potentially be an effective therapy in critically afflicted COVID‐19 patients. Methods: In this clinical trial study, from April until June 2020, 68 COVID‐19 patients (35 vs. 33 controls) with severe critical symptoms, and PaO2/FiO2 (P/F) ratio less than 200 mmHg either received a single standard therapy or a combination of standard treatment for COVID‐19 combined with hemoperfusion (hemofilter, HA330 D Javfron) for 4 h, in 3 consecutive days. The length of hospital stay and mechanical ventilation, the resolution of radiologic abnormalities, and the mortality rate were defined as the primary outcomes. Results: Demographic characteristics, the acute physiology, and chronic health evaluation score of both groups were similar (p > 0.05). Importantly, we noticed a significant mortality rate reduction in the perfused group compared with controls (37.1% vs. 63.6%, p = 0.02), this positive effect was stronger among those with a P/F ratio higher than 75 (mortality rate of 84.7% for P/F ratio < 75 vs. 15.4% for P/F ratio ≥ 75, p = 0.02). Conclusions: The results imply that early start of hemoperfusion could be more effective and significantly reduce the mortality rate among COVID‐19 patients with critical diseases. [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]

• SARS-CoV-2 subtly disrupts the equations of immune responses in COVID-19 patients. • The virus activates infected macrophages and CD4+ T cells to induce cytokine storm. • Cytokine storm and direct interaction of viruses inhibit NK cell cytolytic effect. • Exhausted NK cell fails to lyse infected cells to avoid their unleashed cytokine release. • Adoptive transfer of cytolytic NK cell may reduce cytokine storm while decreasing viral load. The global outbreak of coronavirus-2019 (COVID-19) still claims more lives daily around the world due to the lack of a definitive treatment and the rapid tendency of virus to mutate, which even jeopardizes vaccination efficacy. At the forefront battle against SARS-CoV-2, an effective innate response to the infection has a pivotal role in the initial control and treatment of disease. However, SARS-CoV-2 subtly interrupts the equations of immune responses, disrupting the cytolytic antiviral effects of NK cells, while seriously activating infected macrophages and other immune cells to induce an unleashed "cytokine storm", a dangerous and uncontrollable inflammatory response causing life-threatening symptoms in patients. Notably, the NK cell exhaustion with ineffective cytolytic function against the sources of exaggerated cytokine release, acts as an Achilles' heel which exacerbates the severity of COVID-19. Given this, approaches that improve NK cell cytotoxicity may benefit treatment protocols. As a suggestion, adoptive transfer of NK or CAR-NK cells with proper cytotolytic potentials and the lowest capacity of cytokine-release (for example CD56dim NK cells brightly express activating receptors), to severe COVID-19 patients may provide an effective cure especially in cases suffering from cytokine storms. More intriguingly, the ongoing evidence for persistent clonal expansion of NK memory cells characterized by an activating phenotype in response to viral infections, can benefit the future studies on vaccine development and adoptive NK cell therapy in COVID-19. Whether vaccinated volunteers or recovered patients can also be considered as suitable candidates for cell donation could be the subject of future research. [ABSTRACT FROM AUTHOR]

Introduction: The on-going Corona-Virus Disease 2019 (COVID-19) pandemic has spread rapidly across the globe. Tocilizumab is a recombinant monoclonal antibody to Interleukin-6 (IL-6) receptor. An increasing number of studies across the world is reporting the use of tocilizumab in treating COVID-19 patients or at risk of developing cytokine storm. Apart from clinical and laboratory parameters, High Resolution Computed Tomographic (HRCT) chest scan is a promising tool to identify patients very early in the course of COVID-19 disease. Aim: The purpose of this retrospective research study is to find whether high chest CT Severity Score (CTSS) on HRCT thorax scan predict the clinical requirement of tocilizumab injection in COVID-19 patients. Materials and Methods: In this retrospective study, during the period from May 2020 to July, 2020, 250 patients with confirmed Reverse Transcriptase-Polymerase Chain Reaction (RT-PCR) diagnosed of COVID-19 on first or repeat sample and who also underwent HRCT scan of the chest, were assigned chest CTSS. From data obtained, patients were categorised into two groups based on mild and severe CTSS. Patients with higher CTSS have a higher future possibility of developing the cytokine storm and hence the requirement of tocilizumab can be reliably predicted. All statistical analysis was performed in IBM SPSS version 20. Results: Out of a total of 250 patients, 72 patients were given tocilizumab injection. The average CTSS was 29.8±6.38 in the tocilizumab injection group. Only 8% of patients with mild CTSS received tocilizumab injection while 60% of patients with severe CTSS received tocilizumab injection (p<0.001). Out of 72 patients who received tocilizumab injection, 16.7% had mild CTSS while 83.3% had severe CTSS (p<0.001). Average values of inflammatory markers like CRP, D-Dimer, Ferritin, LDH, and IL-6; were significantly higher in severe CTSS and tocilizumab group (p<0.001). Conclusion: CTSS may be used as a new decisive tool in triaging in-hospital COVID-19 patients. Categorising patients in mild and severe CTSS early in the disease course, even before the marked worsening of laboratory parameters and development of cytokine storm may help initiate early treatment and thereby save many lives. [ABSTRACT FROM AUTHOR]