Alcoholic liver disease (ALD) refers to a range of progressive liver conditions caused by chronic and excessive alcohol consumption. One-third of the US population consumes alcohol above the recommended levels, increasing their risk of ALD. There are three stages of ALD, which may or may not occur sequentially. The first stage is typically asymptomatic and involves the development of (potentially) reversible alcoholic fatty liver. Continued alcohol consumption will lead to alcoholic hepatitis, the second stage, which often becomes chronic. Clinical findings in this stage include jaundice, fatigue, and fever. In the third and final stage, the patient develops alcoholic cirrhosis. Patient history, transaminase levels, and imaging studies are crucial for diagnosis and show different patterns of hepatic injury. Nonalcoholic steatohepatitis is a differential diagnosis and is currently regarded as an important cause of cirrhosis. Treatment of ALD requires complete cessation of alcohol use.
The management of alcoholic hepatitis, including its diagnosis and treatment, is described in detail elsewhere.
- Second most common cause of liver cirrhosis in the United States
- 28% of the US population exceeds the recommended limits of alcohol consumption.
- Lifetime prevalence of alcohol abuse: 18%
- ∼ 10–20% of heavy drinkers develop cirrhosis.
Epidemiological data refers to the US, unless otherwise specified.
- Hepatic degradation of ethanol to acetyl-CoA by alcohol dehydrogenase results in NADH excess (see breakdown of ethanol for more details) → ↑ NADH drives the formation of glycerol 3-phosphate (G3P) from dihydroxyacetone phosphate (DHAP) → ↑ in both G3P and fatty acids causes increased triglyceride synthesis in the liver and accompanying inflammation → steatohepatitis → chronic inflammation leads to hepatic fibrosis and sclerosis → portal hypertension and eventually cirrhosis
The stages of ALD may overlap and do not necessarily occur in sequence.
Alcoholic fatty liver (reversible)
- Mostly asymptomatic
- Some patients report feeling a sensation of pressure in the upper abdominal area.
- Hepatomegaly: soft in consistency
- Regresses after cessation of alcohol consumption
- Acute exacerbation with risk of hepatic failure is rare.
Alcoholic hepatitis (reversible in mild cases)
See “Alcoholic hepatitis.”
- Final stage of ALD
- See “Clinical features” in .
- AST (aspartate aminotransferase) > ALT (alanine aminotransferase) (both ↑ ALT and ↑ AST)
- ↑ GGT
- ↑ Serum ferritin
- Macrocytic anemia 
- ↑ CDT(carbohydrate-deficient transferrin)
See “Alcoholic hepatitis.”
- See .
- Diagnosis confirmed by biopsy
- Alcoholic fatty liver: accumulation of lipid droplets in the hepatocytes with gradual single cell necrosis within the lobules
- Macrovesicular steatosis with hydropic swelling and ballooning degeneration of hepatocytes within the lobules
- Damaged hepatocytes typically contain Mallory-Denk bodies (hyaline inclusion bodies that contain keratin filaments and appear eosinophilic on HE staining).
- Immunoreaction: neutrophilic granulocytes within hepatic tissue
- Pericellular and sinusoidal fibrosis
- Alcohol-related cirrhosis
- Epidemiology: very widespread
- Pathophysiology: ↑ Insulin resistance
- Clinical features
- Complications: cirrhosis, hepatocellular carcinoma
The differential diagnoses listed here are not exhaustive.
Mainly characterized by a constellation of clinical features resulting from decreased hepatic function:
Other organ damage following chronic alcohol use
- Acute hemolytic anemia after excessive alcohol use over the course of several years, characterized by the following triad:
We list the most important complications. The selection is not exhaustive.