Gastroenterology: Liver disease

• Basics: Interpreting Liver Blood Tests | Approach to Jaundice | Gilbert's Syndrome and Inherited Jaundice
• Viral hepatitis: Hepatitis A and E | Hepatitis B and D | Hepatitis C
• Fatty liver: Alcohol-related Liver Disease | MASLD (Fatty Liver Disease)
• Autoimmune: Autoimmune Hepatitis | Primary Biliary Cholangitis | Primary Sclerosing Cholangitis
• Genetic and drug-related: Haemochromatosis | Wilson's Disease | Alpha-1 Antitrypsin Deficiency | Drug-induced Liver Injury | Liver Disease in Pregnancy
• Revision: Drug Reference Table | Spot the Diagnosis | Exam-style Scenarios | Key Points | Guidelines and Further Reading

🫀 Liver disease is one of the few major causes of death that is rising in the UK. It is usually silent until late, so it is often found through "abnormal LFTs". The three biggest causes - alcohol, fatty liver and viral hepatitis - are all preventable or treatable. Cirrhosis and liver tumours have their own chapter.
Your four questions for every patient: Is the pattern hepatocellular, cholestatic or isolated bilirubin? What is the cause (alcohol, metabolic, viral, autoimmune, genetic, drugs)? How much fibrosis is there - is this cirrhosis? Is the liver failing (jaundice, low albumin, high INR, encephalopathy, ascites)?

Interpreting Liver Blood Tests

What each test means:

• ALT and AST - enzymes released by damaged liver cells (hepatocellular injury). AST also comes from muscle and heart.
• ALP - from bile ducts (cholestasis), but also bone (growth, Paget's, fractures, metastases) and the placenta (pregnancy). A raised GGT alongside confirms it is from the liver.
• GGT - raised by alcohol, fatty liver, cholestasis and enzyme-inducing drugs. On its own it is non-specific.
• Bilirubin - raised in haemolysis, Gilbert's, liver disease and bile duct blockage.
• Albumin and INR - show liver function (synthesis). Low albumin and high INR suggest advanced disease - though albumin also falls in illness, and the INR also rises with vitamin K deficiency.
• Platelets - a low count is often the first sign of cirrhosis (portal hypertension causes splenic pooling).

Patterns:

Abnormal LFTs - what to do (BSG 2018 guideline):

• Take an alcohol history (units and AUDIT-C), drug and supplement history, BMI and metabolic risk.
• Liver aetiology screen:
  • Liver ultrasound.
  • Hepatitis B surface antigen and hepatitis C antibody.
  • Autoantibodies - antimitochondrial (AMA), anti-smooth muscle, antinuclear - and immunoglobulins.
  • Ferritin and transferrin saturation.
  • Coeliac serology.
  • In selected people: caeruloplasmin (under 40), alpha-1 antitrypsin.
• Assess fibrosis in fatty liver or alcohol (FIB-4, ELF, FibroScan).
• Don't just repeat the tests and ignore mildly abnormal results - mild ALT rises can hide significant fibrosis.

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Approach to Jaundice

What it is: Yellowing of the skin and eyes when bilirubin is above about 40–50 µmol/L.

• Pre-hepatic (unconjugated):
  • Haemolysis - anaemia, high reticulocytes, high LDH, low haptoglobin.
  • Gilbert's syndrome.
  • Normal-coloured urine ("acholuric jaundice").
• Hepatic:
  • Hepatitis (viral, alcohol, drugs, autoimmune).
  • Cirrhosis.
  • Infiltration.
  • Sepsis.
  • Heart failure.
• Post-hepatic (obstructive):
  • Gallstones in the common bile duct.
  • Pancreatic cancer, cholangiocarcinoma.
  • PSC.
  • Strictures.
  • Dark urine, pale stools, itch.

Key steps:

• Urgent ultrasound - are the bile ducts dilated?
• Dilated ducts: Bile duct obstruction - MRCP or CT, then ERCP if needed.
• Normal ducts: Liver disease or haemolysis - liver screen.
• Painless jaundice with weight loss in an older person is pancreatic or biliary cancer until proven otherwise. NICE NG12: urgent CT or suspected cancer referral for jaundice at 40 or over.
• Fever, pain and jaundice (Charcot's triad) - cholangitis, an emergency (see the Gastroenterology Emergencies chapter).
• Check the INR - vitamin K if it is prolonged by obstruction.

