This case was reported in a literature article and described the occurrence of autoimmune hepatitis in a 31-year-old female subject who was vaccinated with hepatitis A vaccine inactivated (manufacturer unspecified), yellow fever vaccine (non-GSK). The subject had no significant past medical history. She had neither history of high-risk behavior nor a family history of jaundice or liver disease. She had returned 2 days prior from a 5-day trip to a foreign country. On an unspecified date (before her trip), the subject received unspecified dose of Hepatitis A vaccine (unknown route of administration, lot number not provided), unspecified dose of Yellow fever vaccine (unknown route of administration). On an unspecified date, 11 days after vaccination with Hepatitis A vaccine and Yellow fever vaccine, the subject her first symptoms. She presented to the emergency room (ER) with complaints of fever, dark urine, and nausea/vomiting for 10 days. Symptoms of nausea/vomiting and itching started on the first day of travel and continued to progress during the trip. She denied any pain, dyspnea, or diarrhea. Her temperature on admission was normal (37 deg. C), as well as her other vital signs. Her physical examination was significant for severe jaundice and mild hepatomegaly, without splenomegaly and encephalopathy. She had no stigmata of chronic liver disease. Laboratory blood examination revealed white blood cell count of 3,500/mcL (normal range: 4,500-11,000/mcL), hemoglobin of 12 g/dL (normal range: 11.7-15.0 g/dL), platelets of 256,000/mcL (normal range: 150,000-450,000/mcL), International Normalized Ratio (INR) of 1.1. Electrolytes, creatinine and blood urea nitrogen were normal. Her total 9.4 mg/dL) and direct (6.3 mg/dL) bilirubin levels were significantly elevated, as well as her levels of alanine aminotransferase (ALT) of 575 U/L (1-53 U/L) and aspartate aminotransferase (AST) of 1276 U/L (1-50U/L). The subject's levels of alkaline phosphatase of 162 U/L (30-110 U/L) and gamma-glutamyl transpeptidase of 152 U/L (10-54 U/L) was mildly elevated. Albumin (3.4 g/dL) and total protein (6.7 g/dL) levels were within normal limits. Viral serologies for Epstein-Barr virus (EBV), leptospira, and hepatitis A, B, C, and E were negative. Additionally, autoimmune markers including antinuclear antibodies, anti-liver-kidney microsome antibodies, antimitochondrial antibodies and anti-smooth muscle antibodies were negative. Serum quantitative immunoglobulin G (IgG) levels were mildly elevated at 1870 mg/dL (less than 1728 mg/dL). A yellow fever DNA polymerase chain reaction result was negative. She was discharged to home after several days of observation with stable, though still elevated blood tests (ALT 566 U/L, AST 192 U/L and total bilirubin 9.7 mg/dL). Weekly follow-up blood tests showed increased transaminase activities and she was subsequently readmitted 3 weeks later for rising liver tests (ALT 750 U/L, AST 208 U/L, total bilirubin 17.7 mg/dL). No new symptoms or signs were noted on readmission. A percutaneous liver biopsy was performed; initial liver biopsy evaluation: Enlargement of portal tracts by mixed necroinflammatory infiltrate and portal to central bridging necrosis. No fibrous septum was seen on trichrome stain. Plasma cells and eosinophils were present in the area of bridging necrosis. Despite the negative autoimmune serum markers, a presumptive diagnosis of autoimmune hepatitis (AIH) was made. Using International Autoimmune Hepatitis Group (IAIHG) criteria, the pretreatment likelihood of AIH was considered probable. She was started on prednisone 40 mg daily and showed a dramatic improvement in both the ALT (90 U/L) and AST (95 U//L) blood test results. She was discharged to home again on a slow prednisone taper and azathioprine 50 mg daily. Within 3 months, she was taking only 5 mg of prednisone daily and 50 mg of azathioprine daily and had normal ALT (25 U/L), AST (16 U/L), and total bilirubin (0.7 mg/dL) blood values. She was instructed to stop prednisone and continue taking azathioprine 50 mg daily. Subsequent follow-up 2 months later revealed that she had self-discontinued azathioprine shortly after her last visit because of nausea and vomiting. Her liver tests were as follows: ALT 7 U/L, AST 17 U/L, total bilirubin 0.4 mg/dL, and IgG of 1870 mg/dL. Autoimmune markers were repeated and remained negative. Nearly a year after her initial presentation, she underwent a repeat percutaneous liver biopsy; evidence of resolving hepatitis was noted compared with the initial biopsy. Given the biopsy results, she was restarted on prednisone 10 mg and azathioprine 50 mg daily to prevent disease progression. Prednisone has been tapered off and she is tolerating the azathioprine without any nausea/vomiting. Her ALT and AST remained less than 20 U/L. The 1-year post-treatment liver biopsy specimen showed significant decrease in the portal inflammation with focal mild interface hepatitis and minimal lobular activity. The areas of bridging necrosis had been replaced by thin fibrous septa, which were devoid of inflammation. Ceroid-containing macrophages were present in portal tracts and rarely in the lobules, indicative of previous damage. The findings were those of chronic hepatitis with mild activity (grade 2 of 4) and fibrous septum formation (stage 2 of 4). This case raised the possibility that vaccination with HAV or yellow fever may have been the triggering agent which would be a novel triggering factor for AIH. As with drugs implicated in triggering AIH, whether vaccination-induced or unmasked, underlying AIH in this patient was debatable. Autoimmune hepatitis after vaccinations has been previously reported. Many with an acute presentation of AIH have histological evidence of chronic disease on liver biopsy, indicating the presence of subclinical disease for a long time. That did not appear to be true in this case base on the initial liver biopsy, which showed acute hepatitis with bridging necrosis without fibrous septum formation. Alternately, that the vaccination itself induced yellow fever hepatitis with accompanying autoimmune features seems unlikely given the history of vaccines and the undetectable yellow fever DNA by polymerase chain reaction in this patient. What has been noted is that the lag time between exposure to a triggering factor and onset of symptoms can be quite variable in AIH. In this case, the lag time was very brief, just 11 days. Of course vaccination and the onset of AIH may have been unrelated events. Fortunately, in this case, there was little evidence of subclinical disease even though she had discontinued treatment prematurely. Liver biopsy taken 1 year after the initial presentation showed mild activity, and thin, fibrous septa had replaced the bridging necrosis. The length of treatment with and without prednisone is controversial and may need to be tailored to individual cases. In this case, our plan is to continue her on azathioprine therapy over 1 year and then reassess with a repeat liver biopsy. Her overall prognosis is good given her response to treatment, but continued close follow-up is recommended.