Alcohol-Related Liver Disease: Alcoholic Hepatitis, Treatment and Transplant in India

Alcohol-related liver disease runs from reversible fatty liver to alcoholic hepatitis and cirrhosis. Severe alcoholic hepatitis — a Maddrey discriminant function of 32 or more — is a medical emergency. In the 1,103-patient STOPAH trial, pentoxifylline did not improve survival and prednisolone gave no benefit at 90 days. Stopping alcohol completely remains the single treatment that changes outcome at every stage.
— Dr Chetan Kalal, DM Hepatology, Gleneagles Hospital Mumbai

Consider a 44-year-old businessman from Navi Mumbai who has drunk half a bottle of whisky most evenings for fifteen years. He has never missed a day of work. Then, over three weeks, his eyes turn yellow, his abdomen swells, and he develops a low fever. His family assumes it is “jaundice” and keeps him at home on boiled food. By the time he reaches hospital his bilirubin is over 20 mg/dL, his INR is 2.3 and his kidneys are beginning to fail. That is severe alcoholic hepatitis — and in India it is often the first time the patient or his family learns that his liver was sick at all. (This is an illustrative scenario, not a specific patient.)

Alcohol-related liver disease (ALD) is one of the commonest reasons Indians are admitted to a liver unit, and the patients are young. In more than 1,200 patients with alcohol-related acute-on-chronic liver failure enrolled across Asia by the AARC — the APASL working group I have contributed to for years — 98% were men and the average age was 42.5. My own randomised trial work at ILBS New Delhi tested aggressive nutrition therapy in malnourished men with alcohol-related cirrhosis. This guide explains how the disease progresses, how severity is measured, what the evidence really says about steroids and pentoxifylline, and when liver transplantation becomes the right conversation.

From fatty liver to cirrhosis: how alcohol damages the liver

Alcohol injures the liver along a spectrum, and most heavy drinkers move through it silently. The first stage, alcohol-related fatty liver, develops in most people who drink more than about 40 g of alcohol a day, and it can resolve with abstinence; only a subset go on to more advanced disease. The second, alcoholic hepatitis, is active inflammation and liver cell death; it can be mild and unnoticed, or severe and life-threatening. The third is fibrosis progressing to cirrhosis, in which scar tissue replaces normal liver and blood flow through the organ is disrupted.

These stages overlap. Many patients admitted with alcoholic hepatitis already have cirrhosis underneath; their hepatitis is an acute insult on chronic disease, which is precisely what acute-on-chronic liver failure means. Whether someone progresses depends on how much and for how long they drink, but also on factors no drink counter captures: genetics, sex (women develop liver damage at lower intakes), coexisting hepatitis B or C, malnutrition, and — increasingly in India — the metabolic triad of obesity, diabetes and fatty liver from diet.

That last point deserves emphasis because it is changing the disease in front of us. In an AARC analysis of 1,216 patients with alcohol-associated ACLF, overweight or obesity independently raised 30-day mortality (adjusted hazard ratio 1.91). A 2025 AARC study found that diabetic patients with alcohol-related ACLF had 90-day survival of 32%, against 57% in matched non-diabetic patients. The modern Indian ALD patient is often a heavy drinker and metabolically unwell, and that combination is worse than either alone.

Early disease is detectable before symptoms. Liver tests, an ultrasound, and a FibroScan to measure liver stiffness can show whether fibrosis is developing while it can still regress. Our alcohol-related liver disease clinic page describes how we assess these patients at Gleneagles.

Alcoholic hepatitis: recognising the emergency and measuring severity

Severe alcoholic hepatitis typically follows a period of heavy drinking, often within weeks of the last drink. The classical features are rapidly deepening jaundice, fever without infection, a tender enlarged liver, swelling of the abdomen with fluid (ascites), muscle wasting, and in severe cases confusion, bleeding and kidney failure. The STOPAH investigators summarised the stakes plainly: short-term mortality in severe disease exceeds 30%.

Doctors grade severity with scores rather than impressions. The oldest is the Maddrey discriminant function, calculated from prothrombin time and bilirubin; a value of 32 or more defines severe disease and was the entry threshold for the trials that shaped treatment. MELD, the score used for transplant allocation, is also widely used. In the ACLF framework that AARC developed for Asian patients, organ failures are counted and scored as well, because a patient with alcoholic hepatitis plus kidney failure plus encephalopathy is in a different prognostic world from one with jaundice alone.

