Abstract

Patients with hemophilia who received clotting factor concentrates before the availability of heat-treated factors in the mid-1980s were almost universally infected with hepatitis C virus (HCV). Until recently, the clinical impact of chronic hepatitis C was largely overshadowed by human immunodeficiency virus (HIV) infection in this risk group. With recent advances in treating HIV infection, there is greater emphasis on the morbidity and mortality associated with chronic hepatitis C in the hemophilic population. A recent study from the United Kingdom demonstrated that mortality from chronic liver disease in hemophilic patients was 16.7 times greater than in the general population, and death resulting from liver cancer, 5.6 times greater. Before the advent of protease inhibitors, which can alter the natural history of HIV infection, co-infection with HIV appeared to accelerate the course of chronic hepatitis C. Levels of HCV RNA were dramatically increased after HIV seroconversion, and liver failure was found in 9% of patients, exclusively among those co-infected with HIV. HCV genotypes generally reflect the predominant genotype of the donor population, but multiple genotypes may be present. Liver biopsy may be performed safely via the percutaneous or transjugular route in hemophilic patients with chronic hepatitis C, although there is an increased cost because of the expense of factor replacement. Response to interferon in this population has been similar to that expected in the general population. Large trials are underway to evaluate the role of combination therapy with interferon and ribavirin for the treatment of patients with hemophilia and hepatitis C.

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