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The challenging patient: HCV and alcoholic liver disease

A 54-year-old man first learned that he had liver disease 5 years ago. He was complaining of aches and pains when his wife noticed that his eyes had turned yellow. He presented to the emergency room and was referred to the transplant evaluation clinic. Liver transplantation evaluation confirmed that the patient was infected with hepatitis C virus (HCV) genotype 1a. The viral copy number was 1.4 million copies/mL HCV RNA. In addition to jaundice, he had ascites and mild encephalopathy. He had been married for 25 years with 2 children. In the past he worked in construction, but he had not been able to work for 2 years before his initial presentation because of chronic back pain. Before recognition of liver disease, his normal pattern was to drink 2-4 beers a day. He answered negatively to all 4 CAGE questions. He stopped all alcohol when he was given the advice to stop on account of liver disease. He had no reaction to stopping alcohol. He had a history of one conviction for driving while impaired 25 years ago. He went to drivers education classes to get his license back. He agreed that he had “experimented” with intravenous drugs when he was a teenager. He was also tattooed when he was 18. There is a history of probable alcoholism affecting his mother. Antiviral therapy was not attempted, and the patient was placed on the transplant waiting list. Four years ago, he underwent orthotopic liver transplantation. Histopathological examination of the explanted liver revealed micronodular cirrhosis without neoplasm. He received posttransplantation immunosuppression with tacrolimus, mycophenolate mofetil, and prednisone. He had no episodes of acute cellular rejection. Fifteen months after the transplant, when his immunosuppression had been reduced to just tacrolimus, he was treated with pegylated interferon alfa-2a and ribavirin. He was unable to tolerate this because of depression and because of “feeling terrible.” It was stopped after 8 weeks. Two years ago, results of a percutaneous liver biopsy showed one core of hepatic tissue with 14 portal tracts. The portal tracts contained moderate inflammation, comprising mostly lymphocytes and plasma cells, with occasional eosinophils and neutrophils. A few nodular lymphoid aggregates were also seen. There was mild interface hepatitis. One to 3 necroinflammatory foci were found per lobule. Occasional ballooned hepatocytes and acidophil bodies were seen. The parenchyma was negative for marked steatosis, Mallory hyaline, cholestasis, alpha-1 antitrypsin-like globules, and iron deposits. A Trichrome-stained slide showed portoportal fibrous bridging with rare portocentral fibrous bridging. There was mild pericellular fibrosis. In summary, these histopathological appearances were characterized as chronic HCV, grade 2, stage III, with mild pericellular fibrosis. For the past year, his main problem has been recurrent persistent intractable ascites. He underwent a transjugular intrahepatic portosystemic shunt placement 3 months ago. He was admitted to the hospital 2 months ago with encephalopathy. He was treated with increased lactulose, and although the symptoms improved, they did not resolve completely.