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Alcoholic hepatitis is a distinct clinical entity characterised by jaundice and liver failure that generally occurs after decades of heavy alcohol use. Recovery from alcoholic hepatitis is determined by abstinence from alcohol, the presence of mild clinical symptoms and the implementation of appropriate therapy. Unfortunately, patients with severe alcoholic hepatitis have a high mortality rate of about 40% to 50% despite optimal medical management.1 A significant percentage of patients succumb to bacterial infections with infection-attributed mortality of 12% to 54%2 underscoring the importance of bacterial translocation and an impaired immune response. Moreover, patients with alcoholic hepatitis have a profound, often sepsis-like hyper-inflammatory state which suggests the possibility that proinflammatory mediators such as cytokines contribute to alcoholic hepatitis by promoting systemic inflammation and systemic inflammatory response syndrome.
Tumour necrosis factor α (TNFα) has been proposed to be the critical cytokine involved in the pathogenesis of alcoholic hepatitis, which is mostly based on animal models of experimental alcoholic liver disease.3 Inhibition of TNFα attenuates alcoholic liver injury in rats.4 Elevated plasma TNFα is a significant predictor of decreased long-term survival in patients with severe alcoholic hepatitis.5 However, clinical trials using an anti-TNFα strategy resulted in disappointing outcomes.6 ,7 In patients with moderate to severe alcoholic hepatitis, etanercept was associated …
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