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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- Spectrum: fatty liver (steatosis, reversible) → alcoholic hepatitis → fibrosis → cirrhosis (irreversible but progression can be halted with abstinence)
- Alcoholic hepatitis: acute presentation with jaundice, hepatomegaly, fever, coagulopathy on background of heavy alcohol use
- Maddrey discriminant function (DF) ≥32 = severe alcoholic hepatitis → consider prednisolone 40 mg OD for 28 days
- Complete alcohol abstinence is the MOST important intervention at every stage — the only treatment that improves survival
- Screen for complications: varices (OGD if cirrhotic), HCC (6-monthly USS), nutritional deficiencies (thiamine, B12, folate)
Overview
Alcoholic liver disease (ALD) is a spectrum of hepatic pathology caused by chronic excessive alcohol consumption. The earliest stage is simple steatosis (fatty liver), present in >90% of heavy drinkers and fully reversible with abstinence. Approximately 10–20% progress to alcoholic hepatitis (acute inflammation and hepatocyte necrosis) or fibrosis leading to cirrhosis. The risk is dose-dependent, with sustained consumption of >50 units/week (men) or >35 units/week (women) significantly increasing risk. Co-factors accelerating progression include female sex, obesity, hepatitis C co-infection, genetic polymorphisms, and continued drinking.
Epidemiology
Alcohol-related liver disease is the most common cause of liver-related death in the UK and the third most common cause of premature death overall. Approximately 6,000 deaths per year in the UK are directly attributable to ALD. Hospital admissions for ALD have doubled in the last two decades. ALD accounts for approximately 60% of liver cirrhosis cases in the UK. The burden falls disproportionately on deprived communities.
Clinical Features
Symptoms
Fatty liver: usually asymptomatic; may have vague RUQ discomfort
Alcoholic hepatitis: rapid onset jaundice, malaise, anorexia, nausea, RUQ pain, fever
Symptoms of decompensated cirrhosis: ascites, variceal bleeding, confusion, pruritus
Features of alcohol dependence: tremor, sweating, withdrawal symptoms
Signs
Hepatomegaly (may be tender in alcoholic hepatitis, shrunken in advanced cirrhosis)
Jaundice (deep in alcoholic hepatitis)
Spider naevi, palmar erythema, Dupuytren contracture
Parotid enlargement
Gynaecomastia and testicular atrophy (hyperoestrogenaemia)
Ascites, splenomegaly, caput medusae (portal hypertension)
Asterixis/flapping tremor (hepatic encephalopathy)
Investigations
First-line
LFTsAST:ALT ratio >2 is suggestive of ALD (unlike viral/autoimmune where ALT > AST). GGT raised (enzyme inducer). Bilirubin elevated in alcoholic hepatitis
FBCRaised MCV (macrocytosis — direct toxic effect of alcohol on erythropoiesis). Thrombocytopenia if portal hypertension/hypersplenism
Coagulation (INR/PT)Prolonged in severe hepatitis and cirrhosis — used in Maddrey DF calculation
Alcohol historyAUDIT-C or full AUDIT questionnaire. Units per week. Duration. CAGE questions
Second-line
Maddrey discriminant functionDF = 4.6 × (patient PT − control PT) + bilirubin (µmol/L)/17.1. DF ≥32 = severe alcoholic hepatitis
FibroScanNon-invasive fibrosis assessment — determine degree of fibrosis/cirrhosis
Abdominal USSHepatic steatosis (bright echogenic liver), signs of cirrhosis (nodular surface, splenomegaly), ascites
Specialist
Liver screenExclude co-existent liver disease: hepatitis B/C serology, autoantibodies (ANA, SMA, AMA), ferritin/transferrin saturation, caeruloplasmin, alpha-1-antitrypsin
Liver biopsyIf diagnostic uncertainty — shows steatosis, Mallory-Denk bodies, ballooning degeneration, neutrophilic infiltrate (alcoholic hepatitis)
OGDVariceal screening if cirrhosis confirmed
1
All stages — abstinence
- Complete alcohol cessation is the single most important intervention — improves survival at every stage
- Brief intervention in primary care
- Referral to specialist alcohol services for detoxification and psychosocial support
- Consider pharmacological support: acamprosate, naltrexone, or disulfiram for maintaining abstinence
- Medically assisted alcohol withdrawal: chlordiazepoxide (reducing regimen) if significant dependence
2
Severe alcoholic hepatitis (DF ≥32)
- Prednisolone 40 mg OD for 28 days (if no contraindications: active sepsis, GI bleeding, renal failure)
- Assess response at day 7 using Lille score: if Lille >0.45 = non-responder → stop prednisolone (futile)
- Pentoxifylline no longer recommended (no survival benefit in STOPAH trial)
- Nutritional support: high-protein, high-calorie diet + thiamine (Pabrinex IV) + B vitamins
3
Cirrhosis management
- Manage complications: ascites (spironolactone ± furosemide, salt restriction), varices (band ligation, propranolol prophylaxis), encephalopathy (lactulose, rifaximin)
- HCC surveillance: 6-monthly USS ± AFP
- Assess for liver transplant if: abstinent ≥6 months (varies by centre), decompensated cirrhosis, or non-response to medical therapy
4
Nutritional
- IV Pabrinex (vitamins B and C) for all admissions — prevents Wernicke encephalopathy
- Oral thiamine 100 mg TDS long-term
- Dietitian review — many patients are malnourished
- Correct electrolyte abnormalities (hypomagnesaemia, hypophosphataemia, hypokalaemia)
Complications
- Cirrhosis: Irreversible but progression halted by abstinence. ~50% 5-year survival if decompensated
- Variceal bleeding: From portal hypertension — major cause of death in ALD cirrhosis
- Hepatic encephalopathy: Confusion, asterixis, coma — precipitated by infection, GI bleeding, constipation, electrolyte disturbance
- Hepatocellular carcinoma: 1–5% annual risk in ALD cirrhosis
- Hepatorenal syndrome: Functional renal failure in advanced cirrhosis — type 1 (rapid, poor prognosis) and type 2 (gradual)
UKMLA Exam Tips
- 1AST:ALT ratio >2:1 = think alcoholic liver disease (unique to ALD; viral hepatitis typically ALT > AST)
- 2Maddrey DF ≥32 = severe alcoholic hepatitis → prednisolone 40 mg OD for 28 days
- 3Lille score at day 7: >0.45 = non-responder → STOP steroids (no benefit, increased infection risk)
- 4STOPAH trial: prednisolone showed short-term mortality benefit; pentoxifylline showed NO benefit
- 5Mallory-Denk bodies (eosinophilic intracytoplasmic inclusions) on biopsy are characteristic but not pathognomonic for ALD
- 6IV Pabrinex BEFORE glucose/carbohydrate loading — giving glucose to thiamine-deficient patients precipitates Wernicke encephalopathy
practicetest your knowledge on alcoholic liver diseaseApply what you've learnt with UKMLA-style questions from the iatroX Q-Bank — gastroenterology and beyond.
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