03492nas a2200361   4500008004100000020001400041024001700055245017000072210006900242260028100311300001300592490000700605520193200612653004402544653005402588653001502642653005502657653003202712653004802744653001102792653001102803653005402814653003302868653001602901100002402917700002202941700001802963700001902981700002303000700002303023700003503046856004903081       2014                        eng d  a1537-2995  awdn, 041736000aAcute hemolysis after intravenous immunoglobulin amid host factors of ABO-mismatched bone marrow transplantation, inflammation, and activated mononuclear phagocytes.0 aAcute hemolysis after intravenous immunoglobulin amid host facto  aUnited StatesbMichelis,Fotios V. Blood and Marrow Transplant Program, Princess Margaret Hospital, University Health Network, Toronto, Ontario, Canada; Research & Development, Canadian Blood Services, Toronto, Ontario, Canada; Transfusion Medicine Laboratory, Universityc2014  a681 - 900 v543 aBACKGROUND: Hemolysis may follow intravenous immunoglobulin (IVIG), with product, dosing, and host factors contributing. The importance of recipient features remains unclear., CASE REPORT: A 52-year-old obese woman, 10 years after ABO-mismatched (recipient O, donor A) marrow transplantation, presented with immune thrombocytopenia (ITP). IVIG at 100 g/dayx2 days was followed by hemoglobinuria and angina and dyspnea, with frank hemoglobinemia and anemia (hemoglobin 12.9 to 8.4 over 24 hr, to a nadir of 6.9 g/dL)., STUDY DESIGN AND METHODS: Serologic methods established ABO, A1, Lewis, and Secretor type, while monocyte monolayer assay (MMA) examined erythrophagocytosis with control or patient monocytes, and the implicated IVIG lot to opsonize control (group A1, A2, B, O) or patient red blood cells (RBCs). Baseline, hemolytic, and convalescent markers (including cytokines) were assessed., RESULTS: Passive anti-A was identified on reverse type and eluted from sensitized RBCs (immunoglobulinG 1+, C3d-). Le(a-b+) typing and saliva confirmed H Secretor status. MMA revealed significant activity between patient RBCs, monocytes, and IVIG. However, normal A1 cells opsonized with IVIG were not significantly phagocytosed by either normal or patient monocytes. Proinflammatory markers were significantly elevated before and after IVIG., CONCLUSIONS: Synergizing host factors (including obesity-unadjusted dosing and existing inflammation) marked this severe post-IVIG hemolytic crisis. Group A antigen restriction to myeloid tissues, with H Secretor phenotype, may have contributed, rendering this bone marrow transplant chimera vulnerable to anti-A in a manner analogous to the idiosyncratic effect of therapeutic anti-D in certain D+ ITP recipients. However, MMA suggested a macrophage activation state as contributory, perhaps precipitated by existing inflammation.Copyright © 2013 American Association of Blood Banks.10a*ABO Blood-Group System/im [Immunology]10a*Bone Marrow Transplantation/ae [Adverse Effects]10a*Hemolysis10a*Immunoglobulins, Intravenous/ae [Adverse Effects]10a*Phagocytes/im [Immunology]10aBlood Group Incompatibility/im [Immunology]10aFemale10aHumans10aImmunoglobulins, Intravenous/tu [Therapeutic Use]10aInflammation/im [Immunology]10aMiddle Aged1 aMichelis, Fotios, V1 aBranch, Donald, R1 aScovell, Iain1 aBloch, Evgenia1 aPendergrast, Jacob1 aLipton, Jeffrey, H1 aCserti-Gazdewich, Christine, M  uhttps://www.notifylibrary.org/reference/4446