Clin Mol Hepatol Volume_18 Number_2 June 2012 Figure 1. Abdominal CT scan. Note the absence of splenomegaly and formation of collateral vessels, suggesting the low likelihood of portal hypertension. Evidence of liver cirrhosis is not clear, although there is a large volume of ascites. cm and weight 41 kg). She was previously diagnosed as having RA in November 2006. From the time of diagnosis to September 2009 she made regular visits to the out-patient department of rheumatology and received several treatments consisting of dif- ferent disease modifying antirheumatic drugs (DMARDs) such as sulfasalazine and hydroxychloroquine, in addition to very low dose oral steroids (2.5 mg/day of prednisone) and COX-2 inhibi- tor. At that time her serum was positive for HBsAg and HBeAb with undetectable HBV DNA (<86 IU/mL) but negative for HBsAb, HBeAg, and HCV Ab. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) remained persistently nor- mal. All other laboratory tests were unremarkable except a mild degree of anemia (hemoglobin 11.2 g/dL). The follow-up test for liver function obtained at December 2008 was completely within normal limit, with a platelet count of 255×103/mm3. At September 2009, markedly increased HBV DNA titer (> 170,000,000 IU/mL) and abnormal results of liver function tests such as serum ALT 44, AST 76 U/L, total bilirubin 2.0 mg/dL, total protein 5.3, albumin 2.5 g/dL, and prothrombin time (PT) (16.7 sec, 58%, INR 1.52) were first detected. Platelet count was 134×103/mm3. Serum creatinine level was 0.9 mg/dL, while routine urinalysis revealed no signs of proteinuria or albuminuria. About two weeks later, she was ad- mitted to the department of gastroenterology for further work-up and management. Pitting edema of both lower extremities were evident on physical examination, with mildly distended abdomen. She denied the intake of any other unprescribed medications or al- cohol. There were no evidences of hepatitis A and C virus, Epstein- Barr virus, cytomegalovirus, or herpes simplex virus infection. Abdominal ultrasonography revealed a mildly coarse parenchymal 226 HBV DNA >1.7×108 IU/mL HBV DNA = 64,500 IU/mL Figure 2. Clinical course of the patient. HD, hospital day. echogenicity and moderate amount of ascites, with no evidence of liver cirrhosis. Both endoscopy and computed tomography (Fig. 1) also revealed large amount of ascites without signs of portal hy- pertension. Since her serum and ascites albumin levels at the time of ascites tapping were 2.2 and 0.3 g/dL respectively, serum asci- tes albumin gradient (SAAG) was 1.9, higher than 1.1, indicating that the ascites was transudate. Thus, acute flare-up of hepatitis B caused by HBV reactivation was diagnosed. All DMARDs, COX- 2 inhibitor and steroid were stopped. Immediate antiviral therapy with clevudine at a daily dose of 30 mg was initiated along with hepatotonics and diuretics. Despite prompt administration of anti- viral agent and some virological response toward the reactivated HBV evidenced by a great decrease in HBV DNA titer (64,500 IU/ mL) at one month, laboratory tests still revealed elevated levels of AST (69 IU/L) and ALT (32 IU/L), increased total (5.9 mg/dL) and direct (3.3 mg/dL) bilirubin, decreased total protein (4.6 g/ dL) and albumin (2.5 g/dL), decreased cholesterol (49 mg/dL) and prolonged PT (24.8 sec, 34%, INR 2.66), aggravated anemia (Hgb 9.0 g/dL) and first signs of thrombocytopenia (108×103/mm3), indicating the progression of liver failure. Despite continued anti- viral administration, liver failure continued to progress (Fig. 2) and multi-organ failure eventually developed, and she died after 50 days since administration of antiviral agent. DISCUSSION HBV infection is by far the most common chronic viral infection affecting the liver in the world, with over 400 million subjects infected, and it is the leading cause of cirrhosis and hepatocellular carcinoma.8 Reactivation of HBV replication in patients undergoing immunosuppressive therapy is a well recognized and frequently reported complication of considerable clinical importance.1-3,9-10 http://dx.doi.org/10.3350/cmh.2012.18.2.225 http://www.e-cmh.org