Age: 31.0
Sex: F
Vaccine: HEPA, YF, HEPA, YF
Symptoms: Chromaturia, Epstein-Barr virus antibody negative, Foreign travel, Gamma-glutamyltransferase increased, Haemoglobin normal
Clinical narrative: Initial case was received via a search of the scientific literature on 19 October 2009. A 31-year-old female patient, with no reported medical history, developed autoimmune hepatitis after receiving Yellow Fever vaccine and Hepatitis A vaccine (manufacturers and lot numbers not reported). Eleven days post-vaccination, she began experiencing nausea, vomiting, and itching. She subsequently traveled for five days. Two days after her return, she presented to the emergency room with a 10-day history of nausea and vomiting, in addition to fever and dark urine. She denied pain, dyspnea, and diarrhea. She had no history high risk factor behavior, and no family history of jaundice or liver disease. Vital signs were normal. A physical examination revealed severe jaundice and mild hepatomegaly. Laboratory testing revealed the following: white blood count 3500 uL (normal 4500-11,000); hemoglobin 12 g/dL (normal 11.7-15), platelets 256,000 uL (normal 150,000 - 450,000), and international normalized ration (INR) 1.1. Electrolytes, creatinine, and blood urea nitrogen (BUN) were normal. Total (9.4 mg/dL) and direct (6.3 mg/dL) bilirubin levels were significantly elevated. Alanine aminotransferase (ALT) was 575 U/L (normal 1 - 53), aspartate aminotransferase (AST) was 1276 U/L (normal 1-50), alkaline phosphatase was 162 U/L (normal 30 - 110), and gamma-glutamyl transpeptidase was 152 U/L (normal 10 - 54). Albumin and total protein were normal, and viral serologies for Epstein-Barr virus, leptospira, and hepatitis A, B, C, and E were negative. Autoimmune markers for antinuclear antibodies, anti-liver-kidney microsome antibodies, antimitochondrial antibodies, and anti-smooth muscle antibodies were negative. Serum quantitative immunoglobulin G levels were mildly elevated at 1870 mg/dL (normal - less than 1728). Yellow fever DNA polymerase chain reaction result was negative. She was discharged to home after several days of observation with stable, although elevated, blood tests; however, she was readmitted three weeks later with 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, which revealed acute hepatitis with bridging necrosis and marked expansion of the portal tracts by lymphoplasmocellular infiltrates. Pathology revealed eosinophils, lobular inflammation, scattered acidophilic bodies, foci of parenchymal necrosis, perivenular necroinflammatory lesions, cholestatis, and portal central bridging necrosis. Periportal hepatocyte regeneration was also evident. A diagnosis of probable autoimmune hepatitis (AIH) was made. She was treated with prednisone 40 mg daily, and subsequently showed an improvement in ALT (90 U/L) and AST (95 U/L) results. She was discharged to home on a slow prednisone taper and azathioprine 50 mg daily. After three months she instructed to stop prednisone and continue taking azathioprine 50mg daily, however she self-discontinued azathioprine due to nausea and vomiting. Two months later, ALT was 7 U/L, AST 17 U/L, total bilirubin 0.4 mg/dL, and IgG 1870 mg/dL. Autoimmune markers remained negative. One year after initial presentation, she underwent a repeat percutaneous liver biopsy which showed evidence of chronic hepatitis with mild activity and fibrous septum formation. As a result, she was restarted on prednisone 10 mg and azathioprine 50mg daily. She had subsequently tapered off the prednisone, and was tolerating the azathioprine without nausea or vomiting. According to the authors, the patient's overall prognosis was good. Documents held by sender: None.