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Gilbert's Syndrome and Inherited Jaundice

• Gilbert's syndrome:
  • A common (about 5%), harmless inherited reduction in the liver enzyme that conjugates bilirubin (UGT1A1).
  • Mild unconjugated hyperbilirubinaemia (usually under 70 µmol/L), with normal ALT, ALP and FBC.
  • Worse with fasting, illness, stress or exertion.
  • Diagnose by the pattern - repeat tests, exclude haemolysis. No treatment needed.
  • Some drugs (e.g. irinotecan) are more toxic.
• Crigler–Najjar syndrome: Severe lack of the same enzyme - high unconjugated bilirubin in infants. Type 1 risks kernicterus (phototherapy, transplant). Type 2 responds to phenobarbital.
• Dubin–Johnson and Rotor syndromes: Benign conjugated hyperbilirubinaemia. Dubin–Johnson gives a black liver on biopsy.
• Neonatal jaundice lasting over 2 weeks with pale stools - exclude biliary atresia urgently (surgery before 60 days gives the best results).

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Hepatitis A and E

Both are spread by the faecal–oral route, cause acute hepatitis, and are usually self-limiting.

• Hepatitis A:
  • Contaminated food or water, travel, outbreaks in nurseries, men who have sex with men, people who inject drugs.
  • Flu-like illness, then jaundice; dark urine; tender liver.
  • More severe in adults and older people than in children.
  • Diagnosis: HAV IgM.
  • No chronic infection. Rarely, acute liver failure.
  • Supportive care; notifiable.
  • Vaccine for travellers, close contacts, and people with chronic liver disease.
• Hepatitis E:
  • Now the commonest cause of acute viral hepatitis in the UK - genotype 3, from undercooked pork, sausages and game.
  • Often mild or without symptoms, especially in older men.
  • Diagnosis: HEV IgM and HEV RNA.
  • Chronic infection can occur in immunosuppressed people (transplant recipients, chemotherapy) - reduce immunosuppression; ribavirin.
  • Neurological features: Guillain–Barré syndrome, neuralgic amyotrophy.
  • Pregnancy (genotype 1, from travel to Asia or Africa) - high risk of liver failure and death.
  • Cook pork thoroughly; blood donations are screened.

💡 Clinical Pearl: Test for hepatitis E in anyone with unexplained hepatitis, including suspected drug-induced liver injury - it is often missed.

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Hepatitis B and D

How it spreads:

• Mother to baby (the commonest route worldwide).
• Sex.
• Blood (injecting drugs, needlestick, unscreened transfusions).
• Commonest in people born in Asia, Africa and Eastern Europe.

Who becomes chronically infected:

• About 90% of infected babies.
• About 5% of infected adults.

Reading the serology:

Chronic hepatitis B - management (NICE CG165):

• Refer to a hepatology service; test the household and sexual contacts, and vaccinate them.
• Assess: HBV DNA, ALT, HBeAg, and fibrosis (FibroScan).
• Treat if:
  • Significant fibrosis or cirrhosis.
  • Raised ALT with high HBV DNA.
  • Family history of HCC.
• Drugs:
  • Tenofovir (disoproxil 245 mg or alafenamide 25 mg daily) or entecavir (0.5 mg daily) - usually lifelong; cure is rare.
  • Peginterferon (48 weeks) for selected patients.
• HCC surveillance (6-monthly ultrasound) in cirrhosis and other high-risk groups (e.g. older Asian men, African-born people, family history) - HCC can occur without cirrhosis in hepatitis B.
• Reactivation: Before chemotherapy, rituximab or other strong immunosuppression, test HBsAg and anti-HBc. Give antiviral prophylaxis (entecavir or tenofovir) if positive - reactivation can cause fatal hepatitis.
• Pregnancy:
  • Screened antenatally.
  • Tenofovir in the third trimester for high viral load.
  • Baby: Hepatitis B vaccine at birth (plus immunoglobulin if the mother is high-risk), then vaccine doses in the routine schedule, and testing at 12 months.
• Prevention: Hepatitis B vaccine is part of the UK childhood schedule (6-in-1), and is given to healthcare workers and other at-risk groups. Check anti-HBs response.

Hepatitis D (delta):

• A defective virus that only infects people who already have hepatitis B.
• Causes the most severe and rapidly progressive viral hepatitis.
• Test all HBsAg-positive people for anti-HDV.
• Treatment: bulevirtide (NICE TA896), peginterferon.

