Alcoholic Liver Disease

Overview

Alcoholic liver disease refers to a set of characteristic pathological changes that occur in individuals who ingest large amounts of alcohol over a long period of time.

Incidence

Alcoholic Liver Disease is the most common cause of liver disease in most developed countries and occurs in alcohol abusers.

Morphology

Alcoholic Liver Disease can appear as any of three morphological patterns which can also overlap. The vast majority (>90%) of those with disease display alcoholic hepatic steatosis which can appear even after a single episode binge drinking. However, 10-20% patients additionally display alcoholic hepatitis which is thought to be a precursor of alcoholic cirrhosis.

This pattern of steatosis begins with the appearance of microvesicular lipid droplets in a centrilobular pattern. Over time, the lipid droplets grow to a macrovesicular pattern that can involve the entire hepatic lobule. Grossly, the liver may look enlarged, yellow, and fatty. Alcoholic hepatic steatosis is completely reversible and will resolve with cessation of drinking.

This pattern of hepatitis is characterized by ballooning (swelling) of hepatocytes which can also undergo spotty necrosis. Hepatocytes may also possess mallory bodies which are amorphous accumulations of cytoskeletal proteins. Inflammation is primarily characterized by the presence of neutrophils around injured hepatocytes. Fibrosis may be seen especially in the Space of Disse and around the terminal hepatic venule. Alcoholic hepatitis heralds the onset of irreversible hepatic injury and is considered an early stage in the development of alcoholic cirrhosis.

This pattern of cirrhosis develops slowly and over time, representing completely irreversible injury to the liver. Fibrosis begins to develop between major histological landmarks (i.e. between adjacent portal tracts and between portal tracts and the terminal hepatic venule). Nodules of regenerating hepatic tissue develop within these increasingly thick walls of fibrotic tissue and can be observed grossly as surface nodularity on the liver. Over time, these nodules are obliterated through a process of ischemia and necrosis as they are increasingly ensnared by fibrosis. In the end, the liver becomes a shrunken, scarred shell of its former self.

Pathogenesis

The pathogenic mechanisms which induce the morphological changes above are multiple and complex; however, several risk factors are worth mentioning.
Alcohol Intake Amount and Length: The risk of developing disease is proportional to the amount of alcohol that is ingested per day and the length of time at which this is maintained. In general, intake of more than 100g/day for one or two decades is considered a strong risk factor for irreversible injury
Gender: Women appear to be more prone to liver injury than men
Hepatitis C Virus: Concomitant infection with HCV significantly increases the risk of developing cirrhosis

Clinical Consequences

Clinical consequences of alcoholic hepatic steatosis are subtle and often subclinical. Subtle hepatomegaly may be the only evidence with mild elevation of serum aminotransferases and occasionally hyperbilirubinemia.

Although alcoholic hepatitis develops over time it will often present suddenly with symptomology that may include fever, abdominal pain, and hepatomegaly. Sudden bouts of alcoholic hepatitis are fatal in a significant minority of cases (~30-50%). Elevation of serum aminotransferases is usually observed along with hyperbilirubinemia.

Alcoholic Cirrhosis will present with symptoms of cirrhosis which are discussed on its own page.

Hepatic Failure is frequently an endpoint of alcoholic liver disease
Mallory-Weiss Syndrome or other massive GI Bleeding episode can occur
Hepatorenal Syndrome
Hepatocellular Carcinoma may occur as alcoholic liver disease is a major risk factor for this malignancy.

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