P0690 - The Impact of Hepatitis C Virus Treatment Response on Clinical Course in Patients Diagnosed With Concurrent Autoimmune Hepatitis

Swathi Kari, MD¹, Briton Lee, MD², Mai Sedki, MD, MPH³, Catherine Magee, FNP, MPH⁴, Melawit Tekeste, MS⁵, Isaac Avila-Vargas, BA⁵, Aparna Goel, MD⁶, Michele M. Tana, MD, MHS^5
1Sutter Gould Medical Foundation, Modesto, CA; ²New York University Langone Medical Center, New York, NY; ³Stanford University Medical Center, Stanford, CA; ⁴Zuckerberg San Francisco General Hospital, San Francisco, CA; ⁵University of California San Francisco, San Francisco, CA; ⁶Stanford University, Redwood City, CA

Introduction: The pathogenesis of autoimmune hepatitis (AIH) remains unclear, with molecular mimicry as a proposed mechanism. Following exposure to HCV, cross-reactive T cells may target host structures with similarity to HCV, leading to AIH. In this case series, we highlight the potential link between HCV and AIH and provide a step toward clarifying the etiopathogenesis of AIH in some patients.

Methods: A retrospective analysis of patients diagnosed with chronic hepatitis C (CHC) and AIH from 1/1/2005 to 12/31/2017 was conducted at Stanford University and University of California San Francisco. After an electronic search for diagnosis codes, charts were reviewed to confirm diagnoses and collect demographics, lab results, liver biopsies and clinical course. CHC diagnosis was confirmed by 1) detectable HCV viral load or 2) positive HCV antibody and receipt of HCV treatment. A diagnosis of AIH was established by one of the following: 1) liver biopsy consistent with AIH, 2) history of treatment for AIH, 3) diagnosis of AIH by a gastroenterologist or 4) International Autoimmune Hepatitis Group score of “probable” or “definite”.

Results: 14 CHC-AIH patients were identified. HCV was diagnosed before AIH in 9, concurrently in 5. 2 patients also had HIV. Of 12 patients with a liver biopsy, 11 (91.6%) had portal inflammation, 10 (83.3%) had plasma cell-rich infiltrate, 9 (75%) had interface hepatitis, 2 (16.6%) had emperipolesis, and 1 (8.3%) had confluent dropout necrosis. 12 of 14 patients were treated with direct-acting antivirals (DAAs), of whom 10 achieved SVR, 1 died and 1 was lost to follow-up. Of 7 patients with available pre- and post-treatment labs, all had decreases in ALT, with complete normalization in 6. Once carrying dual diagnosis, 2 of 14 patients received AIH treatment first, but both eventually received DAAs and achieved SVR. After SVR, immunosuppression remained stable in both.

Discussion: In this series of patients with concurrent CHC-AIH, AIH was usually diagnosed after or contemporaneously with HCV. While AIH was often the predominant histologic process, the majority of patients eventually received DAA therapy, and SVR rate was 83%. ALT normalized in most patients at the end of HCV therapy, indicating that viral clearance decreased AIH activity. These findings highlight a potential role of viruses in AIH pathogenesis.




Disclosures:


Swathi Kari, MD¹, Briton Lee, MD², Mai Sedki, MD, MPH³, Catherine Magee, FNP, MPH⁴, Melawit Tekeste, MS⁵, Isaac Avila-Vargas, BA⁵, Aparna Goel, MD⁶, Michele M. Tana, MD, MHS⁵. P0690 - The Impact of Hepatitis C Virus Treatment Response on Clinical Course in Patients Diagnosed With Concurrent Autoimmune Hepatitis, ACG 2021 Annual Scientific Meeting Abstracts. Las Vegas, Nevada: American College of Gastroenterology.