Abstract

Already in 1943, Beeson observed a connection between the transfusion of blood products and the emergence of hepatitis [1]. Jaundice developed in 7 patients 1–4 months after the administration of whole blood or plasma. Further reports on the development of hepatitis in hemophilic patients were published in the mid-70s [2, 3, 4]. Today it is generally accepted that the hepatitis C virus causes the majority of cases of post-transfusion hepatitis in the western world. It is responsible for most of the chronic liver disorders observed in hemophilic patients treated with clotting factor concentrates. The hepatitis C infection can be associated with replacement therapy involving clotting factor concentrates applied in the early 1970s [2, 5, 6].

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