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Hepatitis C

How it spreads:

• Blood - mainly injecting drug use (shared needles and equipment).
• Older blood transfusions (before 1991 in the UK).
• Medical treatment abroad.
• Tattoos.
• Less often sexual (especially men who have sex with men with HIV) or mother to baby.

Natural history:

• Most acute infections are silent; about 75% become chronic.
• Over decades, chronic infection can cause cirrhosis and HCC - faster with alcohol, obesity, HIV and older age.
• Outside the liver:
  • Cryoglobulinaemia (vasculitis, glomerulonephritis).
  • Porphyria cutanea tarda.
  • Lichen planus.
  • Diabetes.
  • Lymphoma.

Testing:

• HCV antibody (exposure), then HCV RNA (current infection). About 1 in 4 clear the virus naturally - antibody-positive but RNA-negative.
• Test anyone who has ever injected drugs, received blood before 1991, or has abnormal LFTs. Also people from high-prevalence countries and people in prison.

Treatment:

• Direct-acting antivirals (DAAs) - tablets for 8–12 weeks, with cure rates over 95%.
• Pan-genotypic regimens:
  • Sofosbuvir/velpatasvir (12 weeks).
  • Glecaprevir/pibrentasvir (8 weeks).
• Cure = SVR12 - undetectable HCV RNA 12 weeks after finishing treatment.
• Check drug interactions (e.g. amiodarone with sofosbuvir - severe bradycardia; some statins, antiepileptics and the pill). Check hepatitis B status - HBV can reactivate during treatment.
• Cure does not give immunity - reinfection is possible, so continue harm reduction.
• Cirrhosis: Continue HCC surveillance even after cure.
• NHS England has an elimination programme - treatment is offered through operational delivery networks, including in drug services and prisons.

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Alcohol-related Liver Disease

Spectrum:

• Fatty liver (most heavy drinkers; reversible with abstinence).
• Alcohol-related hepatitis (see the Gastroenterology Emergencies chapter).
• Fibrosis.
• Cirrhosis (10–20% of long-term heavy drinkers).
• HCC.

Risk:

• Rises with the amount and duration of drinking, female sex, obesity, viral hepatitis, smoking and genetics (PNPLA3).
• UK low-risk guidance: no more than 14 units a week, spread over 3 days or more.

Assessment:

• Alcohol history in units; AUDIT-C (screening) and AUDIT.
• Bloods:
  • GGT.
  • MCV (macrocytosis).
  • AST:ALT ratio over 2.
  • Low platelets.
• FibroScan (NICE: offer to people drinking harmfully - over 50 units a week for men or over 35 for women, for several months - to look for cirrhosis).
• Screen for other causes and for dependence (withdrawal symptoms, morning drinking).

Management:

• Abstinence - the most important treatment at every stage. It improves survival even in cirrhosis.
• Brief interventions, referral to alcohol services; psychological support; mutual aid groups.
• Planned detoxification if dependent (chlordiazepoxide reducing regimen; see the Gastroenterology Emergencies chapter for withdrawal and Wernicke's).
• Thiamine for everyone at risk (oral 100 mg three times daily for long-term use).
• Relapse prevention drugs (with psychosocial support):
  • Acamprosate (reduces craving).
  • Naltrexone (avoid in liver failure and with opioids).
  • Disulfiram (avoid in liver disease).
  • Baclofen is used off-label in liver disease.
• Nutrition - malnutrition and muscle loss are common; dietitian review.
• Manage cirrhosis complications (see the Cirrhosis chapter). Transplant is possible for selected abstinent patients.

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MASLD (Fatty Liver Disease)

What it is: Metabolic dysfunction-associated steatotic liver disease - the new name for non-alcoholic fatty liver disease (NAFLD). Fat builds up in the liver in people with metabolic risk factors. It affects about 1 in 4 to 1 in 3 UK adults and is now the commonest liver disease.

Definition: Fatty liver plus at least one cardiometabolic risk factor:

• BMI 25 or more (23 in Asian people), or a large waist.
• Type 2 diabetes, prediabetes or raised glucose.
• BP 130/85 or more, or on treatment.
• Raised triglycerides.
• Low HDL cholesterol.

Related terms:

• MASH (metabolic dysfunction-associated steatohepatitis) - fat with inflammation and liver cell damage; it can progress to fibrosis and cirrhosis.
• MetALD - MASLD plus moderate alcohol intake.

