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• W4211004823 endingPage "739" @default.
• W4211004823 startingPage "699" @default.
• W4211004823 abstract "Alcoholic liver disease (ALD) represents three overlapping and likely related conditions: steatosis, inflammation (steatohepatitis), and fibrosis/cirrhosis. Although the vast majority of heavy drinkers develop steatosis, less than 25% develop more serious forms of ALD. Symptoms and signs associated with ALD are not specific and mostly reflect the severity of the underlying liver injury. Steatosis, ballooning degeneration of hepatocytes, apoptotic bodies, perisinusoidal fibrosis, and Mallory-Denk bodies are the most characteristic histological features of ALD. Although the risk of ALD increases with increasing consumption of alcohol above a threshold of 30-40 g/day, many other risk factors including obesity, female gender, genetically determined iron overload, chronic hepatitis C infection, and genetic factors including PNPLA3, TM6SF2, and genes connected with oxidant stress appear to influence the probability of developing serious ALD. Much has been learned about potential mechanisms of injury that contribute to ALD. Activation of SREBP-1, reactive oxygen species, and potentially activation of the FXR receptor are involved in hepatic steatosis. Loss of integrity of the gut mucosa, possibly as a direct effect of alcohol, contributes to activation of the toll-like receptor complex (TLR) and subsequent release of proinflammatory cytokines including IL1β, TNF-α, and others that clearly play important roles in the hepatic inflammation associated with heavy alcohol consumption. Abstinence remains the cornerstone of therapy for ALD, but anti-inflammatory medications such as methylprednisolone have been shown to improve 30-day survival in patients with severe forms of acute alcoholic hepatitis (AAH). Unfortunately, the improved survival is not sustained beyond a short time due to subsequent infections which has stimulated the need for better treatments with fewer side effects. Nutritional support (30-40 kcal/kg and 1.0-1.5 g of protein/kg body weight) is also beneficial in recovery from AAH. In those patients who are either abstinent for a sustained time or in those who have good insight and family support shortly after presentation with ALD, liver transplantation may be life-saving when other options fail. Future treatments will focus on newly identified targets that interrupt the accumulation of fat within the liver, the inflammatory cascade, or regeneration of the liver after injury from alcohol." @default.
• W4211004823 created "2022-02-13" @default.
• W4211004823 creator A5006482005 @default.
• W4211004823 creator A5008621012 @default.
• W4211004823 date "2017-10-23" @default.
• W4211004823 modified "2023-10-14" @default.
• W4211004823 title "Alcoholic Liver Disease" @default.
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