Alcohol-Related Liver Disease (ARLD)
From fatty liver to cirrhosis — assessment, abstinence and pharmacological management
Alcohol-related liver disease (ARLD) encompasses a spectrum of conditions caused by excessive alcohol consumption — from simple steatosis (fatty liver) through alcoholic hepatitis to cirrhosis and liver failure. It is the leading cause of liver-related mortality in the UK. Early recognition and sustained abstinence are the cornerstones of management, but pharmacological treatment and specialist support play an important role. Careful evaluation of disease severity and safe alcohol withdrawal are essential.
The Spectrum of ARLD
ARLD progresses along a spectrum. Alcoholic steatosis (fatty liver) develops in up to 90% of heavy drinkers and is reversible with abstinence. Alcoholic hepatitis (AH) is an acute inflammatory condition superimposed on underlying liver disease — it ranges from mild to severe and can be life-threatening. Alcoholic cirrhosis represents end-stage fibrotic disease with progressive loss of liver function. Not all heavy drinkers progress to cirrhosis — genetic factors, sex (women are more susceptible), pattern of drinking, and nutritional status all influence the disease course.
Assessing Severity — Alcoholic Hepatitis
Severe alcoholic hepatitis (SAH) carries a 28-day mortality of up to 40% without treatment. The Modified Discriminant Function (Maddrey's DF) is used to identify severe disease: DF = 4.6 × (patient's PT − control PT) + bilirubin (µmol/L ÷ 17.1). A DF ≥32 defines severe AH and indicates consideration for corticosteroid therapy. The Glasgow Alcoholic Hepatitis Score (GAHS) and MELD score are also used. The Lille score, calculated at day 7 of steroid treatment, identifies non-responders — a score >0.45 predicts non-response and steroids should be stopped.
Alcohol Withdrawal Management
All patients admitted with ARLD must be assessed for alcohol withdrawal. The Clinical Institute Withdrawal Assessment for Alcohol (CIWA-Ar) score guides treatment. Chlordiazepoxide (a long-acting benzodiazepine) is the preferred agent for alcohol withdrawal in the UK — given in a reducing regimen over 5–7 days. Lorazepam is preferred in severe hepatic impairment (shorter half-life, no active metabolites). Pabrinex (IV thiamine) must be given to ALL patients with ARLD — prophylactically for those at risk of Wernicke's encephalopathy, and therapeutically for those with confirmed Wernicke's. Oral thiamine alone is insufficient in significant ARLD due to poor GI absorption.
Pharmacological Treatment of Severe Alcoholic Hepatitis
Prednisolone 40 mg daily for 28 days is the first-line treatment for severe alcoholic hepatitis (DF ≥32 or GAHS ≥9). It reduces short-term mortality but has no effect on long-term survival. Contraindications include active infection, GI bleeding, and renal failure — these must be excluded before starting. Pentoxifylline is no longer recommended as first-line treatment (STOPAH trial). N-acetylcysteine may be added to prednisolone in selected patients. Nutritional support — enteral nutrition via NG tube if oral intake is inadequate — is essential and improves outcomes. This article has been prepared following careful evaluation of NICE, BSG, and EASL guidance on alcohol-related liver disease.
Supporting Sustained Abstinence
Abstinence is the only intervention that improves long-term prognosis across all stages of ARLD. Acamprosate (calcium homotaurine) reduces craving by modulating glutamate activity — it is started after detoxification and continued for up to 1 year. Naltrexone (opioid antagonist) reduces the rewarding effects of alcohol — licensed in the UK for relapse prevention, but use with caution in hepatic impairment (monitor LFTs monthly for 3 months). Disulfiram causes an unpleasant reaction if alcohol is consumed and acts as a deterrent — rarely used due to hepatotoxicity risk in ARLD. All patients should be referred to structured alcohol treatment services for psychological support including motivational interviewing and CBT.