ABSTRACT
Dysregulation of liver enzymes aspartate transaminase (AST) and alaninetransaminase (ALT) are common in CO VID-19 patients. De Ritis ratio (ASTIALT) ratio is a noninvasive, cost-effective test however usefulness of De Ritis ratio in COVID-19 is unclear. Intraindividual variation of AS T and ALT are large leading to misclassification as normal on repeat testing compared to De Ritis ratio which may not be relatively large as predicted by the product of the individual variances. This was a retrospective study which included subject's male and female adults aged 18-50 years. Dyslipidemic, obese, hypothyroid, nephrotic syndrome, diabetes mellitus, pregnant women were excluded from the study. The study aimed to determine the levels of AST, ALT and De Ritis ratio and investigate association of De Ritis ratio between COVID-19 admitted patient's survivors and inhospital mortality in 500patients admitted to ESIC Medical College and Hospital, Faridabad.The De Ritis ratio was significantly lower in survivors than nonsurvivors (median: 0.94;IQR: 0.71-1.2 vs 1.53;IQR: 1.11-2.46,P= .04)whereas no significant differences was seen in ALT and AST concentrations. In ROC Curve analysis, the AUC value of the De Ritis ratio was 0.80(95% CI 0.56 to 0.65, P < 0.0001) with sensitivity and specificity of 70.64% and 70.27%, respectively as compared toAST (0.60) and ALT (0.64).De Ritis ratio along with correlation with inflammatory markers can be used as a significant biomarker in prognosis and management of COVID-19 admitted patients without incurring any additional cost.
ABSTRACT
Introduction: Coronavirus disease 2019 has challenged the global healthcare system since 2019. Cytokine storm due to the release of pro-inflammatory cytokine scan lead to systemic inflammation reaction. Dysregulation of lipid profile and liver enzymes Aspartate Transaminase (AST) and Alanine Transaminase (ALT) are reported in COVID-19 patients. De Ritis ratio (AST/ALT) ratio is a non-invasive, costeffective test however its usefulness in COVID-19 is unclear. Aim(s): To determine serum host serum lipid levels and serum levels of AST, ALT and De Ritis ratio in admitted patients and its correlation with inflammatory markers. Materials and Methods :It was a retrospective study conducted from June 2020 to December 2020, included 500 COVID-19 admitted patients. AST, ALT, Total Cholesterol, Triglycerides, Low Density Lipoprotein, High Density lipoprotein, Ferritin, Procalcitonin, hsCRP estimated in Autoanalyzer and Interleukin-6 by ELISA. Result(s): A significant increase in Serum Triglycerides and decrease in HDL-C was observed with no remarkable finding in other lipid parameters. A statistically significant (p<0.05) correlation was observed between TG (positive), HDL (negative)and inflammatory markers such as hsCRP, PCT, Ferritin, IL-6. The De Ritis ratio was significantly lower in survivors than non-survivors whereas no significant differences was seen in ALT and AST concentrations. In ROC Curve analysis, the AUC value of the De Ritis ratio was 0.80(95% CI 0.56 to 0.65, p<0.0001) with sensitivity and specificity of 70.64% and 70.27%, respectively as compared to AST (0.60) and ALT (0.64). Conclusion(s): Liver enzymes and lipid profile are cost-effective and easily accessible in all laboratories. Its correlation with inflammatory markers can be used as a significant biomarker in prognosis and management of COVID-19 admitted patients without incurring any additional cost.
ABSTRACT
Background: Urokinase plasminogen activator receptor (uPAR/PLAUR) is a cell surface receptor on monocytes and macrophages (MO/MPs), which when cleaved, forms soluble uPAR (suPAR). Previous work has shown that uPAR is differentially induced in MO/MPs after coronavirus (CoV) infection and contributes to hyperfibrinolysis. In contrast to cellular uPAR's fibrinolytic function (implicated in CoV-induced coagulopathy), suPAR is a MP chemotactic factor implicated in perpetuating tissue injury after CoV infection. However, it is unclear if induced levels of cellular uPAR correlate with the elevated levels of suPAR after CoV infection and how suPAR expression is regulated after influenza virus (IAV) infection. Method(s): Published scRNA sequencing data (GSE149689) of PBMCs from patients (COVID-positive and IAV-positive) and healthy controls was analyzed. In vitro, we performed infections of immortalized murine MPs (RAW264.7) with the CoVs MHVA59 or MHV1, or the IAV (A/PR/8/34;H1N1) at the indicated MOI for 24 hours. uPAR and urokinase levels were measured by ELISA. Urokinase activity of conditioned media was measured using a commercially available colorimetric assay. Result(s): ScRNA analysis revealed differential expression of PLAUR in MOs from COVID and IAV-positive relative to healthy controls, with the highest PLAUR expression in COVID-positive samples (Fig. A-B). Infection of RAW264.7 cells with CoV and IAV induced cellular uPAR expression, but only CoV infection induced suPAR expression (Fig. C). In contrast to uPAR, the expression of both cellular and soluble urokinase levels was induced after infection with either CoVs or IAV (Fig. D). Finally, induction of urokinase activity of conditioned media after viral stimulation was observed after infection with either CoVs or IAV (Fig. E). Conclusion(s): CoV but not IAV infection induces the expression of both cellular and soluble uPAR in MO/MPs. Both CoV and IAV induce the expression of cellular and soluble urokinase, and urokinase activity. Understanding this virus specific effect on uPAR/suPAR in innate immune cells may reveal the pathogenesis of virus-associated coagulopathy and tissue injury.
ABSTRACT
Introduction Coronavirus disease 2019 (COVID-19) caused by the SARS coronavirus 2 has challenged the global healthcare system since 2019. Lipids are integral component of this enveloped virus that play an essential role in in its life cycle starting from fusion of viral membrane to host cell, viral replication and exocytosis. It also disrupts metabolic profile due to the release of pro-inflammatory cytokines leading to systemic inflammation reaction. Aim and Objective Therefore, it was aimed to find association between human host serum lipid levels and its association with inflammatory markers. Materials and Methods It was a retrospective study conducted from June 2020 to December 2020, included 500 COVID-19 admitted patients tested positive by Oral/Nasopharyngeal swab by Real time PCR. Total Cholesterol, Triglycerides (TG), Low Density Lipoprotein (LDL-C), High Density lipoprotein (HDL), Ferritin, Procalcitonin (PCT), High sensitive C Reactive protein (hsCRP) estimated in Vitros XT 7600 Autoanalyzer and Interleukin-6(IL-6) by ELISA. Results A significant increase in Serum Triglycerides(185mg/dL) and decrease in HDLC(30mg/dL) was observed with no remarkable finding in other lipid parameters. A statistically significant (p<0.05)positive correlation was observed between TG and inflammatory markers such as hsCRP, PCT, Ferritin, IL-6. Likewise, a negative correlation was detected between HDL-C and hsCRP, PCT, Ferritin, IL-6. Conclusion Lipid profile and host cell metabolism is altered in COVID 19 patients either by cellular infection or by systemic inflammation. Hence it is important to study lipid profile alterations in synergism with inflammatory markers. It may act as guiding step in management and prognosis of this disease.