ID: 37: SILENT BUT DEADLY CYTOMEGALOVIRUS TRIGGERING AUTOIMMUNE HEPATITIS

Introduction To consider that viruses, more specifically cytomegalovirus (CMV), can trigger autoimmune hepatitis. Case Report 54 year-old female presents with new onset jaundice, which was associated with abdominal distension, lower extremity edema and 10 pound weight gain. She has no history of intravenous drug use, blood transfusions, any new sexual partners in over 8 years or a family history of liver disease. The physical examination was remarkable for spider angiomata, icteric sclera, ascites, and edema. The results of the biochemical analysis of the blood were the following: Liver enzymes were all elevated ALP 162 U/L, GGT 65 U/L, AST 154 U/L, ALT 72 U/L. Furthermore, her autoimmune workup was significant for an elevated ANA titer of 1:640, anti-smooth muscle ab titer 1:40 and a significant increase in immunoglobulins specifically IgG which was 4100 mg/dL. Interestingly, CMV Ab IgM was positive at 36.6 u/mL as well as CMV Ab IgG, which was positive at u003e10.00 u/mL. The rest of the work up was unremarkable in regards to hepatitis A, B, C, HIV, HSV, Epstein Barr virus (EBV), alpha1 antitrypsin, ceruloplasmin, iron level, ferritin and antimitochondrial ab. A liver biopsy was performed which showed heavy infiltration with lymphoplasmacytic inflammatory cells, interface hepatitis, bridging necrosis, and fibrosis. These pathologic and laboratory findings led us to a definitive diagnosis of autoimmune hepatitis (AIH) Type 1. In the setting of positive CMV IgG and IgM ab titers, we suggest that the trigger for AIH in this case was a preceding CMV infection. Her evolution was satisfactory under corticosteroid and azathioprine therapy. Discussion Autoimmune hepatitis is a chronic hepatocellular inflammation and necrosis of unknown cause. The most supported pathogenesis of AIH postulates that a combination of environmental triggers, failure of immune system tolerance and a genetic predisposition that may induce a T cell–mediated immune attack against the liver. Case studies in the literature report AIH being triggered by virus and drugs. There is evidence of cross-reactivity between anti-LKM1 and antibodies against homologous regions of cytomegalovirus (exon CMV130-135). This case could explain an association between cytomegalovirus infection and autoimmune hepatitis. As clinicians, it is difficult to diagnose autoimmune hepatitis because its presentation can be acute, severe, asymptomatic or chronic. Diagnosis requires multiple findings and exclusions of similar diseases. When excluding, make sure viral etiologies are part of the differential, which in this case is CMV. If indeed a trigger is required to set off a sequence of events leading to autoimmune hepatitis in these predisposed individuals, viruses are among the most likely candidates.