Summary

Alcohol-Related Liver Disease (ALD) encompasses a spectrum of liver damage caused by excessive alcohol consumption, ranging from simple steatosis (fatty liver) through alcoholic steatohepatitis (ASH) to fibrosis and ultimately cirrhosis. ALD is the most common cause of liver cirrhosis in Western countries. Acute alcoholic hepatitis (AAH) is a severe inflammatory condition with 30-50% 28-day mortality in severe cases. Abstinence from alcohol is the cornerstone of management at all stages, and is the only intervention proven to improve long-term outcomes.

Key Facts

• Prevalence: 90% of heavy drinkers develop fatty liver; 20-40% progress to fibrosis/cirrhosis
• Risk threshold: Greater than 14 units/week increases risk; greater than 35 units/week high risk
• Biochemistry: AST:ALT ratio greater than 2:1; elevated GGT; macrocytosis
• Mortality: Severe AAH has 30-50% 28-day mortality without treatment
• Key management: Abstinence (only proven intervention); steroids for severe AAH
• Transplant eligibility: Typically requires 6 months abstinence

Clinical Pearls

The AST:ALT Ratio: In ALD, AST is typically greater than ALT in a 2:1 ratio. If ALT greater than AST, consider alternative diagnoses (viral hepatitis, NAFLD). This ratio helps differentiate ALD from other causes.

Maddrey's Discriminant Function: MDF = 4.6 × (PT patient - PT control) + Bilirubin (μmol/L) / 17.1. Score greater than 32 indicates severe disease with benefit from corticosteroids if no contraindication.

The Lille Score: Calculate at day 7 of steroid treatment. Score greater than 0.45 indicates non-response — stop steroids (no benefit and increased infection risk).

Why This Matters Clinically

ALD is a major cause of liver-related morbidity and mortality. Severe AAH requires rapid assessment and treatment decisions. Early recognition and intervention can prevent progression to cirrhosis. Abstinence support is critical at all stages — even in cirrhosis, abstinence improves outcomes and may allow liver regeneration.

Structured Approach

General:

• Nutritional status (cachexia, muscle wasting)
• Stigmata of chronic liver disease
• Level of consciousness (encephalopathy grade)

Abdominal:

• Hepatomegaly (tender in AAH)
• Splenomegaly (portal hypertension)
• Ascites (shifting dullness, fluid thrill)

Peripheral Signs:

• Spider naevi, palmar erythema
• Jaundice (scleral icterus)
• Asterixis (hepatic flap)
• Peripheral oedema

Special Tests

Natural History

• Fatty liver: Reversible with abstinence
• AAH: 30-50% 28-day mortality if severe
• Cirrhosis: 5-year survival 60% with abstinence vs 30% with continued drinking

Outcomes with Treatment

Prognostic Factors

Good Prognosis:

• Fatty liver stage
• Abstinence maintained
• Lille responder (less than 0.45)
• Lower MELD score

Poor Prognosis:

• MDF greater than 32
• Lille non-responder
• Hepatorenal syndrome
• Encephalopathy
• Continued alcohol use

Key Guidelines

1. EASL Clinical Practice Guidelines: Alcohol-Related Liver Disease (2018) — European Association for the Study of the Liver. J Hepatol 2018
2. NICE NG50 (2016) — Cirrhosis in over 16s: assessment and management. NICE NG50
3. ACG Clinical Guideline: ALD (2018) — American College of Gastroenterology.

Landmark Trials

STOPAH Trial (2015) — Steroids vs Pentoxifylline for Alcoholic Hepatitis

• 1103 patients; 2x2 factorial design
• Key finding: Prednisolone reduced 28-day mortality; pentoxifylline did not
• Clinical Impact: Supports steroids for severe AAH; pentoxifylline not recommended

Lille Study (2007) — Early identification of steroid non-responders

• Developed Lille score at day 7
• Key finding: Non-responders (greater than 0.45) have no benefit from continued steroids
• Clinical Impact: Stop steroids at day 7 if Lille greater than 0.45

Evidence Strength

What is Alcohol-Related Liver Disease?

Alcohol-related liver disease (ALD) happens when drinking too much alcohol over time damages your liver. The liver is an amazing organ that can repair itself, but if you keep drinking heavily, it gradually becomes scarred and stops working properly.

There are stages:

1. Fatty liver: Fat builds up in your liver. Usually no symptoms. Reversible if you stop drinking.
2. Alcoholic hepatitis: Your liver becomes inflamed. You may feel unwell, tired, and become jaundiced (yellow skin).
3. Cirrhosis: Your liver becomes scarred and hardened. This is serious and can be life-threatening.

Why does it matter?

Your liver does hundreds of essential jobs — filtering your blood, making proteins, and processing nutrients. When it fails, you can develop serious problems like fluid in the tummy (ascites), confusion (encephalopathy), and bleeding. Severe alcoholic hepatitis can be fatal without treatment.

How is it treated?

1. Stop drinking: This is the most important treatment at all stages. With fatty liver, stopping drinking lets your liver recover. Even with cirrhosis, stopping improves survival.
2. Nutrition: Many people with ALD are malnourished. Good nutrition helps your liver heal.
3. Steroids: For severe alcoholic hepatitis, steroid tablets can reduce inflammation and improve survival.
4. Managing complications: If you have cirrhosis, you may need treatment for fluid retention, confusion, or bleeding.
5. Liver transplant: For those with end-stage disease who have stopped drinking.

What to expect

• Recovery depends on how much damage has occurred and whether you stop drinking
• Fatty liver can completely recover within weeks to months of abstinence
• Cirrhosis is permanent, but stopping drinking prevents further damage

When to seek help

See a doctor urgently if you have:

• Yellowing of your skin or eyes (jaundice)
• Swollen tummy (ascites)
• Confusion or drowsiness
• Vomiting blood or passing black stools
• Fever with abdominal pain