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Background Hemophilia A is an X‐linked inherited bleeding disorder caused by deficiency of coagulation factor VIII. Factor VIII is activated as part of the intrinsic coagulation cascade. It plays a crucial role as the cofactor in the intrinsic “tenase” complex activating factor X to assist in clot formation. Absence or mutation of this coagulation factor leads to excessive bleeding. Clinical manifestations of hemophilia relate to bleeding from impaired hemostasis, sequelae from bleeding, or complications of coagulation factor infusion. Diagnostic criteria for Hemophilia A include factor VIII activity level below 40% of normal, presence of a mutated F8 gene, and the absence of von Willebrand disease (F8 gene ‐ Genetics Home Reference ‐ NIH. https://ghr.nlm.nih.gov/gene/F8). Patients who have this intrinsic defect in the coagulation cascade have a characteristically prolonged PTT. It is theorized that the majority of factor VIII is synthesized mainly in the liver, by way of liver sinusoidal endothelial cells (Arruda VR. Haematologica. 2015;100(7):849–850). Extrahepatic production also occurs in the endothelial cells, kidneys, and lymphatic tissue. In 1969, Marchioro et al showed that transplantation of normal liver to hemophilia dog could normalize plasma factor VIII levels (Marchioro T L, Science. 1969;163(3863):188–190). These results were subsequently proven in humans. Liver transplantation from hemophilia A donors without factor VIII inhibitor is not commonly performed due to the perceived risk of developing hemophilia A in the recipient. There is currently limited literature aimed at elucidating this risk. We present a case of liver transplantation in a hemophilia A donor to a recipient with no history of hemophilia A with literature reviewis a case report, objective and method do not apply. Objective and method We did a case report and literature review of a liver transplant receipient fro ma hemohpila A donor. Results The receipient of the liver from hemophilia A donor did not develop hemophilia post transplant and had normal factor VIII levels. conclusion To our knowledge, this is only the second case in humans of hemophilia A patient as a donor in liver transplantation. As the indications for liver transplantation have expanded, there is a need to expand the donor list, and possibly not exclude this population as viable donor option.

Hemophilia B, also called Christmas disease, is an X-linked inherited bleeding disorder that predominantly affects males, and it is caused by deficiency of coagulation factor IX. Factor IX is a coagulation factor produced in the liver. Liver transplantation from hemophilia B donors is neither widely documented nor performed due to presumed risk of developing increased bleeding tendency in the recipient due to potential acquired factor IX deficiency. In this review, we present a case of liver and kidney transplantation from a donor with mild hemophilia B to a recipient with no history of hemophilia B and literature review. This is a relatively rare situation with only two other prior case reports of acquired Hemophilia B through liver transplantation noted in 2015. The 2 cases presented in the literature lead to acquired hemophilia B in liver transplant recipients since donors were not screened due to mild disease and low suspicion level. In our case, the donor was known to have mild Hemophilia B and the recipient had a rapid decline -thus it is imperative to weigh risks and benefits of transplantation from this donor population. While those individuals with mild hemophilia B disease (and low bleeding burden) should be considered as an alternative donor for liver transplantation, appropriate counseling should be done with the recipient about possible bleeding risks and OLT should only occur after patient consent. A multidisciplinary approach should involve hematology in case factor replacement therapy is needed post transplantation and for long term follow up.

Hemophilia B, also called Christmas disease, is an X-linked inherited bleeding disorder that predominantly affects males, and it is caused by deficiency of coagulation factor IX. Factor IX is a coagulation factor produced in the liver. Liver transplantation from hemophilia B donors is neither widely documented nor performed due to presumed risk of developing increased bleeding tendency in the recipient due to potential acquired factor IX deficiency. In this review, we present a case of liver and kidney transplantation from a donor with mild hemophilia B to a recipient with no history of hemophilia B and literature review. This is a relatively rare situation with only two other prior case reports of acquired Hemophilia B through liver transplantation noted in 2015. The 2 cases presented in the literature lead to acquired hemophilia B in liver transplant recipients since donors were not screened due to mild disease and low suspicion level. In our case, the donor was known to have mild Hemophilia B and the recipient had a rapid decline – thus it is imperative to weigh risks and benefits of transplantation from this donor population. While those individuals with mild hemophilia B disease (and low bleeding burden) should be considered as an alternative donor for liver transplantation, appropriate counseling should be done with the recipient about possible bleeding risks and OLT should only occur after patient consent. A multidisciplinary approach should involve hematology in case factor replacement therapy is needed post transplantation and for long term follow up.