Autoimmune hepatitis isnāt something you catch from someone else. Itās not caused by alcohol, viruses, or poor diet. It happens when your immune system turns on your own liver, attacking healthy tissue like itās an invader. This leads to chronic inflammation that, over time, can scar the liver, cause cirrhosis, or even liver failure. The good news? Itās treatable. The catch? Treatment requires patience, monitoring, and often, long-term medication.
How Is Autoimmune Hepatitis Diagnosed?
Thereās no single test that confirms autoimmune hepatitis. Instead, doctors piece together clues from blood work, imaging, and a liver biopsy. If youāre feeling unusually tired, have dark urine, yellowing skin, or unexplained joint pain, and your liver enzymes are sky-high, itās 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-whatās called Type 1 AIH. Less common is Type 2, marked by LKM1 antibodies, which tends to affect younger people. But hereās the key update from the 2025 European Association for the Study of the Liver (EASL) guidelines: autoantibody types no longer change how youāre treated. Whether youāre ANA-positive or LKM1-positive, the first-line drugs stay the same. Thatās a big shift from older practices. The real gold standard? A liver biopsy. Itās the only way to see the telltale sign: interface hepatitis. Thatās 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, thatās about 35 to 60 mg a day. The goal isnāt to stay on this dose forever. Itās 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. Thatās 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. Thatās 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 doesnāt work as fast as prednisone, but it suppresses the immune system in a different way-long-term and with fewer immediate side effects. Itās 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 youāre on 5-10 mg of prednisone instead of 30-40 mg. Thatās a massive reduction in side effects. Studies show combination therapy cuts steroid-related complications from 70% to just 30%. Thatās not just a minor improvement-itās life-changing. But azathioprine isnāt 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. Thatās 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. Donāt 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 hereās 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. Thatās not rare-itās documented. But remission doesnāt mean cure. About 60-80% of patients need to stay on some form of treatment indefinitely. If you stop, relapse rates hit 50-90%. Thatās why doctors donāt rush to stop therapy. If youāve 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 Doesnāt Work?
About 10-15% of patients donāt respond well after 12-18 months. Thatās called treatment failure. The next step is switching to a second-line drug. Mycophenolate mofetil (CellCept) is the most common alternative. Itās taken as 1-1.5 grams twice daily. Itās effective in about 60-70% of non-responders and tends to be easier on the stomach than azathioprine. Itās also used when azathioprine causes pancreatitis or low blood counts. Other options include calcineurin inhibitors like cyclosporine or tacrolimus, especially in patients who canāt 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%.
Edith Brederode
January 19, 2026 AT 14:05Just started my azathioprine journey last month and honestly? My moon face is kinda wild š But my ALT dropped from 380 to 68 in 6 weeks. Steroids are brutal, but this combo? Life-changing. Also, TPMT test was $180 at my clinic-totally worth it. Donāt skip it.
clifford hoang
January 20, 2026 AT 00:07They say it's autoimmune... but what if it's just the EMFs from 5G towers messing with your liver? š Iāve been tracking my symptoms since 2021 and the timing lines up with when my neighborhood got the new cell tower. They donāt want you to know the truth. Steroids? Just suppressing symptoms while the real enemy grows. Ask yourself: who profits from lifelong meds?
Arlene Mathison
January 20, 2026 AT 19:01YOU GOT THIS. I was diagnosed with AIH in 2020, felt like my body was betraying me. Now? Iām hiking, teaching yoga, and my last biopsy showed F0. Yes, Iām on 5mg prednisone every other day and azathioprine. Itās not easy, but itās manageable. Your liver is stronger than you think. Keep showing up for your bloodwork. Youāre not alone.
Emily Leigh
January 22, 2026 AT 00:55Okay butā¦ why are we still using 1970s drugs? š I mean, prednisone? Azathioprine? We have CRISPR. We have AI-driven drug discovery. Why am I being told to take pills that give me depression and cellulite? This feels like medical stagnation. Also, āinterface hepatitisā? Sounds like a bad sci-fi movie title.
Greg Robertson
January 23, 2026 AT 21:27Hey, just wanted to say thanks for posting this. Iāve been reading up on AIH since my diagnosis last year and this is the clearest breakdown Iāve found. Iām on the combo too-6 months in, feeling way better. The fatigueās still there sometimes, but Iām not passing out anymore. Small wins, right?
Crystal August
January 24, 2026 AT 09:01How dare you normalize lifelong medication? This is what Big Pharma wants. Youāre being manipulated into dependency. Why not try fasting? Or turmeric? Or acupuncture? I healed my own liver with lemon water and breathwork. Youāre being sold a lie. Steroids are poison. Period.
Nadia Watson
January 24, 2026 AT 10:48Thank you for sharing such a detailed and thoughtful overview. Iām a nurse in rural Oregon, and Iāve seen too many patients dismissed because their autoantibodies were āinconclusive.ā The IAHIG scoring system is a game-changer. Iāve started advocating for TPMT testing here-only 2 of 12 clinics do it. We need more awareness. P.S. Sorry for the typos-typing on my phone while on break š
Courtney Carra
January 25, 2026 AT 01:02Is it just me, or does it feel like our immune systems are screaming for help because weāve lost touch with nature? Weāre over-sanitized, over-medicated, under-sleepingā¦ and then we get diagnosed with an āautoimmuneā disease? Maybe itās not just the liver-itās the soul. Azathioprine suppresses the body, but what if we need to suppress the stress? š¤
thomas wall
January 26, 2026 AT 18:45While the clinical data presented is methodologically sound, one cannot overlook the profound ethical implications of institutionalizing lifelong immunosuppression. The normalization of pharmaceutical dependency in chronic autoimmune disease represents a systemic failure of preventative medicine. One must question: are we healing, or merely managing decline? The absence of holistic dietary intervention in this discourse is, frankly, alarming.