Glucocorticosteroids for people with alcoholic hepatitis

Pavlov, Chavdar S; Varganova, Daria L; Casazza, Giovanni; Tsochatzis, Emmanuel; Nikolova, Dimitrinka; Gluud, Christian

doi:10.1002/14651858.cd001511.pub3

Cited by 27 publications

(15 citation statements)

References 112 publications

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“…AH, as a uniquely alcohol-associated liver disease, causes acute liver inflammation as a result of prolonged and heavy alcohol abuse (Im, 2019). Moreover, AH is characterized by steatosis, fibrosis, necroinflammation, and potential complications to liver disease (Pavlov et al, 2017). In the past, study of the pathogenesis of AH chiefly focused on factors such as ethanol metabolism, malnutrition, abnormal methionine metabolism, and production of endotoxins.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: microRNA-155 Modulates Hepatic Stellate Cell Proliferation, Apoptosis, and Cell Cycle Progression in Rats With Alcoholic Hepatitis via the MAPK Signaling Pathway Through Targeting SOCS1

et al. 2020

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The aim of this study was to investigate the regulatory function of the non-coding microRNA-155 (miR-155) and suppressor of cytokine signaling 1 (SOCS1) in alcoholic hepatitis (AH) and its potential mechanism associated with the mitogen-activated protein kinase (MAPK) signaling pathway. Levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), albumin (ALB), total bilirubin (TBIL), malondialdehyde (MDA), and superoxide dismutase (SOD) were measured in a rat model of AH. The biological prediction website microRNA.org and dual-luciferase reporter gene assay were used to identify whether SOCS1 was a direct target of miR-155, and the effects of miR-155 and SOCS1 on the viability, cycle progression, and apoptosis of hepatic stellate cells were assessed using RT-qPCR, Western blot assay, MTT assay, Annexin V/PI double staining, and PI single staining. The levels of ALT, AST, MDA, and TBIL and the liver cell morphology were all prominently changed in AH model rats. miR-155 suppressed SOCS1 by specifically binding to SOCS1-3'-UTR to activate the MAPK signaling pathway. SOCS1 had low expression while miR-155 was highly expressed in AH rats. miR-155 promoted hepatic stellate cell viability and cycle progression and reduced cell apoptosis by silencing SOCS1. Together, we find that silenced miR-155 could upregulate SOCS1 and inactivate the MAPK signaling pathway, thereby inhibiting the proliferation of alcoholic hepatic stellate cells and promoting cell apoptosis.

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Section: Introductionmentioning

confidence: 99%

RETRACTED: microRNA-155 Modulates Hepatic Stellate Cell Proliferation, Apoptosis, and Cell Cycle Progression in Rats With Alcoholic Hepatitis via the MAPK Signaling Pathway Through Targeting SOCS1

et al. 2020

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“…Equally important is the ongoing pursuit of better treatments for AH that may make a significant impact on outcomes. This is especially pertinent given the underwhelming evidence for the efficacy of corticosteroids [ 15 ] which had been by many seen as central to the treatment of AH [ 27 ], despite conflicting trial data.…”

Section: Discussionmentioning

confidence: 99%

“…Most recently the largest randomised controlled trial (RCT) in the field of ArLD failed to show a clear benefit of corticosteroid therapy [ 13 ]. A small positive benefit on early mortality was found in network meta-analysis of several trials [ 14 ], however this was not supported by the most recent direct meta-analysis [ 15 ], and any short-term benefits of corticosteroid are not maintained in the longer-term.…”

Section: Systematic Review: Trends In Survival From Alcoholic Hepatitmentioning

confidence: 99%

Survival from alcoholic hepatitis has not improved over time

2018

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Purpose/BackgroundWe aimed to describe changes in survival in alcoholic hepatitis (AH) over time by examining published data.MethodsA systematic literature search of Ovid Embase and PubMed was undertaken using the MESH terms ‘hepatitis, alcoholic’ to identify randomised controlled trials (RCT) and observational studies (OS) in alcoholic hepatitis. Data were extracted from included studies regarding 28-day, 90-day, 180-day mortality, as well as biochemical and clinical data.ResultsAfter review of the literature search results, 77 studies published between 1971 and 2016 were analysed, which included data from a total of 8,184 patients. Overall mortality from AH was 26% at 28 days, 29% at 90 days and 44% at 180 days after admission. No changes in mortality over time were observed in univariable analysis at 28 days or 90 days after admission (Pearson correlation r -0.216, p = 0.098, and r 0.121 p = 0.503 respectively). A small but statistically significant increase in mortality was seen in 180-day mortality (r 0.461 p = 0.036). However, after meta-regression to adjust for other factors associated with mortality at each time point, no changes in mortality were seen. Sub-group analysis did not reveal any changes in mortality over time in different study types, or when only biopsy-proven or severe disease were considered.ConclusionThere has been no improvement in mortality from AH. This is not explained by changes in severity of disease. This emphasises the urgent need for effective treatments for this alcoholic hepatitis.

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“…42 Glucocorticoids have also been shown to be associated with steatosis or glycogenic diseases. 43 The mechanism of drug-induced hepatotoxicity mainly involves mitochondrial dysfunction, oxidative stress, endoplasmic reticulum stress, lipid dystrophy and insulin resistance. 44 Zhan et al 45 found that lopinavir/ritonavir was an independent risk factor for severe liver injury in COVID-19 patients.…”

Section: Molecular Mechanism Of Liver Injury In Covid-19mentioning

confidence: 99%

Mechanism of Sars-Cov-2 Invasion Into the Liver and Hepatic Injury in Patients With Covid-19

Zhang

et al. 2022

Mediterr J Hematol Infect Dis

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A large number of studies have shown that patients with Coronavirus disease 2019 (COVID-19) have different degrees of liver injury. However, the mechanisms of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) invasion into the liver are still not fully understood. This review mainly summarizes the recently published works on the abnormal liver biochemical indicators and the mechanism of viral invasion with liver injury in COVID-19 patients. Generally, SARS-CoV-2 infection of the liver was caused by blood circulation or retrograde infection of digestive tract, which led to the liver injury through direct cytopathic effect induced by virus or immunopathological effect caused by excessive inflammation. Besides these, hypoxia, endothelial injury and drug-induced jury were also the main reasons of liver injury in COVID-19 patients. In the liver function indicators, elevated alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, gamma-glutamyl transpeptidase, and lactate dehydrogenase levels with reduced albumin levels were observed in COVID-19 patients.

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Glucocorticosteroids for people with alcoholic hepatitis

Cited by 27 publications

References 112 publications

RETRACTED: microRNA-155 Modulates Hepatic Stellate Cell Proliferation, Apoptosis, and Cell Cycle Progression in Rats With Alcoholic Hepatitis via the MAPK Signaling Pathway Through Targeting SOCS1

RETRACTED: microRNA-155 Modulates Hepatic Stellate Cell Proliferation, Apoptosis, and Cell Cycle Progression in Rats With Alcoholic Hepatitis via the MAPK Signaling Pathway Through Targeting SOCS1

Survival from alcoholic hepatitis has not improved over time

Mechanism of Sars-Cov-2 Invasion Into the Liver and Hepatic Injury in Patients With Covid-19

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