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Objectives: We report a case of an 83 year old man who developed oxaliplatin immuneinduced syndrome (OIIS) after his 19th cycle of FOLFOX (5FU, leucovorin, oxaliplatin). When oxaliplatin was omitted from his next cycle of chemotherapy he continues to show signs of drug-induced immune thrombocytopenia (DITP) and was found to have drug-dependent, platelet-reactive antibodies (DDPA) to leucovorin and palonosetron as well as oxaliplatin. Methods: The patient was admitted for monitoring but required no transfusions and thrombocytopenia resolved without treatment during his first admission. Drug-dependent antibody testing was performed on his blood by the Blood Center of Wisconsin (Diagnostic Laboratories; Milwaukee, WI). Results: No RBC or platelet IgG or IgM antibodies were detected in the absence of any drugs, but upon addition of palonosetron, leucovorin, or oxaliplatin, the tests became strongly positive for anti-RBC IgG and anti-platelet IgG antibodies. Discussion: Repeated administration of oxaliplatin can result in drug-induced immune thrombocytopenia (DITP) or autoimmune hemolytic anemia (AIHA). This phenomenon has recently been termed OIIS and may additionally include Evan's syndrome or thrombotic microangiopathy (TMA). Here we describe a patient who developed OIIS with drugdependent, platelet-reactive antibodies (DDPA) to leucovorin and palonosetron. To our knowledge, these two drugs have never been described in the literature as a cause of DDPA. We suggest that OIIS in addition to oxaliplatin-induced thrombocytopenia may be associated with the development of DDPAs to other drugs causing clinically significant thrombocytopenia which is important to recognize and manage with discontinuation of provoking agents. [ABSTRACT FROM AUTHOR]

We hypothesized that diagnoses may be associated with alloantibody 'responder' status and examined associations between disease states and alloimmunization. Patients with ≥1 alloantibody and non-alloimmunized controls were analysed. Pearson's coefficients were calculated to determine associations between alloimmunization and diseases; significant correlations were selected to construct a network. Inflammatory disorders and diseases requiring chronic transfusion support were associated with responder status. Mitigation steps may be considered in patients with these disorders. [ABSTRACT FROM AUTHOR]

Background and Objectives Fetuses affected by maternal RBC alloantibodies may have prolonged anaemia after birth, leading one to question whether maternal alloantibody transfer may occur outside the placenta. In response to a recent publication describing breast milk transfer of clinically significant amounts of maternal antiplatelet IgA antibodies from mother to nursing infant, we hypothesized that maternal RBC alloantibodies may also be capable of being transferred in breast milk. Materials and Methods The presence and clinical significance of breast milk alloantibody transfer were tested through a series of pregnancy, fostering and transfusion experiments, using a murine model in which transgenic RBCs express the human KEL glycoprotein. Results Maternal anti- KEL immunoglobulins, induced through transfusion or pregnancy, were detected in the aqueous phase of breast milk. Further, efficient transfer of maternal anti- KEL IgG and IgA to nursing pups was observed in fostering experiments. The breast milk-acquired alloantibodies were clinically significant in wild-type pups in a transfusion setting, binding to 'incompatible' KEL RBCs and leading to premature clearance from the circulation. Although breast milk-acquired alloantibodies also bound to the RBCs of transgenic KEL-positive fostered pups, no anaemia resulted. Conclusions Taking these murine data in combination with recently published human data of maternal antiplatelet IgA antibodies in breast milk leading to sequelae in some infants, it is theoretically possible that maternal anti- RBC IgA alloantibodies may also be transferred in human breast milk and may lead to sequelae in some infants under some circumstances. [ABSTRACT FROM AUTHOR]

Mice provide tractable animal models for studying the pathophysiology of various human disorders. This review discusses the use of mouse models for understanding red-blood-cell (RBC) clearance. These models provide important insights into the pathophysiology of various clinically relevant entities, such as autoimmune haemolytic anaemia, haemolytic transfusion reactions, other complications of RBC transfusions and immunomodulation by Rh immune globulin therapy. Mouse models of both antibody- and non-antibody-mediated RBC clearance are reviewed. Approaches for exploring unanswered questions in transfusion medicine using these models are also discussed. [ABSTRACT FROM AUTHOR]