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Aim: Coronavirus disease 2019 (COVID-19) mostly proceeds with mild respiratory symptoms, but sometimes severe pneumonia, cytokine storm, and acute respiratory distress syndrome can develop. Anti-cytokine treatments are being tried for cytokine storm. In this study, we aimed to examine the effect of tocilizumab on mortality associated with COVID-19. Material(s) and Method(s): The study included 146 patients with moderate-to-severe acute respiratory distress syndrome diagnosed with COVID-19. The patients were divided into two groups, receiving only standard treatment (ST group, n=44), and tocilizumab treatment in addition to standard treatment (TCZ group, n=102). Groups were compared in terms of demographic, clinic, and laboratory data. Also, mortality rates were determined to detect the effect of tocilizumab on mortality. Result(s): Overall, 36.3% (n=53) of the patients were female, 63.7% (n=93) were male, and the mean age was 69.5+/-14.2 years. The mortality rate was 29.4% (n=30) in the TCZ group and 52.3% (n=23) in the ST group (p=0.009). While C-reactive protein, fibrinogen, and lactate levels on admission to the intensive care unit (ICU) were similar across the groups, the TCZ group had higher ferritin levels (p=0.006). On discharge from ICU, the TCZ group had a significant decrease in C-reactive protein (p<0.001), while their ferritin levels decreased to levels in the ST group (p=0.134). The absence of tocilizumab in the treatment regimen was associated with a 2.63-fold increase in the mortality risk. Conclusion(s): Tocilizumab reduces the mortality in COVID-19 patients in ICU. However, further studies are warranted to better elucidate the efficacy and side effects of tocilizumab. Copyright © 2022, Duzce University Medical School. All rights reserved.
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Introduction: The presence of tissue damage in the lungs, kidneys, heart, or other organs can be detected by monitoring the level of Lactate Dehydrogenase (LDH) in the blood and considered a reliable biomarker in early prediction of patients' prognosis. Aim(s): To determine extent of correlation between LDH level with the spectrum and in-hospital outcome of Coronavirus Disease-2019 (COVID-19) infected patients. Material(s) and Method(s): This retrospective research was undertaken during March 2020 to May 2020, based on the data of 205 COVID-19 infected patients, reported at Dammam Medical Complex, Dammam, Eastern Province, Saudi Arabia. Patients' records were retrieved and the following data were recorded-age, gender, nationality, co-morbidities, lactate dehydrogenase level, number of days since the patient tested positive (Up to 7,14 and >14 days), COVID-19 symptoms [mild, moderate, or severe as per British Thoracic Society guidelines (CURB (Confusion, Blood Urea Nitrogen, Respiratory Rate, Blood Pressure)-65)]. The data was collected and tabulated as mean+/-SD, frequency and percentages. Analysis was carried out using specialized software of Statistical Package for Social Sciences (SPSS) version 20.0. Result(s): On analysis of the collected data of all 205 included patients, the LDH level was found significantly high among males, 46-60 years old, and among non-Saudi patients. The severity of COVID-19 symptoms and LDH levels were found to have a strong relationship (p-value<0.001). Patients between the ages of 46 and 60 were more likely (4.3 times) to have poor outcomes, and diabetes mellitus was predicted to be 2.32 times more likely to be associated with poor COVID-19 outcomes. Raised LDH levels were >5 times more likely to lead to in-hospital poor outcomes compared to those with borderline LDH levels. Conclusion(s): LDH level is a reliable predictor for the cause of COVID-19. The results of the present study suggest that patients aged 46-60 years, diabetic patients, or those suffering from severe symptoms of COVID-19 have raised levels of LDH. Copyright © 2023 Journal of Clinical and Diagnostic Research. All rights reserved.
