Liver injury in COVID-19 - The culprit may not be COVID-19!
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ABSTRACT:
SUBMITTER: Singh A
PROVIDER: S-EPMC7977008 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Patients with novel coronavirus disease 2019 (COVID-19) experience various degrees of liver function abnormalities. Liver injury requires extensive work-up and continuous surveillance and can be multifactorial and heterogeneous in nature. In the context of COVID-19, clinicians will have to determine whether liver injury is related to an underlying liver disease, drugs used for the treatment of COVID-19, direct effect of the virus, or a complicated disease course. Recent studies proposed several theories on potential mechanisms of liver injury in these patients. This review summarizes current evidence related to hepatobiliary complications in COVID-19, provides an overview of the available case series and critically elucidates the proposed mechanisms and provides recommendations for clinicians.
| S-EPMC7268949 | biostudies-literature
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| S-EPMC7129165 | biostudies-literature
Project description:IntroductionThe prevalence and significance of acute liver injury in patients with COVID-19 are poorly characterized.MethodsPatients with confirmed COVID-19 who were hospitalized in geographically diverse medical centers in North America were included. Demographics, symptoms, laboratory data results, and outcomes were recorded. Linear and logistic regression identified factors associated with liver injury, in-hospital mortality, and length of stay (LOS).ResultsAmong 1555 patients in the cohort, most (74%) had an elevated alanine aminotransferase (ALT) during hospitalization, which was very severe (> 20 × upper limit of normal [ULN]) in 3%. Severe acute liver injury (ALI) was uncommon, occurring in 0.1% on admission and 2% during hospitalization. No patient developed acute liver failure (ALF). Higher ALT was associated with leukocytosis (per mL3) (β 10.0, 95% confidence interval (CI) 6.7-12.6, p < 0.001) and vasopressors use (β 80.2, 95%CI 21.5-138.8, p = 0.007). In-hospital mortality was associated with ALT > 20 × ULN (unadjusted OR 6.0, 95%CI 3.1-11.5, p < 0.001), ALP > 3 × ULN (unadjusted OR 4.4, 95%CI 2.5-7.7, p < 0.001), and severe ALI (unadjusted OR 6.8, 95%CI 3.0-15.3, p < 0.001) but lost significance after adjusting for covariates related to severe COVID-19 and hemodynamic instability. Elevated ALP and ALT were associated with longer LOS, admission to intensive care, mechanical ventilation, vasopressor use, and extracorporeal membrane oxygenation use (p < 0.001).ConclusionsTransaminase elevation is common in hospitalized patients with COVID-19. Severe ALI is rare, and ALF may not be a complication of COVID-19. Extreme elevations in liver enzymes appear to be associated with mortality and longer LOS due to more severe systemic disease rather than SARS-CoV-2-related hepatitis.
| S-EPMC8419385 | biostudies-literature
Project description:Coronavirus disease 2019 (COVID-19) is a global pandemic that has caused widespread loss of life. Notably, in this disease, severe inflammatory reactions characterized by cytokine storms are caused by severe acute respiratory syndrome coronavirus 2. The cytokine storms may promote hyper-ferritinemia which can further intensify the inflammation. Moreover, elevated ferritin levels trigger nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy, in which ferritin is degraded and iron is released. Excess iron released from ferritinophagy can promote ferroptosis and cellular damage. Therefore, we propose that NCOA4-mediated ferritinophagy can be targeted to limit the ferroptosis and prevent the multi-organ damage and severity in COVID-19 patients.
