Elevated troponin levels predict the reduced efficacy of Paxlovid in COVID-19 patients.
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ABSTRACT:
SUBMITTER: Zhao D
PROVIDER: S-EPMC10069933 | biostudies-literature | 2023 Apr
REPOSITORIES: biostudies-literature
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Elevated troponin levels predict the reduced efficacy of Paxlovid in COVID-19 patients.
Zhao Deze D He Yi Y Dian Yating Y Meng Yu Y Zeng Furong F Deng Guangtong G
The Journal of infection 20230403 2
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Project description:Elevations in troponin levels have been shown to predict mortality in patients with coronavirus disease 2019 (COVID-19). The role of inflammation in myocardial injury remains unclear. We sought to determine the association of elevated troponin with mortality in a large, ethnically diverse population of patients hospitalized with COVID-19, and to determine the association of elevated inflammatory markers with increased troponin levels. We reviewed all patients admitted at our health system with COVID-19 from March 1 to April 27, 2020, who had a troponin assessment within 48 hours of admission. We used logistic regression to calculate odds ratios (ORs) for mortality during hospitalization, controlling for demographics, co-morbidities, and markers of inflammation. Of 11,159 patients hospitalized with COVID-19, 6,247 had a troponin assessment within 48 hours. Of these, 4,426 (71%) patients had normal, 919 (15%) had mildly elevated, and 902 (14%) had severely elevated troponin. Acute phase and inflammatory markers were significantly elevated in patients with mildly and severely elevated troponin compared with normal troponin. Patients with elevated troponin had significantly increased odds of death for mildly elevated compared with normal troponin (adjusted OR, 2.06; 95% confidence interval, 1.68 to 2.53; p < 0.001) and for severely elevated compared with normal troponin (OR, 4.51; 95% confidence interval, 3.66 to 5.54; p < 0.001) independently of elevation in inflammatory markers. In conclusion, patients hospitalized with COVID-19 and elevated troponin had markedly increased mortality compared with patients with normal troponin levels. This risk was independent of cardiovascular co-morbidities and elevated markers of inflammation.
| S-EPMC7550867 | biostudies-literature
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| S-EPMC7091621 | biostudies-literature
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| S-EPMC9546778 | biostudies-literature
Project description:Background & aimsEndothelial injury and dysfunction play a detrimental role in the pathogenesis of infections. Endothelium-related molecules have been reported as potential diagnostic and/or prognostic biomarkers of infection. The prognostic value of these biomarkers in patients with cirrhosis and infections remains elusive.MethodsIn this study, we investigated the performance of key soluble endothelial injury biomarkers, including intercellular adhesion molecule 1 (ICAM1), von Willebrand factor (vWF), vascular endothelial growth factor receptor 1 (VEGFR1), and angiopoietin 1 and 2 (Ang1, 2) as mortality predictors in patients with cirrhosis and severe COVID-19 or bacterial sepsis.ResultsA total of 66 hospitalized patients (admitted to the COVID-19 ward or liver intensive care unit [ICU]) were included. Twenty-two patients had COVID-19 alone, while 20 patients had cirrhosis plus COVID-19. Twenty-four patients had cirrhosis plus bacterial sepsis. Among patients with cirrhosis, the most common aetiology of liver disease was alcohol. ICAM1 was increased (p = 0.003) while VEGFR1 (p <0.0001) and Ang1 (p <0.0001) were reduced in patients with COVID-19 and cirrhosis, compared to patients with COVID-19 alone. Endothelial biomarker levels did not differ significantly between patients with cirrhosis and severe COVID-19 or bacterial sepsis in the ICU. In these patients, ICAM1 levels significantly and independently predicted mortality (hazard ratio 3.24; 95% CI 1.19-8.86) along with model for end-stage liver disease (MELD) score, renal and coagulation failures. The AUC for ICAM1 was 0.74, MELD was 0.60 and combined ICAM1 and MELD was 0.70. ICAM1 also positively correlated with the composite organ failure scores recorded 3-5 days post ICU admission (CLIF-OF and SOFA) in this subgroup of patients.ConclusionThe study indicates that in patients with cirrhosis, elevated plasma ICAM1 serves as an independent predictor of severe COVID-19- or sepsis-associated 28-day mortality.Lay summaryBacterial sepsis and COVID-19 lead to increased mortality in patients with cirrhosis. In this study, we demonstrate that high plasma levels of ICAM1, an endothelial injury biomarker, is one of the important factors predicting mortality in critically ill cirrhotic patients with severe COVID-19 or bacterial sepsis.
