Autoimmune Markers Do Not Impact Clinical Presentation or Natural History of Steatohepatitis-Related Liver Disease

Academic Article


  • Background and Aim: Autoimmune (AI) markers are reported in patients with steatohepatitis-related liver disease. However, their clinical significance is unclear. Methods: Charts of patients due to alcoholic liver disease (ALD) or nonalcoholic fatty liver disease (NAFLD) were stratified for antinuclear antigen (ANA > 1:80), antismooth muscle antibody (ASMA > 1:40), or antimitochondrial antibody (AMA > 1:20). Study outcomes were patient survival and complications of liver disease. Results: Of 607 patients (401 NAFLD), information about AI markers was available for 398 (mean age 50 ± 15 year; 52 % males; median body mass index (BMI) 38; 44 % diabetic; 62 % nonalcoholic steatohepatitis (NASH) as type of steatohepatitis; median MELD score 9). A total of 78 (19.6 %) patients were positive for AI markers without differences for ALD versus NAFLD, cirrhosis versus no cirrhosis, and NASH versus no NASH. There were no differences for age, gender, BMI, cirrhosis at presentation, MELD score, endoscopic findings, and histology based on AI markers. Serum ALT was higher among patients with AI markers (65 ± 46 vs. 59 ± 66 IU/l; P = 0.048). Data remained unchanged on analyzing NAFLD patients. None of the 11 ANA-positive patients (1:640 in 4) showed findings of AI hepatitis. Biopsy in three AMA-positive patients showed mild bile duct damage in one patient. On median follow-up of about 3 years, there were no differences in liver disease outcomes (ascites, encephalopathy, variceal bleeding), hepatocellular carcinoma, transplantation, and survival. Conclusions: Autoimmune markers are frequently present in steatohepatitis-related liver disease patients. Their presence is an epiphenomenon without histological changes of autoimmune hepatitis. Further, their presence does not impact clinical presentation and follow-up outcomes.
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    Digital Object Identifier (doi)

    Author List

  • Ravi S; Shoreibah M; Raff E; Bloomer J; Kakati D; Rasheed K; Singal AK
  • Start Page

  • 3788
  • End Page

  • 3793
  • Volume

  • 60
  • Issue

  • 12