Synopsis
Diagnose autoimmune hepatitis rigorously, identify acute liver failure and use monitored induction and maintenance immunosuppression to prevent progressive fibrosis.
- Autoimmune hepatitis is an immune-mediated necroinflammatory liver disease that can present at any age, from incidental aminotransferase elevation to acute liver failure.
- The diagnosis combines biochemistry, immunoglobulin G, autoantibodies, compatible histology and deliberate exclusion of viral, metabolic, obstructive and drug-related liver injury.
- Antinuclear and smooth-muscle antibodies support type 1 disease; anti-LKM1, anti-LC1 or anti-SLA can help in selected seronegative or atypical presentations.
Key red flags
Fatigue, anorexia, nausea, right-upper-quadrant discomfort, dark urine, jaundice and arthralgia accompany a predominantly hepatocellular biochemical injury.
Investigation priorities
Define injury pattern, severity and trajectory.
Management branches
A hepatitic blood pattern, raised IgG or unexplained inflammatory hepatitis raises autoimmune hepatitis.
- Assess jaundice, encephalopathy, INR, glucose and haemodynamics first and admit urgently when synthetic function is impaired.
- Obtain IgG and a structured autoantibody panel while excluding viral hepatitis, Wilson disease where relevant, biliary obstruction, alcohol and medicine or supplement injury.
Key medicines
PrednisoloneFor usual adult induction, the 2025 BSG guideline recommends approximately 0.5 mg/kg by mouth once each morning and not usually more than 40 mg daily, followed by response-led tapering under hepatology supervision.
AzathioprineA hepatologist selects the weight-based dose within current BSG and BNF guidance after TPMT assessment, commonly introducing it during induction and titrating to response, tolerability and blood monitoring rather than using a fixed universal regimen.