Autoimmune hepatitis isn’t something you catch from someone else. It’s not caused by alcohol, viruses, or poor diet. It happens when your immune system turns on your own liver, attacking healthy tissue like it’s an invader. This leads to chronic inflammation that, over time, can scar the liver, cause cirrhosis, or even liver failure. The good news? It’s treatable. The catch? Treatment requires patience, monitoring, and often, long-term medication.
How Is Autoimmune Hepatitis Diagnosed?
There’s no single test that confirms autoimmune hepatitis. Instead, doctors piece together clues from blood work, imaging, and a liver biopsy. If you’re feeling unusually tired, have dark urine, yellowing skin, or unexplained joint pain, and your liver enzymes are sky-high, it’s time to dig deeper. Blood tests look for two main things: elevated liver enzymes (ALT and AST) and high levels of immunoglobulin G (IgG). In active disease, ALT and AST can be five to ten times higher than normal. IgG levels often exceed 1.5 times the upper limit of normal. Autoantibodies like ANA (antinuclear antibodies) or SMA (smooth muscle antibodies) are also checked. These are found in about 80% of cases-what’s called Type 1 AIH. Less common is Type 2, marked by LKM1 antibodies, which tends to affect younger people. But here’s the key update from the 2025 European Association for the Study of the Liver (EASL) guidelines: autoantibody types no longer change how you’re treated. Whether you’re ANA-positive or LKM1-positive, the first-line drugs stay the same. That’s a big shift from older practices. The real gold standard? A liver biopsy. It’s the only way to see the telltale sign: interface hepatitis. That’s when immune cells pile up at the edge of liver lobules, chewing through tissue. A good biopsy needs at least 20 portal tracts to be reliable. The procedure uses a thin needle guided by ultrasound and carries a very low risk-about 1 in 1,000-for serious bleeding. Doctors also use the Revised International Autoimmune Hepatitis Group (IAIHG) scoring system. You earn points for clinical symptoms, lab results, histology, and by ruling out other causes like hepatitis B or C. A score above 15 means probable AIH. Above 20? Definite AIH. This system helps avoid misdiagnosing other liver conditions that mimic it.Why Steroids Are the First Line of Defense
Prednisone (or its active form, prednisolone) has been the backbone of AIH treatment since the 1970s. It works fast. Most patients see their liver enzymes drop within two weeks. That quick response is actually a clue-it helps confirm the diagnosis. The typical starting dose is 0.5 to 1 mg per kilogram of body weight per day, capped at 60 mg daily. For someone weighing 70 kg, that’s about 35 to 60 mg a day. The goal isn’t to stay on this dose forever. It’s to get inflammation under control, then taper down. By week 6 to 8, the dose is usually lowered to 10-15 mg per day. Tapering too fast can cause a rebound flare. Too slow, and you risk side effects. That’s why close monitoring every 2-4 weeks in the early phase is critical. Blood tests check ALT, AST, and IgG levels to track progress. But steroids come with a price. About 70% of people on prednisone alone develop side effects. Weight gain, especially around the face (moon face), fluid retention, insomnia, mood swings, and increased appetite are common. Long-term use raises the risk of osteoporosis (20% of patients), diabetes (15%), and cataracts (10%) within five years. That’s why steroids are almost never used alone.Azathioprine: The Steroid-Sparing Partner
Azathioprine (brand name Imuran, or generic azathioprine) is the drug that makes steroid therapy bearable. It doesn’t work as fast as prednisone, but it suppresses the immune system in a different way-long-term and with fewer immediate side effects. It’s started early, usually at 50 mg per day, then increased to 1-2 mg per kg per day (up to 150 mg). The goal? Cut steroid doses by 70-80% within six months. That means you’re on 5-10 mg of prednisone instead of 30-40 mg. That’s a massive reduction in side effects. Studies show combination therapy cuts steroid-related complications from 70% to just 30%. That’s not just a minor improvement-it’s life-changing. But azathioprine isn’t risk-free. It can cause nausea, vomiting, and pancreatitis in about 5-10% of people. The most serious risk? Bone marrow suppression, which can crash your white blood cell count. That’s why testing for TPMT enzyme levels is now standard before starting. TPMT (thiopurine S-methyltransferase) is a liver enzyme that breaks down azathioprine. About 0.3% of people have a genetic variant that makes them TPMT-deficient. Without testing, these patients can develop life-threatening low blood counts within weeks. Testing costs $250-$400 in the U.S., and while 89% of U.S. academic centers do it now, only 45% of community clinics still skip it. Don’t let that be you.
What Does Success Look Like?
Complete biochemical response means your ALT and AST return to normal, and your IgG drops to within the normal range. That happens in 60-80% of patients within 18-24 months. Histological remission-meaning the liver tissue looks normal on biopsy-is achieved in 50-70% after two to three years of treatment. And here’s the hopeful part: the damage can reverse. Many patients with early-stage fibrosis (F2 or F3) see their scarring improve to F0 or F1 after long-term treatment. One patient on a patient forum described her biopsy going from F3 to F0 after two years on low-dose steroids and azathioprine. That’s not rare-it’s documented. But remission doesn’t mean cure. About 60-80% of patients need to stay on some form of treatment indefinitely. If you stop, relapse rates hit 50-90%. That’s why doctors don’t rush to stop therapy. If you’ve been in remission for two to three years, your doctor might suggest trying to taper off slowly-over six to twelve months. But only 45% of people stay off meds without a flare. If your enzymes rise again, treatment restarts immediately.What If the First Treatment Doesn’t Work?
About 10-15% of patients don’t respond well after 12-18 months. That’s called treatment failure. The next step is switching to a second-line drug. Mycophenolate mofetil (CellCept) is the most common alternative. It’s taken as 1-1.5 grams twice daily. It’s effective in about 60-70% of non-responders and tends to be easier on the stomach than azathioprine. It’s also used when azathioprine causes pancreatitis or low blood counts. Other options include calcineurin inhibitors like cyclosporine or tacrolimus, especially in patients who can’t tolerate azathioprine or mycophenolate. These are powerful drugs with their own side effects-kidney toxicity, high blood pressure-and are usually reserved for complex cases. New drugs are on the horizon. Obeticholic acid (Ocaliva), originally for primary biliary cholangitis, is now in phase 3 trials for AIH and showed a 42% complete response rate in early studies. JAK inhibitors like tofacitinib and IL-6 blockers like clazakizumab are also showing promise in early trials, with response rates around 50-55%.
