• acute viral hepatitis
• autoimmune hepatitis
• hepatitis A infection
• hepatitis‐induced autoimmune‐like hepatitis
• infection‐induced autoimmunity

• Humans
• Male
• Female
• Hepatitis, Autoimmune/pathology
• Retrospective Studies
• Hepatitis A/pathology
• Hepatitis A/complications
• Hepatitis A/immunology
• Child
• Liver/pathology
• Child, Preschool
• Adolescent
• Biopsy
• Histocytochemistry
• Hepatitis A virus/immunology
• Immunoglobulin G/blood
• Autoantibodies/blood
• Pruritus
• Infant

• Hepatitis A
• autoimmune diseases
• autoimmune hepatitis
• immune response

• Humans
• Autoimmune Diseases/diagnosis
• Hepatitis A/complications
• Lupus Erythematosus, Systemic/complications
• Arthritis, Rheumatoid

Introduction: The pathogenesis of autoimmune hepatitis (AIH) is little known. Previous case reports suggest that several viral hepatitis, including hepatitis A, can trigger AIH. Patient: A 55-year-old female showed general weakness and jaundice. The patient was diagnosed with acute hepatitis A and discharged after 14 days of hospitalization with improving liver function. However, blood tests performed 6 days after discharge revealed an increase in liver enzymes and high serum titers of an anti-nuclear antibody and immunoglobulin G. She was readmitted for liver biopsy. Diagnosis: Liver biopsy showed acute hepatitis A along with AIH. According to the revised international autoimmune hepatitis group scoring system, her score was 14 and she was diagnosed as AIH induced by acute hepatitis A. Intervention: Conservative treatments with crystalloid (Lactated Ringer’s Solution), ursodeoxycholic acid, and silymarin were administered. Outcomes: The patient has been followed up on an outpatient basis and neither symptom recurrence nor an increase in liver enzymes has been reported thus far. Lessons: After the treatment of acute hepatitis A, liver function needs to be carefully monitored over time, and the possibility of autoimmune hepatitis should be considered when liver enzymes increases.

• Autoimmune hepatitis
• Epigenetics
• HLA-DR
• Single nucleotide polymorphisms

Autoimmune hepatitis (AIH) is an immune-mediated liver disease affecting all age groups. Associations between hepatitis A virus (HAV) and AIH have been described for many years. Herein, we report a case of an AIH/primary biliary cholangitis (PBC) overlap syndrome with anti-HAV immunoglobulin M (IgM) false positivity.

A 55-year-old man was admitted with manifestations of anorexia and jaundice along with weakness. He had marked transaminitis and hyperbilirubinemia. Viral serology was positive for HAV IgM and negative for others. Autoantibody screening was positive for anti-mitochondria antibody but negative for others. Abdominal ultrasound imaging was normal. He was diagnosed with acute hepatitis A. After symptomatic treatment, liver function tests gradually recovered. Several months later, his anti-HAV IgM positivity persisted and transaminase and bilirubin levels were also more than 10 times above of the upper limit of normal. Liver histology was prominent, and HAV RNA was negative. Therefore, AIH/primary biliary cholangitis (PBC) overlap syndrome diagnosis was made based on the “Paris Criteria”. The patient was successfully treated by immunosuppression.

This case highlights that autoimmune diseases or chronic or acute infections, may cause a false-positive anti-HAV IgM result because of cross-reacting antibodies. Therefore, the detection of IgM should not be the only method for the diagnosis of acute HAV infection. HAV nucleic acid amplification tests should be employed to confirm the diagnosis.

• Autoimmune hepatitis
• Primary biliary cholangitis
• Hepatitis A virus
• Case report

• Hepatitis A
• Hepatitis B
• Hepatitis C
• Hepatitis E
• Rheumatoid factor
• Vasculitis

• Arthritis, Rheumatoid
• Cryoglobulinemia/diagnosis
• Hepatitis B, Chronic
• Humans
• Immune System Diseases
• Vasculitis/diagnosis
• Vasculitis/etiology

Multiple pathogenic mechanisms have been implicated in autoimmune hepatitis, but they have not fully explained susceptibility, triggering events, and maintenance or escalation of the disease. Furthermore, they have not identified a critical defect that can be targeted. The goals of this review are to examine the diverse pathogenic mechanisms that have been considered in autoimmune hepatitis, indicate investigational opportunities to validate their contribution, and suggest interventions that might evolve to modify their impact. English abstracts were identified in PubMed by multiple search terms. Full length articles were selected for review, and secondary and tertiary bibliographies were developed. Genetic and epigenetic factors can affect susceptibility by influencing the expression of immune regulatory genes. Thymic dysfunction, possibly related to deficient production of programmed cell death protein-1, can allow autoreactive T cells to escape deletion, and alterations in the intestinal microbiome may help overcome immune tolerance and affect gender bias. Environmental factors may trigger the disease or induce epigenetic changes in gene function. Molecular mimicry, epitope spread, bystander activation, neo-antigen production, lymphocytic polyspecificity, and disturbances in immune inhibitory mechanisms may maintain or escalate the disease. Interventions that modify epigenetic effects on gene expression, alter intestinal dysbiosis, eliminate deleterious environmental factors, and target critical pathogenic mechanisms are therapeutic possibilities that might reduce risk, individualize management, and improve outcome. In conclusion, diverse pathogenic mechanisms have been implicated in autoimmune hepatitis, and they may identify a critical factor or sequence that can be validated and used to direct future management and preventive strategies.

• Autoimmune hepatitis
• Pathogenesis
• Epigenetics
• Molecular mimicry
• Epitope spread
• Intestinal microbiome

• Animals
• Dysbiosis/immunology
• Epigenesis, Genetic
• Epitopes/immunology
• Gastrointestinal Microbiome
• Genetic Predisposition to Disease
• Hepatitis, Autoimmune/genetics
• Hepatitis, Autoimmune/immunology
• Hepatitis, Autoimmune/physiopathology
• Hepatitis, Autoimmune/virology
• Humans
• Immunosuppression Therapy
• Lymphocytes/virology
• Mice
• MicroRNAs/genetics
• Peptides/immunology
• Risk
• T-Lymphocytes/immunology

• hepatitis and other GI infections
• hepatitis other

• Autoimmune diseases
• Autoimmunity
• Cross reactions
• Cross-reactivity
• Molecular mimicry

• Autoantibodies
• Autoimmune hepatitis
• Genome-wide association studies
• Hormones
• Microbiome
• Primary biliary cholangitis
• Primary sclerosing cholangitis

• Hepatitis A virus
• autoimmune hepatitis
• autoimmunity
• vaccination