| S-EPMC8714652 | biostudies-literature
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| S-EPMC8280619 | biostudies-literature
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| S-EPMC7305728 | biostudies-literature
Project description:Scientists and health professionals are exhaustively trying to contain the coronavirus disease 2019 (COVID-19) pandemic by elucidating viral invasion mechanisms, possible drugs to prevent viral infection/replication, and health cares to minimize individual exposure. Although neurological symptoms are being reported worldwide, neural acute and long-term consequences of SARS-CoV-2 are still unknown. COVID-19 complications are associated with exacerbated immunoinflammatory responses to SARS-CoV-2 invasion. In this scenario, pro-inflammatory factors are intensely released into the bloodstream, causing the so-called "cytokine storm". Both pro-inflammatory factors and viruses may cross the blood-brain barrier and enter the central nervous system, activating neuroinflammatory responses accompanied by hemorrhagic lesions and neuronal impairment, which are largely described processes in psychiatric disorders and neurodegenerative diseases. Therefore, SARS-CoV-2 infection could trigger and/or worse brain diseases. Moreover, patients with central nervous system disorders associated to neuroimmune activation (e.g. depression, Parkinson's and Alzheimer's disease) may present increased susceptibility to SARS-CoV-2 infection and/or achieve severe conditions. Elevated levels of extracellular ATP induced by SARS-CoV-2 infection may trigger hyperactivation of P2X7 receptors leading to NLRP3 inflammasome stimulation as a key mediator of neuroinvasion and consequent neuroinflammatory processes, as observed in psychiatric disorders and neurodegenerative diseases. In this context, P2X7 receptor antagonism could be a promising strategy to prevent or treat neurological complications in COVID-19 patients.
| S-EPMC7738776 | biostudies-literature
Project description: Not available
| S-BSST563 | biostudies-other
Project description:BackgroundA cytokine storm conceivably contributes to manifestations of corona virus disease (COVID-19). Inflammatory cytokines such as interleukin-6 (IL-6) cause acute liver injury while serum detectability indicates systemic inflammation.AimsWe explored a link between systemic IL-6, related acute phase proteins and liver injury in hospitalized COVID-19 patients.Methods655 patients with suspected COVID-19 were screened in the emergency department at the University Hospital of Innsbruck, Austria, between February and April 2020. 96 patients (∼15%) were hospitalized with COVID-19. 15 patients required intensive-care treatment (ICT). Plasma aminotransferases, alkaline phosphatase, bilirubin, and gamma glutamyl transferase, as well as IL-6, C-reactive protein (CRP), ferritin and lactate dehydrogenase (LDH) were determined by standard clinical assays.ResultsOf all hospitalized COVID-19 patients, 41 (42%) showed elevated aspartate aminotransferase (AST) concentration. COVID-19 patients with elevated AST exhibited significantly higher IL-6 (p < 0.001), ferritin (p < 0.001), LDH (p < 0.001) and CRP (p < 0.05) serum concentrations compared to patients with normal AST. Liver injury correlated with systemic IL-6 (p < 0.001), CRP (p < 0.001), ferritin (p < 0.001) and LDH (p < 0.001) concentration. In COVID-19 patients requiring ICT, correlations were more pronounced.ConclusionSystemic inflammation could be a fuel for hepatic injury in COVID-19.
| S-EPMC7416681 | biostudies-literature
Project description:Background and Aim: Liver test abnormalities are common in COVID-19 patients. The aim of our study was to determine risk factors for different liver injury patterns and to evaluate the relationship between liver injury patterns and prognosis in patients with COVID-19. Methods: We retrospectively analyzed patients admitted between January 1st to March 10th, with laboratory-confirmed COVID-19 and followed them up to April 20th, 2020. Information of clinical features of patients was collected for analysis. Results: As a result, a total of 838 hospitalized patients with confirmed COVID-19, including 48.8% (409/838) patients with normal liver function and 51.2% (429/838) patients with liver injury were analyzed. Abnormal liver function tests are associated with organ injuries, hypoxia, inflammation, and the use of antiviral drugs. Hepatocellular injury pattern was associated with hypoxia. The mortality of the hepatocellular injury pattern, cholestatic pattern and mixed pattern were 25, 28.2, and 22.3%, respectively, while the death rate was only 6.1% in the patients without liver injury. Multivariate analyses showed that liver injury with cholestatic pattern and mixed pattern were associated with increased mortality risk. Conclusions: Our study confirmed that hepatocellular injury pattern that may be induced by hypoxia was not risk factor for mortality in SARS-COV-2 infection, while liver injury with mixed pattern and cholestatic pattern that might be induced by SARS-CoV-2 directly might be potential risk factors for increased mortality in COVID-19 patients.
| S-EPMC7606271 | biostudies-literature