Autoimmune hepatitis (AIH) is a chronic liver inflammation of unknown etiology that is characterized by the presence of circulatory autoantibodies and ongoing liver tissue damage. In the past few years, the understanding of this disease has grown, and it is believed that, in a genetically predisposed individual, certain agents such as drugs and viruses can trigger this process of self-induced liver damage.
Dr. Waleed K Al-Hamoudi from Saudi Arabia presented a case of severe AIH following varicella zoster infection in a 23-year-old man. This will be published on February 28, 2009 in the World Journal of Gastroenterology.
A 23-year-old man was referred to their hepatology service on September 1, 2007 with jaundice, anorexia, weight loss and malaise of 2 mo duration. The episode of jaundice was preceded by varicella zoster virus (VZV) infection (chicken pox), which he contracted from close contact with infected family members. Despite recovery from the skin eruption, he had persistent anorexia and intermittent right upper quadrant pain. One month later he developed increasing jaundice. His physical examination revealed jaundice and hepatomegaly 2 cm below the costal margin. His initial laboratory findings were as follows: hemoglobin 149 g/L, white blood cell count 9.9 * 109/L, platelets 512 * 109/L, erythrocyte sedimentation rate 39 mm/h, alanine aminotransferase (ALT) 1066 U/L, aspartate aminotransferase (AST) 755 U/L, alkaline phosphatase (ALP) 185 U/L, total bilirubin 425 ?mol/L, direct bilirubin 318 ?mol/L, and albumin 32 g/L. His globulins were elevated at 46 g/L and his IgG was also elevated at 20.5 g/L. The coagulation profile was normal. Anti-nuclear, anti-smooth muscle, anti-mitochondrial and antiliver/kidney microsomes (ALKM-1) autoantibodies were negative. Perinuclear antineutrophil cytoplasmic antibodies were positive. Hepatitis B surface antigen, anti-hepatitis B core antigen IgM, anti-hepatitis C virus antibodies, anticytomegalovirus (CMV) IgM, anti-Epstein-Barr virus (EBV) IgM, and anti-hepatitis A virus (HAV) IgM were all negative. Anti-VZV IgG antibodies were positive. Ceruloplasmin and iron indices were normal.
The patient refused a liver biopsy, therefore, they started him on a tapering course of prednisone for presumed AIH, at a starting dose of 60 mg. He responded to that dramatically, as he became totally asymptomatic and started gaining weight. Within 2 mo of treatment, his liver enzymes normalized. On tapering his steroids below 10 mg, his liver enzymes increased again. His prednisone dose was increased to 30 mg and 50 mg azathioprine was added, however, because of vomiting and epigastric pain, the latter was changed to mycophenolate mofetil 500 mg twice daily. Follow-up showed improvement in his liver enzymes. In August, 2008, he stopped all his medications as he was feeling well and his liver enzymes were normal.
In conclusion, VZV infection can trigger AIH that may progress to advance liver fibrosis and eventually cirrhosis in genetically predisposed individuals. Therefore, AIH should be considered in any patient with persistently altered liver enzymes following a viral infection. Similarly, patients with AIH should be screened for viral hepatitis.