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Health condition · Clinically reviewed

Acute liver disease, elevated LFTs and the causes behind them.

Most acute liver injury settles once the cause is found and removed. A structured screen, a careful drug history and close monitoring of INR decide whether it stays that way.

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Why trust this guide

  • 01

    Clinically reviewed

    Written by our editorial team and reviewed by a registered UK clinician before publication.

  • 02

    Sourced from guidance

    Checked against NICE, BSG, BASL and UKHSA sources you can see at the end.

  • 03

    Current for 2026

    Reflects modern UK guidance including hepatitis E as the leading cause of acute viral hepatitis and MHRA drug-safety updates.

Key facts

Acute liver disease at a glance.

The essentials, in plain English. What it is, what it is not, and the numbers that matter most in the first 48 hours.

  • What it is

    A sudden inflammatory injury to the liver, usually picked up as raised transaminases (ALT and AST) with or without jaundice, and lasting under six months.

  • Not acute liver failure

    Acute liver disease is the injury pattern. Acute liver failure is the syndrome that follows if the liver decompensates, with coagulopathy (INR over 1.5) and encephalopathy. Different pathway, covered separately.

  • Commonest UK cause 2023 to 2024

    Hepatitis E is now the leading cause of acute viral hepatitis in the UK, mostly food-borne from undercooked pork products.

  • Drug-induced (DILI)

    Paracetamol overdose is the top cause of acute liver failure in the UK. Idiosyncratic culprits include co-amoxiclav, flucloxacillin, nitrofurantoin, NSAIDs, statins and herbal or bodybuilding supplements.

  • Pattern matters

    ALT and AST dominant means hepatocellular injury. ALP and GGT dominant means cholestatic or obstructive. R-ratio guides the differential.

  • Key prognostic marker

    INR (or prothrombin time) is the single most important bedside marker. A rising INR is a red flag for progression toward liver failure.

Why this guide matters

Find the cause. Watch the INR. Escalate early.

Most acute liver disease is treatable once the trigger is identified. A handful of features separate a self-limiting hepatitis from the small minority that becomes acute liver failure.

  • Cause first, everything else follows

    The whole management plan hinges on the diagnosis. A structured viral, autoimmune, metabolic and drug screen is non-negotiable.

  • INR is the honest number

    Bilirubin catches the eye, but INR tells you how the liver is really coping. A rising INR trumps everything else on the chart.

  • Know when to phone a transplant unit

    INR over 1.5 with any encephalopathy is acute liver failure until proven otherwise. That call needs to happen the same day.

Causes

The eight groups a UK clinician works through.

Acute liver injury has a broad differential. Working through these groups methodically is the fastest route to the right diagnosis.

  • 1. Viral hepatitis

    Hepatitis A, B, C, D and E. Hepatitis E is the leading UK cause of acute viral hepatitis in 2023 to 2024, mostly food-borne from undercooked pork. Also EBV, CMV and HSV in the immunosuppressed.

  • 2. Drug-induced (DILI)

    Paracetamol overdose is the top cause of acute liver failure. Idiosyncratic culprits include co-amoxiclav, flucloxacillin, nitrofurantoin, NSAIDs, statins, isoniazid, methotrexate and herbal or bodybuilding supplements.

  • 3. Alcohol-related hepatitis

    Recent heavy drinking, jaundice and a raised AST to ALT ratio (often over 2). Covered in detail on a separate page. Severity is scored with Maddrey and response with Lille.

  • 4. Autoimmune hepatitis

    Type 1 with ANA and ASMA, and raised IgG. Type 2 with anti-LKM antibodies, more common in younger women. Responds to prednisolone and azathioprine.

  • 5. Ischaemic hepatitis

    A very high ALT following sepsis, shock, cardiac arrest or heart failure. Treat the underlying hypoperfusion. LFTs usually improve quickly once perfusion is restored.

