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Alcoholic liver disease

Alcoholic liver disease (ALD), also known as alcohol-related liver disease (ARLD), encompasses a range of conditions resulting from excessive alcohol consumption, including fatty liver, alcoholic hepatitis, and cirrhosis.

It is a leading cause of liver disease in Western countries and a major cause of death related to alcohol overconsumption. While fatty liver (steatosis) is common among heavy drinkers and reversible, more severe forms like alcoholic hepatitis and cirrhosis affect a smaller proportion of individuals.

Risk Factors

The risk of developing ALD is influenced by various factors, including:

  • Quantity of Alcohol: Consuming 60–80 g of alcohol daily for over 20 years significantly increases the risk for men, while for women, it's around 20 g/day.
  • Drinking Patterns: Drinking outside meal times triples the risk.
  • Sex: Women are more susceptible due to lower alcohol dehydrogenase levels, higher body fat proportion, and menstrual cycle influences.
  • Ethnicity: Higher rates are seen in African-American and Hispanic males.
  • Hepatitis C: Concomitant infection accelerates liver damage.
  • Genetic Factors: Genetic predispositions affect both alcoholism and ALD, although specific polymorphisms are not definitively linked.
  • Iron Overload: Conditions like hemochromatosis worsen ALD.
  • Diet: Malnutrition, particularly vitamin A and E deficiencies, exacerbates liver damage.


Pathogenesis of Alcoholic Liver Injury
Pathogenesis of Alcoholic Liver Injury

The exact mechanism of ALD is not fully understood. Chronic alcohol consumption leads to pro-inflammatory cytokine secretion, oxidative stress, lipid peroxidation, and acetaldehyde toxicity, resulting in liver inflammation, apoptosis, and fibrosis. The liver's ability to regenerate complicates the understanding of why only some individuals develop severe ALD.

Fatty Change

Fatty change, or steatosis, involves the accumulation of fatty acids in liver cells, visible as fatty globules under the microscope. Alcohol metabolism increases NADH levels, promoting fatty acid synthesis and triglyceride formation, leading to fatty liver.

Microscopy of Liver Showing Fatty Change
Microscopy of liver showing fatty change, cell necrosis, Mallory bodies

Alcoholic Hepatitis

Characterised by hepatocyte inflammation, alcoholic hepatitis affects 10–35% of heavy drinkers. Inflammatory cytokines are very important in liver injury and cytotoxic hepatomegaly. Increased intestinal permeability and TNF-α activity contribute to this condition.


Cirrhosis, a late-stage serious liver disease, involves inflammation, fibrosis, and scarring, leading to liver failure. Symptoms include jaundice, liver enlargement, and pain. Without abstinence, cirrhosis can result in portal hypertension, coagulation disorders, and other severe complications. While some causes overlap with non-alcoholic liver diseases, the progression and symptoms are similar.


Early ALD often presents with subtle or no abnormal findings, typically detected during routine examinations with elevated liver enzyme levels. Advanced ALD shows stigmata of chronic liver disease, and liver biopsy reveals steatosis and inflammation, similar to nonalcoholic fatty liver disease. Acute alcoholic hepatitis manifests with fever, jaundice, hepatomegaly, and hepatic decompensation.

Laboratory Findings

In alcoholic hepatitis, the AST to ALT ratio exceeds 2:1, with levels usually below 500. This ratio results from pyridoxal phosphate deficiency and alcohol-induced mitochondrial injury. Other findings include macrocytosis, elevated GGT, alkaline phosphatase, and bilirubin levels, and reduced folate levels.


Abstinence from alcohol is very important. Patients with chronic HCV should also avoid alcohol to prevent rapid disease progression.


Evidence for medication use is limited. Corticosteroids may be used for severe inflammation, while treatments like silymarin and S-adenosyl methionine show ambiguous results. Anti-TNF medications and pentoxifylline are not clearly beneficial, and propylthiouracil may be harmful.


Liver transplantation is the definitive treatment for irreversible cirrhosis. Post-transplant survival rates are similar for ALD and non-ALD patients. A six-month sobriety period and psychiatric evaluation are typically required for listing, with relapse leading to delisting.


Prognosis depends on liver histology and cofactors like viral hepatitis. Alcoholic hepatitis progresses to cirrhosis in 10–20% of cases annually, with 70% eventually developing cirrhosis. Despite cessation, only a minority achieve normal liver histology. Mortality rates are high, with alcohol-related deaths being a significant cause of mortality globally.

Self-assessment MCQs (single best answer)

Which of the following is NOT a factor influencing the risk of developing Alcoholic Liver Disease (ALD)?

What is the typical daily alcohol consumption that significantly increases the risk of ALD in women?

Which condition is characterised by the accumulation of fatty acids in liver cells?

In the context of ALD, what does an AST to ALT ratio exceeding 2:1 typically indicate?

What is a common histological finding in a liver biopsy of a patient with alcoholic liver disease?

Which medication is commonly used to treat severe inflammation in alcoholic hepatitis?

What is the definitive treatment for irreversible cirrhosis due to ALD?

What is the typical requirement for a patient with ALD to be listed for liver transplantation?

Which of the following laboratory findings is typically seen in alcoholic hepatitis?

What percentage of individuals with alcoholic hepatitis progresses to cirrhosis annually?


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