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It has been reported that coagulation factor VIII (F. VIII) is produced in the spleen and other organs. Transplantation of splenic whole organ and spleen cells may, therefore, be used to treat patients with hemophilia A. The donor spleen from brain-dead donors was used to prepare spleen cell suspension for transplantation. Twenty-two spleen cell transplantations were performed on 20 patients suffering from severe hemophilia A at our institutes. Two of them underwent a second infusion of spleen cells since there was no increase in plasma F. VIII activity after the first transplantation. All but two patients showed a marked clinical improvement. Increased plasma F. VIII activity was observed in 18 of 20 cases. The peak plasma F. VIII activity in these recipients rose to 10%-15% posttransplantation in 14 cases and to over 15% in 4 cases from pretransplant levels of 0%-3%. Generally, the elevation of plasma F. VIII activity could be detected 4-7 days following transplantation of spleen cells and this lasted from 22 to 58 weeks. Four patients whose peak plasma F. VIII activity was greater than 15% experienced an uneventful course after transplantation. The patients with plasma F. VIII activity over 10% showed less frequent bleeding and prolonged intervals between bleed as well as improvement in hemophilic arthrosis. Two patients who had interval hematuria before transplantation did not have any relapse for up to 2 years after infusion of the spleen cells. These results indicate that spleen cell transplantation may be a promising method for the management of patients with hemophilia A.

Our results show that the p16INK4a gene transfer can inhibit the proliferation and reduce the invasion ability of hepatocellular carcinoma.

Our results strongly imply that the spleen is one of the primary sites of synthesis of factor VIII and that the spleen has an inherent ability to fight malignant diseases. Allografting of whole spleen may be a promising technique for the treatment of patients with unresectable hepatocellular carcinoma and severe hemophilia A.

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It has been reported that coagulation factor VIII (F. VIII) is produced in the spleen and other organs. Transplantation of splenic whole organ and spleen cells may, therefore, be used to treat patients with hemophilia A. The donor spleen from brain-dead donors was used to prepare spleen cell suspension for transplantation. Twenty-two spleen cell transplantations were performed on 20 patients suffering from severe hemophilia A at our institutes. Two of them underwent a second infusion of spleen cells since there was no increase in plasma F. VIII activity after the first transplantation. All but two patients showed a marked clinical improvement. Increased plasma F. VIII activity was observed in 18 of 20 cases. The peak plasma F. VIII activity in these recipients rose to 10%-15% posttransplantation in 14 cases and to over 15% in 4 cases from pretransplant levels of 0%-3%. Generally, the elevation of plasma F. VIII activity could be detected 4-7 days following transplantation of spleen cells and this lasted from 22 to 58 weeks. Four patients whose peak plasma F. VIII activity was greater than 15% experienced an uneventful course after transplantation. The patients with plasma F. VIII activity over 10% showed less frequent bleeding and prolonged intervals between bleed as well as improvement in hemophilic arthrosis. Two patients who had interval hematuria before transplantation did not have any relapse for up to 2 years after infusion of the spleen cells. These results indicate that spleen cell transplantation may be a promising method for the management of patients with hemophilia A.

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