Severity scores do one more thing: they tell the family honestly how ill the patient is. In my experience, the most damaging delay in Indian ALD care is not in the hospital but before it — days or weeks of home remedies while the bilirubin climbs. Any heavy drinker with new jaundice should be assessed by a hepatologist promptly.

Steroids, pentoxifylline and the STOPAH trial

For decades two drugs were recommended for severe alcoholic hepatitis: prednisolone, a corticosteroid, and pentoxifylline. Both rested on small trials. The STOPAH trial, published in the New England Journal of Medicine in 2015, finally tested them properly: 1,103 patients across the UK, randomised in a two-by-two design to prednisolone, pentoxifylline, both, or neither.

The results reset practice. Pentoxifylline did not improve survival at all (odds ratio for 28-day death 1.07). Prednisolone was associated with a reduction in 28-day mortality — 14% versus 17% with placebo — that did not reach statistical significance (odds ratio 0.72, P = 0.06), and there was no benefit at 90 days or one year. Serious infections occurred in 13% of patients given prednisolone against 7% of those who were not.

The practical approach that follows is selective rather than reflexive. Steroids may be considered for patients with severe disease once infection, gastrointestinal bleeding and kidney failure have been looked for and treated, and only under specialist supervision. Response is judged at day seven using the Lille model, which combines age, kidney function, albumin, prothrombin time, and bilirubin at baseline and day seven. A Lille score of 0.45 or higher marks non-response: continuing steroids then adds infection risk without benefit. I am deliberately not giving doses or durations here; those decisions belong to the treating team.

Supportive care often matters as much as the drug. Nutrition is central — most of these patients are severely malnourished, and in our ILBS trial in alcohol-related cirrhosis, energy intake above 25 kcal/kg/day and protein above 0.8 g/kg/day were associated with better 12-month survival regardless of study group. Our guide to nutrition in cirrhosis covers this in detail. Infection surveillance, kidney protection, and management of alcohol withdrawal complete the picture.

Abstinence, relapse and liver transplantation

No medicine for alcohol-related liver disease comes close to the effect of stopping drinking. Abstinence allows fatty liver to resolve, lets inflammation settle, slows or halts fibrosis, and in compensated cirrhosis can keep a patient out of hospital for years. Relapse is common, which is why treatment of alcohol use disorder — counselling, family involvement, and where appropriate medication prescribed by the treating team — is part of liver care, not an optional add-on.

Liver transplantation is the definitive treatment for end-stage alcohol-related cirrhosis and is a common indication for liver transplantation. Most centres, as a 2016 review from an Indian transplant programme notes, require six months of abstinence before transplant. That rule exists for sound reasons: some livers recover substantially once drinking stops, and abstinence is a test of the commitment a transplant requires.

The same review points out that the rule makes little sense for patients with severe alcoholic hepatitis or very advanced decompensation, who are unlikely to survive six months — and most alcoholic hepatitis deaths happen within two months. That is the problem Mathurin and colleagues addressed in a landmark 2011 NEJM study. Across seven French centres, 26 carefully selected patients with a first episode of severe alcoholic hepatitis not responding to medical therapy received early transplantation. Six-month survival was 77% with transplant against 23% in matched patients without one, and the benefit persisted at two years. Selection was strict: fewer than 2% of admitted patients qualified, all had supportive families, no serious coexisting illness, and a commitment to abstinence. Three of the 26 resumed drinking, all after nearly two years or more.

In India, where most transplants depend on a living family donor, these decisions carry an added ethical weight: a healthy relative accepts surgical risk for the patient. Early transplantation for alcoholic hepatitis is therefore considered only after a frank assessment by hepatologists, surgeons and addiction specialists together, with the family fully involved. It is an option for the right patient, never a routine.

For patients and families, the message is simple. Stop drinking completely — not reduce, stop. Get assessed early, while there is still liver to save. And if transplantation is being discussed, have that conversation at a centre with experience in alcohol-related liver disease and a structured abstinence programme. You can read more about our approach to cirrhosis care in Mumbai.

References

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