Who is at risk of progression:

• Type 2 diabetes.
• Obesity.
• Older age.
• Metabolic syndrome.

Most people with MASLD die of cardiovascular disease, not liver disease.

Assessing fibrosis - the key step (NICE NG49 and BSG pathways):

• FIB-4 score (age, AST, ALT, platelets):
  • Under 1.3 (under 2.0 if 65 or over) - low risk; repeat in about 3 years.
  • Over 2.67 - high risk; refer to hepatology.
  • In between - a second test: ELF blood test (10.51 or more suggests advanced fibrosis - refer) or FibroScan (liver stiffness).
• Ultrasound shows fat but cannot show fibrosis.

Management:

• Weight loss - the best treatment:
  • 5% reduces liver fat.
  • 7–10% improves inflammation.
  • 10% or more can reverse fibrosis.
• Mediterranean-style diet; exercise (helps even without weight loss).
• Treat cardiovascular risk: Statins (safe, and should not be withheld for raised ALT), BP and diabetes control. Stop smoking. Keep alcohol low (ideally none if there is advanced fibrosis).
• Diabetes drugs with liver benefit: GLP-1 receptor agonists (semaglutide), SGLT2 inhibitors, pioglitazone (specialist).
• Specific MASH drugs:
  • Resmetirom (approved by the MHRA in June 2026) and semaglutide (conditional MHRA approval for MASH, July 2026) are licensed for MASH with moderate to advanced fibrosis.
  • Both are awaiting NICE appraisal, so they are not yet routinely available on the NHS.
• Bariatric surgery for severe obesity improves MASH.
• Cirrhosis - HCC and variceal surveillance as for any cirrhosis.

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Autoimmune Hepatitis

What it is: The immune system attacks liver cells.

Who gets it:

• Mostly women of any age.
• People with other autoimmune diseases (thyroid, type 1 diabetes, coeliac).

Presentation:

• Abnormal LFTs found by chance.
• Fatigue; arthralgia.
• Acute hepatitis with jaundice - sometimes acute liver failure.
• Cirrhosis at diagnosis in about a third.
• Drug-induced AIH - nitrofurantoin, minocycline, statins, anti-TNF.

Diagnosis:

• Raised ALT and raised IgG.
• Autoantibodies:
  • Type 1 (adults) - antinuclear (ANA) and anti-smooth muscle (ASMA) antibodies.
  • Type 2 (children) - anti-LKM1.
• Liver biopsy - interface hepatitis with plasma cells.
• Exclude viral hepatitis, drugs and Wilson's disease.

Treatment:

• Prednisolone (e.g. 30–40 mg daily, then reducing), with azathioprine (1–2 mg/kg) added after about 2 weeks once bilirubin falls (check TPMT first).
• Budesonide instead of prednisolone in people without cirrhosis (fewer side effects).
• Maintenance: Azathioprine long-term, often for life - relapse is common after stopping.
• Second line: Mycophenolate, tacrolimus.
• Goal: Normal ALT and IgG (biochemical remission).
• Bone protection; HCC surveillance if cirrhotic. Transplant for liver failure.

Overlap syndromes: Features of both AIH and PBC or PSC.

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Primary Biliary Cholangitis

What it is: Autoimmune destruction of the small bile ducts inside the liver. It can lead to cirrhosis.

Who gets it:

• Middle-aged women (about 9 in 10 patients).
• People with other autoimmune conditions - Sjögren's, thyroid disease, systemic sclerosis, coeliac disease.

Symptoms:

• Often none (found on LFTs).
• Fatigue.
• Itching (often before jaundice).
• Dry eyes and mouth.
• Xanthelasma.
• Later: jaundice and liver failure.

Diagnosis - two of these:

• Raised ALP (cholestatic pattern).
• Antimitochondrial antibodies (AMA, M2 subtype) - or PBC-specific ANA (sp100, gp210).
• Typical biopsy (rarely needed).
• Raised IgM.
• Ultrasound to exclude bile duct obstruction.

