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Semin Thromb Hemost 2002; 28(S1): 075-078
DOI: 10.1055/s-2002-30199
Copyright © 2002 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel.: +1(212) 584-4662

Replacement Therapy with Virus-Inactivated Clotting Factor Concentrates in Patients with Severe Hemophilia in Heidelberg

Rainer Zimmermann, Christian Uhle, Angela Huth-Kühne
  • Kurpfalzkrankenhaus and Hemophilia Center and the SRH Group, Heidelberg, Germany
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Publikationsdatum:
17. Mai 2002 (online)

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As early as 1943, Beeson had observed a connection between the transfusion of blood products and the emergence of hepatitis.[1] Jaundice developed in 7 patients 1 to 4 months after the administration of whole blood or plasma. Further reports on the development of hepatitis in hemophilia patients were published in the mid-1970s.[2] [3] [4] Today, it is generally accepted that the hepatitis C virus (HCV) causes most cases of posttransfusion hepatitis in the western world. It is responsible for most of the chronic liver disorders observed in hemophilia patients treated with clotting factor concentrates. The HCV infection can be associated with replacement therapy involving clotting factor concentrates administered in the early 1970s.[2] [5] [6]

Hepatitis C often follows an asymptomatic course, but at least 50% of patients infected with the virus develop chronic hepatitis and up to 30% develop cirrhosis of the liver within 10 to 20 years after diagnosis. Of all those infected, 10% develop a liver cell carcinoma within a further 10 years.[7] [8] Of the variants known, six more frequently occurring genotypes (types 1 to 6) are described, although each type can be differentiated further.[9] The six most common genotypes have varying nucleotide sequences in the 5-noncoding region (NCR).

In 1996, a new hepatitis virus (G) was discovered by means of modern molecular biology techniques.[10] It is said to be responsible for the 10% of cases of non- A-E posttransfusion hepatitis whose etiology was hitherto unknown. Like the HCV, the hepatitis G virus (HGV) is transmitted by the parenteral route. The prevalence of the HGV infection in healthy blood donors is much higher than for the HCV infection, however. It is between 4 and 11%,[11] [12] and for the HCV is below 0.7%.[13] The occurrence of HGV antibodies-unlike HCV antibodies-indicates that the infection has been resolved.[11]

The aim of our study was to investigate the efficacy of viral inactivation methods applied since 1985 on the HCV and the newly discovered HGV in patients with severe hemophilia. Patients included in this study had been treated exclusively with virus-inactivated clotting factor concentrates.

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