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Background and Aim: A novel coronavirus disease 2019 (COVID-19) which was declared a pandemic in March 2020, has spread rapidly around the world and it is still threatening global health. COVID-19 infection may exhibit several clinical manifestations varying from mild respiratory illness to severe pneumonia and acute respiratory distress syndrome (ARDS). Many studies have shown that inflammatory responses play a pivotal role in the severity and prognosis of COVID-19 disease. Galectin-3, a b-galactoside-binding lectin, is a new important player in the pathophysiological processes of inflammation and fibrosis. In this study, we aimed to investigate the relationship between serum Galectin-3 levels at admission and pneumonia severity and inflammatory parameters in COVID-19 patients. Method(s): A total of 68 patients with laboratory, clinical and radiological confirmed COVID-19 were prospectively recruited to the study. The study population was classified into 2 groups as those with severe pneumonia (n=48) and those with mild pneumonia (n=20) based on chest computed tomography images at admission. Ten milliliter of peripheral venous blood were drawn within 24 hours of admission to estimate serum Galectin-3 levels. Patients with chronic renal failure, other inflammatory or rheumatic diseases and/or malignancies, cardiovascular diseases and diabetes mellitus were excluded from the study. We evaluated the relationship between Galectin-3 levels, pneumonia severity and laboratory parameters in COVID-19 patients. Result(s): The demographic and clinical data and laboratory findings of the study population are presented in Table 1. The mean age of the study population was 61.68+/-14.4 years (45 male;23 female). The mean level of Galectin-3 was 29.67+/-16.7 ng/mL. Serum Galectin-3, lactate dehydrogenase (LDH), C-reactive protein (CRP), prohormone B-type natriuretic peptide (pro-BNP), troponin-T, D-dimer and procalcitonin levels, white blood cell (WBC) counts, neutrophil and lymphocyte counts and percentages were significantly different between the groups (Table 1). Serum Galectin-3 levels were found to be higher in severe pneumonia group (p=0.04). In patients with mild pneumonia;Galectin-3 was negatively correlated with neutrophil percentage (r =-0.483 p=0.031) but was positively correlated with lymphocyte percentage and lymphocyte counts (r=0.428, p=0.05;r=0.554, p=0.011, respectively) (Table 2A). However, Galectin-3 was negatively correlated with WBC counts, neutrophil counts and neutrophil percentage (r=-0.317 p=0.028;r=-0.379 p=0.008;r=-0.609 p<0.001, respectively) and positively correlated with lymphocyte percentage (r=0.307;p=0.034) in COVID-19 patients with severe pneumonia (Table 2B). Conclusion(s): In this study, we found a significant relationship between serum Galectin-3 levels and pneumonia severity in COVID-19 patients. Therefore, Galectin-3, a new biomarker of inflammation, may be useful as a prognostic factor in patients with COVID-19.
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Background. There remain important gaps in knowledge concerning the effects of SARS-CoV-2 infection or vaccination on the human blood proteome. Methods. The CCRP is a longitudinal surveillance study with information on SARS-CoV-2 infections, vaccinations and associated humoral immune responses in over 37,000 individuals. We selected a sample of blood spots cards (n=510) from serum antibody studies obtained between October 2020 and April 2021 for mass spectrometry proteomics analysis covering 540 unique plasma proteins. We analyzed the quantified protein differences based on dried blood samples obtained before and after infection or vaccination among previously non-infected individuals (immune naive) after adjustment for batch effects, age, sex, or prior diagnosis of cancer, cardiovascular or autoimmune disease, or diabetes. The majority of infected individuals were minimally symptomatic. Differentially expressed proteins were considered significant with an FDR adjusted p-value of < 0.05 and log2 fold change (L2FC) >0.2. Results. We found 11 and 12 proteins differentially expressed proteins in the naive/infected and naive/vaccinated people respectively, of which 10 were shared. Hepatocyte growth factor receptor (HGF) was upregulated (L2FC 0.24;p < 0.001) only in those who were infected while fibrillarin (L2FC -0.24;p< 0.001) and lambdacrystallin homolog (L2FC -0.29, p < 0.001) were downregulated only in the vaccinated samples (Fig 1). The remaining DE protein were associated with a wide array of functions including metabolic, cytostructural, extracellular matrix and DNA regulatory processes. Conclusion. We found changes in the proteome both from infection and vaccination. HGF, elevated in the infected, has been associated with endothelial inflammation, upregulation of pro-inflammatory cytokines to reduce lung fibrosis and is known to promote tissue repair. Fibrillarin, downregulated in the vaccinated, has been associated with higher rates of bacterial and viral clearance, inflammation reduction, and increased cell survival. These findings suggest detectable complex inflammation from mild to moderate infections. Further investigation is required to understand the mechanism of action and clinical implication of these findings.