Treatment:

• Ursodeoxycholic acid (UDCA) 13–15 mg/kg/day for life - slows progression.
• Check the response at 12 months (ALP and bilirubin). Poor responders have worse outcomes.
• Second line (inadequate response or intolerance of UDCA):
  • Elafibranor (NICE TA1016) or seladelpar (NICE TA1171) - PPAR agonists.
  • Obeticholic acid (TA443) - its licence was withdrawn in the EU in 2024; check its current UK status. Avoid in decompensated cirrhosis; it can worsen itching.
  • Bezafibrate (off-label).
• Itch:
  • Colestyramine first.
  • Then rifampicin (monitor LFTs), naltrexone, or sertraline.
  • Specialist options for severe itch.
• Bone: DEXA; vitamin D and calcium. Check fat-soluble vitamins in advanced disease.
• Transplant for liver failure or intractable itch.

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Primary Sclerosing Cholangitis

What it is: Inflammation and scarring of the large and small bile ducts, inside and outside the liver, causing strictures. It progresses to cirrhosis over years.

Who gets it:

• Young and middle-aged men.
• About 70% have IBD, usually ulcerative colitis.

Symptoms:

• Often none at first (raised ALP).
• Itching, fatigue.
• Episodes of cholangitis (fever, pain, jaundice).

Diagnosis:

• MRCP - multiple strictures and dilatations: "beading".
• p-ANCA is often positive (not specific).
• Exclude IgG4-related sclerosing cholangitis (responds to steroids) and secondary causes.
• Small-duct PSC needs a biopsy.

Management:

• No proven drug treatment. UDCA is used by some, but high doses are harmful.
• Treat itch (as for PBC) and cholangitis (antibiotics).
• Dominant strictures: ERCP with brushings (to exclude cancer) and balloon dilatation.
• Cancer surveillance:
  • Cholangiocarcinoma - lifetime risk 10–20%. Have a high index of suspicion if the patient worsens.
  • Colorectal cancer (with colitis) - yearly colonoscopy from diagnosis.
  • Gallbladder cancer - yearly ultrasound; cholecystectomy for polyps of 8 mm or more.
  • HCC if cirrhotic.
• Liver transplant for advanced disease or recurrent cholangitis. PSC can recur in the new liver.
• All patients with PSC should have a colonoscopy to look for IBD, even without symptoms.

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Haemochromatosis

What it is: An inherited disorder in which the gut absorbs too much iron, which builds up in the liver, pancreas, heart, joints, pituitary and skin.

Genetics:

• Autosomal recessive - usually HFE C282Y homozygous.
• About 1 in 150 people of Northern European (especially Irish and Celtic) descent.
• Many homozygotes never develop disease.
• Women present later (menstruation protects).

Features (usually after 40):

• Fatigue.
• Arthropathy - especially the 2nd and 3rd MCP joints ("iron fist"); chondrocalcinosis.
• Raised LFTs.
• Diabetes.
• Skin bronzing ("bronze diabetes").
• Cardiomyopathy and arrhythmias.
• Hypogonadism (erectile dysfunction, low libido).
• Cirrhosis and HCC.

Diagnosis:

• Raised transferrin saturation (over 50% in men, over 45% in women) - the best screening test.
• Raised ferritin (but ferritin also rises in inflammation, alcohol, fatty liver and cancer).
• HFE gene testing.
• Ferritin over 1,000 µg/L or raised ALT - assess for cirrhosis (FibroScan or biopsy).
• MRI shows liver iron when HFE tests are negative.

Treatment:

• Venesection (about 450–500 mL) weekly or fortnightly until ferritin is about 50 µg/L.
• Then maintenance venesection, usually 2–4 times a year, keeping ferritin under about 100 µg/L.
• Avoid iron and vitamin C supplements and raw shellfish (Vibrio vulnificus). Reduce alcohol.
• Screen first-degree relatives (transferrin saturation, ferritin, HFE).
• Chelation (desferrioxamine) if venesection is not possible.
• Cirrhosis: HCC surveillance continues even after iron is removed.
• Early treatment (before cirrhosis or diabetes) gives a normal life expectancy.

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Wilson's Disease

What it is: A rare autosomal recessive disorder (ATP7B gene) in which copper can't be excreted into bile. Copper builds up in the liver, brain, eyes and kidneys.

Who: Usually presents at 5–40 years. Consider it in any young person with unexplained liver disease or a movement disorder.

Features:

• Liver:
  • Hepatitis; cirrhosis.
  • Acute liver failure with Coombs-negative haemolysis - the ALP is often very low relative to bilirubin.
• Neurological:
  • Tremor ("wing-beating"); dystonia; dysarthria; drooling.
  • Parkinsonism; ataxia.
• Psychiatric: Personality change, depression, psychosis.
• Eyes: Kayser–Fleischer rings (brown copper ring around the cornea - slit lamp; present in nearly all with neurological disease); sunflower cataracts.
• Other: Renal tubular acidosis (Fanconi), arthropathy.

