A 44-year-old white man was diagnosed with chronic hepatitis B in 1999 by his primary-care physician. His laboratory results were as follows: aspartate aminotransferase (AST) 144 IU/L, alanine aminotransferase (ALT) 82 IU/L, hepatitis B surface antigen (HBsAg) positive, hepatitis B e antigen (HBeAg) positive, anti-hepatitis B surface antigen (HBs) negative, and hepatitis B virus (HBV) DNA 7,000,000 IU/mL. The source of HBV was thought to be from use of intravenous drugs 20 years before his evaluation. He was heterosexual and described no other risk factors for acquiring HBV. He did not drink alcohol. No antiviral treatment was started. In 2001, the patient sought care from a gastroenterologist for increased abdominal distension and increasing fatigue. Ultrasonography of the abdomen showed a cirrhotic liver, with a large amount of ascites. An esophagogastroduodenoscopy revealed grade 2 varices with portal hypertensive gastropathy. His renal function was normal. Lamivudine (100 mg) was initiated, along with Aldactone 100 mg every day, Lasix 40 mg every day, and propranolol 20 mg twice a day. Laboratory values were as follows: AST 101 U/L, ALT 56 U/L, bilirubin 2.4 mg/dL, albumin 2.9 g/dL, international normalized ratio of prothrombin time (INR) 1.4. HBV serologies were unchanged. His was lost to follow-up for the next 2 years, but he stated that he continued lamivudine.