  • 6. Obstructive and biliary

    Common bile duct stones, ascending cholangitis, primary sclerosing cholangitis (PSC) and primary biliary cholangitis (PBC). Cholestatic pattern with a raised ALP and GGT.

  • 7. Metabolic and inherited

    Wilson disease (low caeruloplasmin, high 24-hour urinary copper), haemochromatosis (high ferritin and transferrin saturation) and alpha-1 antitrypsin deficiency.

  • 8. Pregnancy-related

    HELLP syndrome, acute fatty liver of pregnancy and severe hyperemesis gravidarum. Any acute LFT derangement in pregnancy needs same-day obstetric and hepatology review.

How the diagnosis is made

From abnormal LFTs to a working diagnosis.

The steps a UK GP or hepatologist will normally follow, in order, so you know what to expect and why each test is being done.

  1. 01

    Assessing

    History and pattern

    Onset, jaundice, itch, right upper quadrant pain, systemic illness, travel, food (pork, shellfish), sexual history, tattoos, IV drug use, alcohol, every prescription, over-the-counter medicine, herbal remedy and supplement.

  2. 02

    Assessing

    Repeat LFTs and classify

    ALT, AST, ALP, GGT, bilirubin (total and conjugated), albumin, INR, U and Es, full blood count and glucose. Calculate the R-ratio to classify hepatocellular, cholestatic or mixed injury.

  3. 03

    Assessing

    Assess severity

    Look for jaundice, coagulopathy (INR over 1.5), hypoglycaemia, acidosis, renal impairment and any sign of encephalopathy. These decide whether admission and transplant-unit discussion are needed.

  4. 04

    Confirming

    Viral serology screen

    Hepatitis A IgM, hepatitis B surface antigen and core IgM, hepatitis C antibody with PCR, hepatitis E IgM, plus EBV, CMV and HSV where the picture fits.

  5. 05

    Confirming

    Autoimmune and metabolic screen

    ANA, ASMA and anti-LKM antibodies with immunoglobulins, ferritin and transferrin saturation, caeruloplasmin and 24-hour urinary copper if under 40, and alpha-1 antitrypsin.

  6. 06

    Confirming

    Imaging

    Ultrasound abdomen with hepatic and portal vein Doppler as the first-line test to look for gallstones, biliary dilatation, hepatic congestion and vascular flow. MRCP if biliary obstruction is suspected.

  7. 07

    Escalating

    Specialist referral

    Hepatology review for unexplained acute hepatitis, suspected autoimmune or metabolic cause, or when INR is rising. Any INR over 1.5 with encephalopathy needs urgent transplant-unit discussion.

Typical timeline: first LFTs to a working diagnosis in days, not weeks.

Symptoms

What acute liver disease actually looks like.

Many people feel non-specifically unwell for days before jaundice appears. Some are picked up on a routine blood test with no symptoms at all.

  • Jaundice

    Yellowing of the sclera and skin. Usually appears once bilirubin passes about 40 to 50 micromol per litre.

  • Right upper quadrant discomfort

    A dull ache or tenderness over the liver, often with a feeling of fullness after meals.

  • Nausea and appetite loss

    Nausea, vomiting, food aversion (especially to fatty food) and unintentional weight loss over days to weeks.

  • Dark urine and pale stools

    Classic signs of cholestasis, driven by conjugated hyperbilirubinaemia and reduced bile flow into the gut.

  • Itch (pruritus)

    Generalised itch without a rash, often worse at night. Points strongly to a cholestatic pattern.

  • Flu-like prodrome

    Fever, malaise, myalgia and headache in the days before jaundice, common in acute viral hepatitis.

  • Bruising and bleeding

    Easy bruising, gum bleeding or a nose bleed can reflect coagulopathy from failing hepatic synthetic function.

  • Red flag - confusion or drowsiness

    Any change in behaviour, sleep reversal, confusion or drowsiness suggests hepatic encephalopathy and is a medical emergency.

Treatment

How acute liver disease is treated in the UK.