| S-EPMC8106200 | biostudies-literature
Project description:Genome-wide association studies have recently identified 3p21.31, with lead variant pointing to the CXCR6 gene, as the strongest thus far reported susceptibility risk locus for severe manifestation of COVID-19. In order the determine its role, we measured plasma levels of Chemokine (C-X-C motif) ligand 16 (CXCL16) in the plasma of COVID-19 hospitalized patients. CXCL16 interacts with CXCR6 promoting chemotaxis or cell adhesion. The CXCR6/CXCL16 axis mediates homing of T cells to the lungs in disease and hyper-expression is associated with localised cellular injury. To characterize the CXCR6/CXCL16 axis in the pathogenesis of severe COVID-19, plasma concentrations of CXCL16 collected at baseline from 115 hospitalized COVID-19 patients participating in ODYSSEY COVID-19 clinical trial were assessed together with a set of controls. We report elevated levels of CXCL16 in a cohort of COVID-19 hospitalized patients. Specifically, we report significant elevation of CXCL16 plasma levels in association with severity of COVID-19 (as defined by WHO scale) (P-value < 0.02). Our current study is the largest thus far study reporting CXCL16 levels in COVID-19 hospitalized patients (with whole-genome sequencing data available). The results further support the significant role of the CXCR6/CXCL16 axis in the immunopathogenesis of severe COVID-19 and warrants further studies to understand which patients would benefit most from targeted treatments.
| S-EPMC8801318 | biostudies-literature
Project description:This study investigates the intricate interplay between Metabolic-associated Fatty Liver Disease (MAFLD) and COVID-19, exploring the impact of MAFLD on disease severity, outcomes, and the efficacy of the antiviral agent Paxlovid (nirmatrelvir/ritonavir). MAFLD, affecting a quarter of the global population, emerges as a potential risk factor for severe COVID-19, yet the underlying pathophysiological mechanisms remain elusive. This study focuses on the clinical significance of Paxlovid, the first orally bioavailable antiviral agent granted Emergency Use Authorization in the United States. Notably, outcomes from phase II/III trials exhibit an 88% relative risk reduction in COVID-19-associated hospitalization or mortality among high-risk patients. Despite conflicting data on the association between MAFLD and COVID-19 severity, this research strives to bridge the gap by evaluating the effectiveness of Paxlovid in MAFLD patients with COVID-19, addressing the scarcity of relevant studies.
| S-EPMC10819977 | biostudies-literature
Project description:BackgroundCOVID-19 causes significant mortality during the recent pandemic. Data regarding the effectiveness of Paxlovid on COVID-19 patients with chronic kidney disease (CKD, eGFR <90 ml/min) are limited.MethodsA retrospective cohort study was performed on the clinical data of the hospitalized adult patients with confirmed COVID-19 infection collected at Renji Hospital from April 7, 2022 to June 21, 2022. The association of Paxlovid treatment with early (within 5 days post diagnosis) or late (5 days or later post diagnosis) initiation time with clinical outcomes was assessed by Cox proportional hazards regression model with time-dependent covariates.Result1279 of 2387 enrollees were included in the study. Patients with early initiation of Paxlovid had a lower all-cause death rate compared to those with late initiation or without Paxlovid treatment (P = 0.046). For the CKD patients with Charlson comorbidity index (CCI) > 7, the early initiation of Paxlovid was associated with a lower all-cause death rate compared to the later initiation or the lack of Paxlovid treatment (P = 0.041). Cox regression analyses revealed that eGFR (HR 4.21 [95%, CI 1.62-10.99]), Paxlovid treatment (0.32 [0.13-0.77]), CCI (4.32 [1.64-11.40]), ICU admission (2.65 [1.09-6.49]), hsCRP (3.88 [1.46-7.80]), chronic liver disease (4.02 [1.09-14.85]) were the independent risk factors for all-cause death for CKD patients after adjusting for demographics and biochemical indexes.ConclusionsAll-cause death, invasive ventilation, and ICU admission were all significantly lowered by an early initiation of Paxlovid treatment in COVID-19 patients with severe CKD.
