Alcohol Misuse and Alcoholic Liver Disease Research Center for ALPD and Cirrhosis Center

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The microsomal ethanol-oxidizing system (MEOS) uses nicotinamide adenine dinucleotide phosphate (NADPH) and molecular oxygen. This enzyme, in addition to catalyzing ethanol oxidation, is also responsible for the biotransformation of other drugs, such as acetaminophen, haloalkanes, and nitrosamines. Ethanol upregulates CYP2E1, and the proportion of alcohol metabolized via this pathway increases with the severity and duration of alcohol use.

Hepatocytes also express very high levels of catalase, an enzyme that inhabits peroxisomes. Catalase normally carries out the detoxification of hydrogen peroxide (H2O2) to water and oxygen. However, when ethanol is present, catalase has an accessory role in ethanol metabolism by using H2O2 to oxidize ethanol to acetaldehyde. Ethanol oxidation by catalase is a relatively minor pathway in the liver, but has a larger ethanol-oxidizing function in the brain (Aragon et al. 1992).

Alcoholic liver disease

Research with rodents subjected to chronic alcohol feeding has shown that ethanol consumption reduces adipose tissue mass by enhancing fat breakdown (i.e., lipolysis) in adipose tissue (Kang et al. 2007; Wang et al. 2016; Wei et al. 2013). The free fatty acids released from adipose tissue are taken up by the liver and esterified into triglycerides, thereby exacerbating fat accumulation in the liver (Wei et al. 2013). Clinical studies also have demonstrated that people with alcohol use disorder who have fatty liver have significantly lower body weight, body mass index, and body-fat mass content than control subjects (Addolorato et al. 1997, 1998). SREBP-1c belongs to a family of transcription factors that control hepatic cholesterol metabolism. However, in heavy drinkers, ethanol oxidation short-circuits hepatic lipid metabolism, converting the liver from a lipid-burning to a lipid-storing organ. Thus, hepatic SREBP-1c is relatively inactive in hepatocytes of abstinent people, residing mostly in the ER.

alcoholic liver disease

During the past several decades, various formulas and algorithms have been proposed for predicting the outcome of severe alcoholic hepatitis. The single most reliable indicator of severity is the presence of hepatic encephalopathy. Mild alcoholic hepatitis is a benign disorder with negligible short-term mortality. However, when alcoholic hepatitis is of sufficient severity to cause hepatic encephalopathy, jaundice, or coagulopathy, mortality can be substantial. However, alcoholic hepatitis can occur among those who drink less and have other risk factors.


However, some degree of hepatitis likely is always present in cirrhotic patients, whereas hepatic fat usually is not prominent in these individuals. The World Health Organization’s (2014)
Global Status Report on Alcohol and Health estimates that 50 percent of all deaths caused by cirrhosis were attributable to alcohol abuse. Patients with alcoholic hepatitis are prone to infections, especially when on steroids; this is particularly important as it might lead to a poor prognosis, acute renal injury, and multi-organ dysfunction. Patients with alcoholic hepatitis are at risk of alcohol withdrawal.

Liver transplantation should be considered as a treatment option for patients with decompensated alcohol related cirrhosis and severe alcoholic hepatitis. The overall clinical diagnosis of alcoholic liver disease, using a combination of physical findings, laboratory values, and clinical acumen, is relatively accurate (Table 3). However, liver biopsy can be justified in selected cases, especially when the diagnosis is in question.

Alcoholic Hepatitis

Cirrhosis caused by alcohol can be a life-threatening disease. Cognitive behavioral therapy (CBT) and medications called benzodiazepines can ease withdrawal symptoms in a person with alcohol dependency. People with severe alcohol dependency may stay at an inpatient rehabilitation facility for closer monitoring.

Even if you have advanced alcoholic cirrhosis, it is possible to feel better and improve your quality of life. Our team approach means that liver disease experts, social workers, and dieticians all come together to deliver personalized care, support, and hope for a better future. It’s the only way you can keep liver damage from getting worse. You may even be able to undo some of the liver damage that’s already happened.

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