Treat the underlying cause, remove hepatotoxins and monitor closely. A small number will need specific antivirals, immunosuppression, endoscopic drainage or transplant assessment.

  • Treat the underlying cause

    The single most useful intervention. Stop the offending drug, treat the infection, relieve the obstruction, start immunosuppression for autoimmune disease, chelate copper in Wilson disease.

  • Stop hepatotoxic agents

    Withdraw alcohol, NSAIDs, herbal remedies, bodybuilding supplements and any non-essential medicine. Review every prescription against a DILI checklist.

  • N-acetylcysteine (NAC)

    Standard of care for paracetamol overdose and considered for non-paracetamol acute liver failure. Given intravenously under specialist guidance.

  • Supportive care

    Fluid balance, glucose, electrolytes, nutrition and thromboprophylaxis. Avoid sedatives that mask encephalopathy.

  • Antiviral therapy

    Nucleos(t)ide analogues (entecavir or tenofovir) for severe acute or reactivated hepatitis B. Ribavirin for severe or persistent hepatitis E in the immunosuppressed.

  • Corticosteroids

    Prednisolone for confirmed autoimmune hepatitis, and considered case by case in severe alcohol-related hepatitis using the Lille and Maddrey scores.

  • Biliary drainage

    ERCP with sphincterotomy and stone extraction for common bile duct stones, or stenting for a stricture, when obstruction is driving the injury.

  • Transplant assessment

    Urgent transfer to a UK liver transplant unit if the King's College criteria are met, or if INR is rising with any grade of encephalopathy.

What this guide is based on

The sources behind every claim on this page.

UK national guidance and specialist society standards, current at the time of last review.

Key references

Guidelines and standards we relied on.

A quiet reminder

This guide is for information, not medical advice.

Your GP or hepatologist knows your history and can tell you which parts apply to you. If in doubt, get seen the same day.

  • NICE. Suspected acute liver injury and abnormal liver function tests (NG165 and CKS).

  • British Society of Gastroenterology (BSG). Guidelines on the management of abnormal liver blood tests.

  • British Association for the Study of the Liver (BASL). Position statements on acute hepatitis and DILI.

  • UK Health Security Agency (UKHSA). Hepatitis E in England and Wales annual reports, 2023 to 2024.

  • MHRA. Drug safety updates on paracetamol, co-amoxiclav, flucloxacillin and nitrofurantoin.

Red flags

When acute liver disease needs urgent attention.

Most acute hepatitis settles. These are the situations where it might not, and where a specialist opinion is needed the same day.

  • Rising INR over 1.5

    The single most important laboratory red flag. It marks failing hepatic synthetic function and needs same-day hepatology input.

  • Any encephalopathy

    Confusion, drowsiness, sleep reversal or a flap. INR over 1.5 with encephalopathy meets the definition of acute liver failure and needs urgent transplant-unit referral.

  • Bilirubin over 100 micromol per litre

    Deep jaundice signals severe injury or persistent obstruction and warrants urgent specialist review.

  • Hypoglycaemia

    The liver runs out of glycogen quickly in severe injury. Unexplained low glucose in someone with hepatitis is a warning sign.

  • Suspected paracetamol overdose

    Any staggered or intentional overdose needs a paracetamol level, N-acetylcysteine and toxicology advice, even when the patient looks well.

  • Ascending cholangitis

    Fever, jaundice and right upper quadrant pain (Charcot's triad) with sepsis. Emergency antibiotics and urgent biliary drainage.

  • Pregnancy with abnormal LFTs

    Consider HELLP, acute fatty liver of pregnancy or severe cholestasis. Same-day obstetric and hepatology review.

  • Wilson disease under 40

    Haemolysis, low alkaline phosphatase and a high bilirubin to ALP ratio suggests Wilson disease and needs urgent transplant-centre input.

  • Ischaemic hepatitis

    A very high ALT (often over 1000) in the context of shock, sepsis or cardiac arrest. Treat the cause of hypoperfusion.

