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Adverse Outcomes in Blood and Blood Component Therapy - page 13 / 19





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Transfusion Associated Graft Versus Host Disease Patients who are heavily immunosuppressed, such as those undergoing intensive anti-cancer chemotherapy, are at risk for development of accidental engraftment and GVHD when they undergo transfusion with cellular blood components, a condition known as TA-GVHD. To prevent this complication, it is routine to irradiate such blood components prior to their transfusion, although the minimum irradiation dose required is uncertain.47 Graft-versus-host disease is usually caused by the engraftment of immunocompetent lymphocytes from bone marrow transplants to an immunocompromised patient. However, even small numbers of viable lymphocytes in blood or blood component transfusions can divide spontaneously and cause GVHD in immunosuppressed recipients. Prevention is by irradiation of all blood products intended for transfusion to such patients. Graft-versus-host disease can occur occasionally in immunocompetent patients if they receive blood from a donor who is homozygous for an HLA haplotype (usually a close relative) for which the patient is heterozygous. Preventive irradiation is therefore required if donor blood is obtained from a first-degree relative. It is also required when transfusing HLA-matched components, excluding stem cells.26

Post Transfusion Purpura Post transfusion purpura (PTP) is a rare complication of transfusion, which results in a sudden dramatic thrombocytopenia developing 5 to 10 days after transfusion of Whole Blood, RBC, FFP or PCs. Patients developing this complication have developed an anti-platelet antibody at the time of a previous, often remote, pregnancy or transfusion. Subsequent transfusion triggers immune mediated destruction of the patient’s own platelets resulting in a profound thrombocytopenia during which platelet levels often drop to <10,000/µl. Over 85 percent of reported cases have been associated with antibodies against the platelet-specific alloantigen HPA-1a, an epitope on glycoprotein (GP) IIIa of the GPIIb/IIIa complex. In addition to anti-HPA-1a, anti-HPA-1b, -3a/b, -4a, and -5b have been found occasionally to induce PTP.48 Post transfusion purpura manifests in adults, primarily women, with mucous membrane hemorrhage, epistaxis, gastrointestinal (GI) bleeding and bleeding from urinary tract. Nine percent of patients develop intracranial hemorrhage. Spontaneous platelet recovery occurs within two weeks. In the interim, patients may be treated with corticosteroids, plasma exchange, high dose IV immunoglobulin and transfusion with PlA1negative platelets.49 The exact pathophysiology is unknown and different mechanisms have been proposed. Due to life-threatening hemorrhages, diagnosis and therapy must not be delayed. The best therapy seems to be infusion of IvIgG.50 Thrombocytopenia is a major cause of morbidity and hospital expense following bone marrow transplantation. Platelet transfusions in these patients are frequently complicated by the recipient's development of antibodies to HLA class I antigens. When these patients become refractory to the transfusion of HLA-matched platelets, the recipient's platelet antigen phenotype must be determined, to ensure that donor platelets will be phenotypically compatible.51

Alloimmunization Platelet refractoriness arising from HLA alloimmunization is a serious complication of transfusion therapy. While transfusions are effective in preventing sickle cell morbidity, their use is complicated by a high incidence of RBC alloimmunization and transfusion-related complications. The risk of alloimmunization continues to increase with RBC exposure, such that 60 percent of chronically transfused adults have become alloimmunized. Furthermore, over half of these patients have antibodies to more than one antigen, which makes it difficult to obtain compatible blood and results in DHTR and occasional life-threatening events. Preliminary data indicate that alloimmunization also increases the rate of RBC autoantibody formation in sickle cell disease (SCD). The mechanism underlying the increased incidence of alloimmunization in these patients may be multifactorial, but the lack of phenotypic compatibility between donor and recipient blood is clearly a major factor.52 Transfusion support is vital to the management of patients with hematologic disorders and malignancies. Many such patients require blood transfusion during the course of their illness, and almost all patients who undergo chemotherapy or radiotherapy become anemic. It is well known that alloimmunization against RBC antigens resulting from the genetic disparities between donor and recipient are one of the risks of blood transfusion. The risk depends on the recipient's exposure to the foreign antigen and its immunogenicity. The number and frequency of the transfusions as well as the recipient’s sex, age, and underlying disease may also influence immunization. Clinically significant RBC alloantibodies develop in more than 30 percent of patients receiving multiple

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