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Background: COVID-19 infection may be associated with coagulopathy, both thrombotic as well as haemorrhagic events. Bleeding manifestations are rather rare. Our case describes a possible association between acquired hemophilia A (AHA) and COVID-19 infection. This causality has been described only in several cases. Aim(s): A 78-year- old male was admitted to hospital for ecchymoses, appearing just over past several days, located on the right breast and the left upper limb, with no history of recent injury. No previous personal or family history of any bleeding symptoms. Concurrently COVID-19 infection was confirmed. During the hospital stay, the skin bruises have further spontaneously extended, covering both the pectoral areas, the abdomen and all extremities. Method(s): Basic laboratory sampling was performed. The isolated presence of striking prolongation of aPTT was discovered (aPTT ratio 4.28, normal range 0.8-1.2). Investigations on prolonged aPTT have been initiated. Result(s): Extremely low activity of factor VIII (0.4%) was found. Further studies have subsequently identified a specific factor VIII inhibitor (24 Bethesda units). During the investigations of the condition no malignancy, autoimmune disorders or drug interactions were disclosed. A 30% COVID pneumonia was discovered by CT imagining. Conclusion(s): The diagnosis of AHA was made, most likely due to an acute onset COVID-19 infection. This association can only be speculated for the time being, however, COVID-19 infection induced autoantibody production and influence on coagulation system is described by a number of studies. We therefore recommend a frequent coagulation monitoring including aPTT in patients admitted with acute COVID-19 infection and the specific/non-specific inhibitor search in cases with otherwise unexplained onset or worsening of haemorrhagic episodes and/or an aPTT prolongation.
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Introduction: Vaccination against SARS-Cov-2 infection has significantly reduced the incidence of severe cases. However, safety concerns have increased as possibly related side effects have been described. It is postulated that vaccination could induce different autoimmune diseases, probably due to cross-reactivity between SARS-Cov-2 proteins and human proteins. To date, more than 20 cases of post-vaccination autoimmune hepatitis (AIH) have been described in the literature. Aims & Methods: The aim of this study was to collect cases of AIH that were detected after vaccination for SARS-Cov-2 in our hospital, and to analyse their characteristics and the possible causality of the vaccine. Cases of probable or definitive autoimmune hepatitis according to the simplified criteria of the International Autoimmune Hepatitis Group that presented less than 90 days after COVID-19 vaccination were collected. All cases had to have a compatible liver biopsy and response to corticosteroids in order to be included. The following data were collected: age, sex, type of vaccine, latency, transaminase and bilirubin (BT) levels at diagnosis, liver biopsy, autoantibodies and IgG, predisposing HLA and treatment received. Result(s): Since the start of vaccination, 5 cases of altered liver biochemistry after vaccination have been detected (Table 1). Four patients were female and one male, with a mean age of 62 years. Sixty percent received Pfizer and 40% Astrazeneca. The mean time from vaccination to detection of laboratory abnormalities was 26 days. No patients showed evidence of liver failure, although there was one case of severe acute hepatitis. ANAs were positive together with elevated IgG levels in all patients. Liver biopsy was performed in 4 cases, which were compatible with AIH. Four patients were treated with systemic corticosteroids with good outcome, and three of them were prescribed azathioprine as maintenance therapy (in one patient it was contraindicated due to a concomitant diagnosis of endometrial neoplasia). Four of the patients had HLA susceptibility for IAH. The score was calculated based on the simplified diagnostic criteria of the International Autoimmune Hepatitis Group, with all patients who underwent biopsy scoring >7 points (definite autoimmune hepatitis). Four of the patients received a new dose of the vaccine at a later date. The second patient had a slight worsening of transaminases, which was related to the concomitant suspension of azathioprine due to digestive intolerance, with an improvement in blood tests when a new course of corticosteroids was started. Conclusion(s): In all of the cases presented, there is a temporal relationship with onset of the alterations less than 90 days after vaccination. Although controversial, it is postulated that vaccination could be the cause of autoimmunity, or rather play a role as a trigger for latent disease. At least 20 cases of probable AIH following vaccination have been reported in the literature, with characteristics similar to the cases presented in this study. However, at present, it is not possible to say with certainty whether the vaccine is the cause of the debut of IAH or whether it is a casual association in predisposed patients. (Table Presented).