Living with it

A treatable condition, with a clear ladder.

Four things that make the biggest difference through recovery. Time, alcohol abstinence, a safer medicine list and follow-up until LFTs are back to baseline.

A quiet reminder

The liver is patient. Give it the conditions to heal.

Recovery is usually complete when the cause is removed. Persistent abnormality beyond six months moves the diagnosis toward chronic liver disease and warrants further review.

  1. 01 Recovery

    Give the liver time

    Most acute hepatitis resolves in weeks to a few months. Rest, hydration and avoiding hepatotoxins are the fundamentals.

  2. 02 Alcohol

    Stop alcohol completely

    Abstain during the illness and for at least six months after LFTs normalise. Longer if the cause was alcohol-related.

  3. 03 Medicines

    Rebuild a safer medicine list

    Never restart the drug that triggered DILI. Review analgesia and any herbal or bodybuilding products with your GP or pharmacist.

  4. 04 Follow-up

    Monitor until fully recovered

    Repeat LFTs at intervals until normal. Persistent abnormality beyond six months moves the diagnosis toward chronic liver disease.

Frequently asked

Everything we get asked about acute liver disease.

Quick answers on causes, tests, red flags and how it differs from acute liver failure.

  • What is acute liver disease and how is it different from acute liver failure?

    Acute liver disease is any sudden inflammatory injury to the liver lasting under six months, usually detected as raised transaminases with or without jaundice. Acute liver failure is the smaller, more serious syndrome where the injured liver decompensates, defined by coagulopathy (INR over 1.5) with hepatic encephalopathy in someone without pre-existing cirrhosis. Acute liver disease is common and often self-limiting. Acute liver failure is rare and needs urgent transplant-unit care, and is covered on a separate page.

  • What is the commonest cause of acute viral hepatitis in the UK?

    Hepatitis E is now the commonest cause of acute viral hepatitis in the UK, based on UKHSA data for 2023 to 2024. It is mostly food-borne from undercooked pork products such as sausages and offal. Most cases in immunocompetent adults are self-limiting, but severe or persistent disease can occur in pregnancy and in immunosuppressed patients, where ribavirin may be considered.

  • Which medicines most often cause drug-induced liver injury (DILI) in the UK?

    Paracetamol overdose remains the top cause of acute liver failure in the UK. Common idiosyncratic culprits include co-amoxiclav, flucloxacillin, nitrofurantoin, isoniazid, methotrexate, NSAIDs, statins and a growing list of herbal and bodybuilding supplements. Any new medicine, over-the-counter product or supplement started in the eight weeks before symptoms is a suspect.

  • What blood tests do I need if my LFTs are abnormal?

    The first-line panel includes ALT, AST, ALP, GGT, bilirubin, albumin and INR to classify the pattern. A non-invasive liver screen then adds hepatitis A IgM, hepatitis B surface antigen and core IgM, hepatitis C antibody with PCR, hepatitis E IgM, autoantibodies (ANA, ASMA, anti-LKM) with immunoglobulins, ferritin and transferrin saturation, caeruloplasmin, alpha-1 antitrypsin and a pregnancy test if relevant. Imaging is usually an abdominal ultrasound with hepatic Doppler.

  • When is acute liver injury an emergency?

    Any of the following needs same-day specialist review: INR over 1.5, encephalopathy of any grade, hypoglycaemia, bilirubin over 100 micromol per litre, ascending cholangitis or a suspected paracetamol overdose. INR over 1.5 combined with encephalopathy meets the definition of acute liver failure and needs urgent transfer to a UK liver transplant unit.

  • Do I need a liver biopsy?

    Not usually. Most acute liver disease is diagnosed from history, blood tests and imaging. Biopsy is reserved for cases where the cause remains unclear after a full non-invasive screen, where autoimmune hepatitis needs confirmation and staging, or where the pattern is not settling as expected.

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