| S-EPMC10290896 | biostudies-literature
Project description:BackgroundThe pathogenesis of coronavirus disease 2019 (COVID-19) is still incompletely understood, but it seems to involve immune activation and immune dysregulation.ObjectiveWe examined the parameters of activation of different leukocyte subsets in COVID-19-infected patients in relation to disease severity.MethodsWe analyzed plasma levels of myeloperoxidase (a marker of neutrophil activation), soluble (s) CD25 (sCD25) and soluble T-cell immunoglobulin mucin domain-3 (sTIM-3) (markers of T-cell activation and exhaustion), and sCD14 and sCD163 (markers of monocyte/macrophage activation) in 39 COVID-19-infected patients at hospital admission and 2 additional times during the first 10 days in relation to their need for intensive care unit (ICU) treatment.ResultsOur major findings were as follows: (1) severe clinical outcome (ICU treatment) was associated with high plasma levels of sTIM-3 and myeloperoxidase, suggesting activated and potentially exhausted T cells and activated neutrophils, respectively; (2) in contrast, sCD14 and sCD163 showed no association with need for ICU treatment; and (3) levels of sCD25, sTIM-3, and myeloperoxidase were inversely correlated with degree of respiratory failure, as assessed by the ratio of Pao2 to fraction of inspired oxygen, and were positively correlated with the cardiac marker N-terminal pro-B-type natriuretic peptide.ConclusionOur findings suggest that neutrophil activation and, in particular, activated T cells may play an important role in the pathogenesis of COVID-19 infection, suggesting that T-cell-targeted treatment options and downregulation of neutrophil activation could be of importance in this disorder.
| S-EPMC7503135 | biostudies-literature
Project description:Pneumonia in hospitalized patients is associated with myocardial injury. In this study, we evaluated risk factors for myocardial injury in hospitalized patients with pneumonia and its prognostic value. We retrieved all patients who were hospitalized in internal medicine departments in a tertiary medical center between 2008 and 2019 with a diagnosis of pneumonia. From 2008 to 2019 a total of 20,683 adult patients were hospitalized in internal medicine wards in the Sheba Medical Center with a diagnosis of pneumonia, 8195 were tested for troponin levels, and 3207 had elevated levels. Risk factors for elevated troponin levels were age, prior diagnosis of ischemic heart disease, and elevated creatinine level upon admission. The in-hospital mortality and 1-year mortality rate were higher among patients who had elevated troponin levels when using a propensity score-based matched analysis. In conclusion, in hospitalized patients with pneumonia elevated troponin levels have a major impact on prognosis. Hence, troponin levels may be used as another tool of risk stratification for patients hospitalized with pneumonia.
| S-EPMC7729902 | biostudies-literature
Project description:BackgroundElevated levels of cardiac troponin T as measured by a high-sensitivity test (hscTnT) are common in geriatric patients with a large spectrum of comorbidities but without acute coronary syndrome (ACS). However, the relative contribution of individual comorbidities has never been clearly addressed. This study aimed to determine the relationship between hscTnT elevation as a response variable and individual comorbidities, and to estimate the impact of individual comorbidities on hscTnT elevation in geriatric patients free of ACS.MethodsA nonexperimental, retrospective, matched, longitudinal cohort study was designed to evaluate the files of 7062 geriatric patients (aged ≥ 65 years) without ACS. The hscTnT levels of the patients have already been measured in all evaluated medical records. The dataset was split into 2 groups (0 and 1) based on the individual comorbidity (0 and 1) and hscTnT levels (≤ 14 ng/L = 0 and > 14 ng/L = 1).ResultsOur results show that although age was positively and significantly correlated with hscTnT (r = 0.17, P < 0.0001), the likelihood of experiencing elevated hscTnT levels in older individuals after having excluded ACS was related to the presence of comorbidities independently of their number (P < 0.0001). The regression coefficients (β) associated with renal insufficiency (0.71), cardiomyopathy (0.63), chronic obstructive pulmonary disease (0.30), diabetes (0.25), and anemia (0.22) indicated that there exists a significant association between these comorbidities and the elevated hscTnT levels (P < 0.001). The receiver operating characteristic curve for predictive modeling was estimated at 71% (P < 0.0001).ConclusionsElevated hscTnT levels were mostly associated with renal insufficiency, cardiac myopathies, chronic obstructive pulmonary disease, diabetes, and anemia in geriatric patients without ACS. Developing guidelines to accurately evaluate hscTnT elevation in geriatric patients with comorbidities, without ACS, is clinically essential.
| S-EPMC7984983 | biostudies-literature