Introduction: Fibrosing cholestatic hepatitis (FCH) is a variant of viral hepatitis reported in hepatitis B virus or hepatitis C virus infected liver, renal or bone transplantation recipients and in leukemia and lymphoma patients after conventional cytotoxic chemotherapy. FCH constitutes a well-described form of fulminant hepatitis having extensive fibrosis and severe cholestasis as its most characteristic pathological findings. Here, we report a case of a 55-year-old female patient diagnosed with rheumatoid arthritis (RA) who developed this condition following methotrexate therapy.

Case Report: This is a case of a 55-year-old female with a RA history and a past medical history of hepatitis B. The RA was diagnosed at September 2012. Methotrexate (15 mg per week) and prednisolone (10 mg per day) treatment was started after diagnosis. Patient was administered to our hospital with jaundice and weakness at April 2013. A complete serological study was performed demonstrating hepatitis B reactivation (HBsAg, HBeAb and HBcAbIgG positive). Elevation of liver transaminase levels, bilirubin levels and bleeding tests were determined (GOT: 1323 UI/mL; GPT: 2272 UI/mL; total bilirubin: 20 mg/dL; direct bilirubin: 10.7 mg/dL; INR: 1.24). Despite treatment with lamuvidine, the hepatitis progressed towards acute hepatic failure (GOT: 849 UI/mL; GPT: 1310 UI/mL; total bilirubin: 34.2 mg/dL; direct bilirubin: 15.7 mg/dL; INR: 1.4).After six cycle of plasmapheresis therapy (with 10 unites of fresh frozen plasma), slight improvement in liver function test was observed at the 3rd week of admission (GOT: 375 UI/mL; GPT: 299 UI/mL; total bilirubin: 16.4 mg/dL; direct bilirubin: 8.4 mg/dL; INR: 1.43). However, elevation on ammonia levels and INR levels were remarked in the 4th week of admission. Abdominal sonography was revealed moderate abdominal ascites without splenomegaly or hepatomegaly. In the 5th week of admission, moderate encephalopathy was developed and deceased donor liver transplantation was performed. The patient was re-operated for bile leak at 18th postoperative days. Patient was discharged at 40 days after liver transplantation. Microscopically lobules were markedly disarrayed because of fibrous expansion of portal tracts, showing prominent ground glass appearance of hepatocytes, and marked canalicular or intracytoplasmic cholestasis. Portal inflammation was mild to moderate, and cholangiolar proliferation was prominent.

Conclusions: Although the ultimate physiopathological mechanism in this condition remains elusive, the extremely high levels of viral replication, the massive HBcAgand HBsAg expression in the liver and the nonsignificant inflammatory component suggest a direct HBV cytopathologic effect. Additional immunosuppression is generally considered as a stimulating factor for FCH. Antiviral therapy with intensive liver support is mainstay of FCH treatment. In the case of liver failure related to FCH, liver transplantation is the only treatment option.