Diagnosis:

• Low caeruloplasmin.
• High 24-hour urinary copper.
• Kayser–Fleischer rings.
• High liver copper on biopsy.
• ATP7B genetic testing.
• MRI brain (basal ganglia changes).

Treatment (lifelong):

• Chelation - penicillamine or trientine. Neurological symptoms can worsen at first.
• Zinc - blocks copper absorption; used for maintenance and in people without symptoms.
• Low-copper diet (avoid shellfish, liver, chocolate, nuts).
• Liver transplant for acute liver failure (curative).
• Screen siblings.

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Alpha-1 Antitrypsin Deficiency

• What it is: An inherited (co-dominant) deficiency of alpha-1 antitrypsin, a protein that protects the lungs from enzyme damage. The abnormal protein (most often the Z variant) gets stuck in liver cells.
• Lungs: Early emphysema (lower zones, panacinar), especially in smokers, often under 45.
• Liver:
  • Neonatal hepatitis (prolonged jaundice).
  • Cirrhosis and HCC in adults.
• Diagnosis:
  • Low serum alpha-1 antitrypsin level.
  • Phenotype (PiZZ is severe; PiMZ is a carrier with mild risk).
  • Liver biopsy - PAS-positive, diastase-resistant globules.
• Management:
  • Stop smoking (critical).
  • Avoid alcohol.
  • Vaccinate.
  • Screen relatives.
  • Monitor liver and lung function.
  • Transplant for end-stage disease.
  • Augmentation therapy is not routinely funded in the UK.
• See also the Airways Disease chapter.

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Drug-induced Liver Injury

Why it matters: A common cause of abnormal LFTs and an important cause of acute liver failure. Always ask about prescribed drugs, over-the-counter drugs, herbal remedies and supplements, gym products and recreational drugs.

Management:

• Stop the drug - most recover, although cholestatic injury can take months.
• Exclude other causes, including hepatitis E.
• Hy's law: ALT over 3 times the upper limit plus bilirubin over 2 times the upper limit, from a drug, carries about a 10% risk of death or transplant - refer urgently.
• TB drugs: Check LFTs at baseline. Stop if ALT is more than 5 times the upper limit, or more than 3 times with symptoms or jaundice, then reintroduce one at a time under specialist care.
• Checkpoint inhibitor hepatitis: Grade it; steroids; hold the drug.
• Report suspected reactions to the MHRA Yellow Card scheme.

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Liver Disease in Pregnancy

In normal pregnancy, ALP rises (from the placenta) and albumin falls. ALT, bilirubin and bile acids should stay normal.

• Hyperemesis gravidarum (first trimester): Mild ALT rise; settles once vomiting stops.
• Intrahepatic cholestasis of pregnancy (second and third trimester):
  • Itching, especially of the palms and soles, without a rash.
  • Raised bile acids (19 µmol/L or more).
  • Risk of stillbirth is raised when bile acids reach 100 µmol/L or more.
  • Timing of birth (RCOG 2022) depends on peak bile acids - e.g. 35–36 weeks if 100 or more, 38–39 weeks if 40–99.
  • UDCA is no longer routinely recommended to improve outcomes (PITCHES trial), but it can be used for itch.
  • Resolves after delivery; recurs in future pregnancies and with the combined pill.
• Pre-eclampsia and HELLP syndrome (Haemolysis, Elevated Liver enzymes, Low Platelets):
  • Third trimester or postpartum; right upper quadrant pain, hypertension.
  • Hepatic haematoma or rupture is a rare but deadly complication.
  • Treatment: delivery, BP control, magnesium sulfate.
• Acute fatty liver of pregnancy (third trimester):
  • Rare but life-threatening.
  • Nausea, vomiting, abdominal pain, jaundice.
  • Hypoglycaemia, AKI, coagulopathy, encephalopathy (Swansea criteria).
  • Linked to a fetal fatty acid oxidation defect (LCHAD deficiency).
  • Urgent delivery and intensive care.
• Other causes:
  • Viral hepatitis (hepatitis E is dangerous in pregnancy).
  • Gallstones.
  • Budd–Chiari syndrome.
  • Pre-existing liver disease (AIH - continue azathioprine; Wilson's - continue treatment at reduced doses).

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Drug Reference Table