Minor histocompatibility (H) antigens are allogeneic target molecules having significant roles in alloimmune responses after human leukocyte antigen–matched solid organ and stem cell transplantation (SCT). Minor H antigens are instrumental in the processes of transplant rejection, graft-versus-host disease, and in the curative graft-versus-tumor effect of SCT. The latter characteristic enabled the current application of selected minor H antigens in clinical immunotherapeutic SCT protocols. No information exists on the global phenotypic distribution of the currently identified minor H antigens. Therefore, an estimation of their overall impact in human leukocyte antigen–matched solid organ and SCT in the major ethnic populations is still lacking. For the first time, a worldwide phenotype frequency analysis of ten autosomal minor H antigens was executed by 31 laboratories and comprised 2,685 randomly selected individuals from six major ethnic populations. Significant differences in minor H antigen frequencies were observed between the ethnic populations, some of which appeared to be geographically correlated.
Humoral rejection was observed 2 years after heart transplantation in a 10-year-old African American girl with sickle cell disease. Hemodynamic compromise developed, and the patient started treatment with extracorporeal membrane oxygenation within 24 hours of admission. With cellular rejection initially believed to be the cause, administration of thymoglobulin and high-dose steroids was initiated. Human leukocyte antigen antibody analysis revealed high titers of donor-specific class I and II antibodies. Aggressive treatment for antibody-mediated rejection was started with plasmapheresis and administration of intravenous immune globulin and rituximab. The patient displayed clinical signs of infection and was treated with antimicrobial, antiviral, and antifungal agents. Computed tomography of the chest suggested asperigillous infection. The patient underwent a left upper lobectomy. The patient recovered and has done well, now 4 years after having received the heart transplant. Antibody-mediated rejection should be considered early in heart transplant patients presenting with hemodynamic compromise and may respond to aggressive antibody and B cell-directed therapy. Vigilance for secondary infections, especially during treatment for rejection, is crucial.
Humoral rejection was observed 2 years after heart transplantation in a 10-year-old African American girl with sickle cell disease. Hemodynamic compromise developed, and the patient started treatment with extracorporeal membrane oxygenation within 24 hours of admission. With cellular rejection initially believed to be the cause, administration of thymoglobulin and high-dose steroids was initiated. Human leukocyte antigen antibody analysis revealed high titers of donor-specific class I and II antibodies. Aggressive treatment for antibody-mediated rejection was started with plasmapheresis and administration of intravenous immune globulin and rituximab. The patient displayed clinical signs of infection and was treated with antimicrobial, antiviral, and antifungal agents. Computed tomography of the chest suggested asperigillous infection. The patient underwent a left upper lobectomy. The patient recovered and has done well, now 4 years after having received the heart transplant. Antibody-mediated rejection should be considered early in heart transplant patients presenting with hemodynamic compromise and may respond to aggressive antibody and B cell-directed therapy. Vigilance for secondary infections, especially during treatment for rejection, is crucial.
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