Autoimmune hepatitis (AIH)

What changes during this transition

Autoimmune hepatitis is chronic immune-mediated hepatocyte destruction — distinct from PBC (cholestatic, AMA-positive, bile-duct injury) and PSC (large/small biliary strictures). Type 1 AIH (~90%) carries ANA + ASMA + anti-actin and presents across the age range with female predominance ~3-4:1. Type 2 AIH (~10%) carries anti-LKM1 + anti-LC1, skews pediatric / young adult, and tends to run more aggressively. A smaller subset is anti-SLA/LP-positive (often used as a relapse-risk marker). Diagnosis is anchored to the IAIHG simplified score (autoantibodies, IgG elevation, histology, exclusion of viral hepatitis), with liver biopsy as the diagnostic gold standard. The standard of care is immunosuppression — prednisone/prednisolone 30-60 mg induction tapered to maintenance, or budesonide (Entocort/Uceris) in non-cirrhotic patients where high first-pass hepatic metabolism gives steroid effect with lower systemic exposure. Budesonide is NOT appropriate in cirrhosis because portosystemic shunting destroys that first-pass advantage and systemic exposure rises. Azathioprine is the standard maintenance steroid-sparing agent (TPMT genotyping or activity testing BEFORE start to avoid catastrophic myelosuppression in deficient patients). Mycophenolate mofetil (MMF) is second-line maintenance for AZA-intolerant or non-responsive patients. Tacrolimus or cyclosporine are refractory-line. Rituximab and infliximab are rare refractory options under hepatology + immunology co-management. End-stage disease goes to liver transplant — and AIH has a 10-20% post-transplant recurrence rate, which is the load-bearing reason transplant is not a 'cure.' The treatment target is not 'feel better.' Per AASLD 2019, EASL 2015, and BSG 2011 guidelines, sustained complete biochemical remission requires ALT/AST normalization + IgG below 1.1× ULN + histologic remission on follow-up biopsy before considering immunosuppression withdrawal. Most patients require indefinite maintenance. HCC surveillance (ultrasound +/- AFP every 6 months) starts once cirrhosis is established. The Autoimmune Hepatitis Association (AIHA) is the major patient organization. Where Juno's library fits — narrowly and with deliberate non-elevation. No peptide has a discovery-card-defensible AIH case. The five drafted substrate entries (BPC-157, TB-500, NMN, Thymosin alpha-1, GHK-Cu) exist for honest /ask answers when users probe. BPC-157's 'liver healing' framing rests on toxic and ischemia-reperfusion animal models — not autoimmune ones — and adding a regeneration peptide while the autoimmune attack is ongoing means hepatocytes regenerate INTO the same immune fire. TB-500 carries the same framing with the additional concern that its under-characterized immunomodulation direction in autoimmune liver disease is exactly what should NOT be added empirically. NMN's NAFLD-context NAD+ work doesn't transfer to immune-mediated hepatocyte destruction. GHK-Cu's dermatologic pedigree and copper-handling concern in chronic liver disease (Wilson disease being the obvious reference) doesn't translate. THYMOSIN ALPHA-1 IS THE SUBSTRATE WHERE THE RULE 6 NON-PROPAGATION PRINCIPLE IS LOUDEST IN THE LIBRARY: TA-1's Tier 1 evidence is in chronic hepatitis B where reawakening T-cell antiviral response against infected hepatocytes is the therapeutic goal. AIH is the polar opposite immunologically — T-cells and B-cells destroying hepatocytes is the disease itself. Rule 6 propagates with the OPPOSITE SIGN — stimulating T-cell function in immune-mediated hepatocyte destruction is mechanistically expected to WORSEN disease. There is no AIH trial of TA-1 because the mechanistic logic predicts harm. The honest editorial frame: hepatology coordination, IAIHG simplified score + biopsy + serology, prednisone/budesonide (non-cirrhotic only) induction + AZA/MMF maintenance, treat-to-target ALT/AST normalization + IgG <1.1× ULN + histologic remission, HCC surveillance once cirrhotic, transplant with 10-20% recurrence awareness, and AIHA resources drive outcomes; no peptide substitutes.