BACKGROUND: Liver failure is an increasing cause of death in human immunodeficiency virus-hepatitis C virus (HIV-HCV) co-infected patients. Here, histopathological features of fatal liver disease in HIV-HCV co-infected patients were comparatively assessed. METHODS: Liver biopsies of seven HIV-HCV co-infected patients with clinically imminent liver death and advanced immune deficiency were studied. Biopsies of seven asymptomatic patients with stable hepatic and immune functions, who were matched according to their documented duration of HIV-HCV co-infection, served as controls. Inflammatory and fibrotic changes as well as hepatocellular steatosis and cholestasis were assessed semiquantitatively by established scores. RESULTS: All patients with fatal liver disease had severe immunodeficiency and jaundice, while biliary ducts were patent. Unexpectedly, the extent of hepatic steatosis, inflammatory activity and fibrosis was strikingly similar in both study groups. Importantly, liver failure was observed even in the absence of marked fibrosis. Lobular bilirubinostasis was the only feature that significantly distinguished patients with advanced immunodeficiency and fatal liver disease from the control group. CONCLUSION: Thus, rapid deterioration of liver function and death can occur in HIV-HCV co-infected patients with advanced immunodeficiency even when liver histology does not reveal markers of end-stage liver disease. Jaundice and marked bilirubinostasis in the absence of biliary tract obstruction seem to herald this complication of chronic hepatitis C in HIV infection.
BACKGROUND:Liver failure is an increasing cause of death in human immunodeficiency virus-hepatitis C virus (HIV-HCV) co-infectedpatients. Here, histopathological features of fatal liver disease in HIV-HCV co-infectedpatients were comparatively assessed. METHODS: Liver biopsies of seven HIV-HCV co-infectedpatients with clinically imminent liver death and advanced immune deficiency were studied. Biopsies of seven asymptomatic patients with stable hepatic and immune functions, who were matched according to their documented duration of HIV-HCV co-infection, served as controls. Inflammatory and fibrotic changes as well as hepatocellular steatosis and cholestasis were assessed semiquantitatively by established scores. RESULTS: All patients with fatal liver disease had severe immunodeficiency and jaundice, while biliary ducts were patent. Unexpectedly, the extent of hepatic steatosis, inflammatory activity and fibrosis was strikingly similar in both study groups. Importantly, liver failure was observed even in the absence of marked fibrosis. Lobular bilirubinostasis was the only feature that significantly distinguished patients with advanced immunodeficiency and fatal liver disease from the control group. CONCLUSION: Thus, rapid deterioration of liver function and death can occur in HIV-HCV co-infectedpatients with advanced immunodeficiency even when liver histology does not reveal markers of end-stage liver disease. Jaundice and marked bilirubinostasis in the absence of biliary tract obstruction seem to herald this complication of chronic hepatitis C in HIV infection.