Trends in the incidence of delayed hemolytic and delayed serologic transfusion reactions

Pineda, Alvaro A.; Vamvakas, Eleftherios C.; Gorden, Lemuel D.; Winters, Jeffrey L.; Moore, S. Breanndan

doi:10.1046/j.1537-2995.1999.39101097.x

Cited by 85 publications

(76 citation statements)

References 15 publications

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“…IgG-mediated HTRs (IgG-HTRs) are more common, but usually less severe, than IgM-HTRs; they can occur acutely or be delayed, typically cause extravascular hemolysis, and occasionally result in renal failure, coagulopathy, and death. 2 Symptomatic immune-mediated red blood cell (RBC) destruction also occurs in autoimmune hemolytic anemia (AIHA), 3 blood group incompatible transplantation, 4 and immune thrombocytopenic purpura (ITP) treated with Rh-immune globulin. 5 Although various different modalities are used to treat HTRs, there is no definitive evidence regarding efficacy.…”

Section: Introductionmentioning

confidence: 99%

Mouse models of IgG- and IgM-mediated hemolysis

Schirmer

Song

Baliff

et al. 2006

Blood

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Well-characterized mouse models of alloimmune antibody-mediated hemolysis would provide a valuable approach for gaining greater insight into the pathophysiology of hemolytic transfusion reactions. To this end, mouse red blood cells (mRBCs) from human glycophorin A transgenic (hGPA-Tg) donor mice were transfused into non-Tg recipients that had been passively immunized with IgG or IgM hGPA-specific monoclonal antibodies (mAbs). In this novel murine "blood group system," mRBCs from hGPA-Tg IntroductionHemolytic transfusion reactions (HTRs) are dangerous complications of blood transfusions. IgM-mediated HTRs (IgM-HTRs) occur acutely, are usually due to ABO incompatibility, typically cause intravascular hemolysis, and can lead to shock, renal failure, coagulopathy, and death. 1 Although infrequent, IgM-HTRs have a high mortality rate. IgG-mediated HTRs (IgG-HTRs) are more common, but usually less severe, than IgM-HTRs; they can occur acutely or be delayed, typically cause extravascular hemolysis, and occasionally result in renal failure, coagulopathy, and death. 2 Symptomatic immune-mediated red blood cell (RBC) destruction also occurs in autoimmune hemolytic anemia (AIHA), 3 blood group incompatible transplantation, 4 and immune thrombocytopenic purpura (ITP) treated with Rh-immune globulin. 5 Although various different modalities are used to treat HTRs, there is no definitive evidence regarding efficacy. Given the sporadic nature of HTRs, designing human trials to evaluate treatment options is difficult. Therefore, to study the mechanisms underlying HTRs, to evaluate the efficacy of existing treatments, and to develop new treatments, a relevant, inexpensive, and tractable animal model is required. 6 A mouse model would be ideal for this purpose, 7 given the abundance of reagents and relevant knockout (KO) and transgenic (Tg) animals. Although mouse blood group polymorphisms exist, 8 and transfused incompatible mouse RBC (mRBCs) are rapidly cleared, 9,10 no one has exploited these findings to develop a model of HTRs. The availability of a Tg mouse expressing human glycophorin A (hGPA; gene symbol designation, GYPA) on mRBCs 11 offers an approach using a well-described glycoprotein target and well-characterized reagents.We describe initial studies validating mouse models of IgG-and IgM-mediated alloimmune hemolysis. Thus, mRBCs from hGPA-Tg donors were transfused into non-Tg recipients that were passively immunized with IgG or IgM hGPA-specific monoclonal antibodies (mAbs). The clearance of the transfused mRBCs was quantified and the roles of complement and Fc␥ receptors were evaluated. Materials and methods AntibodiesPurified mAbs NaM10-2H12 (IgG3), NaM26-3F4 (IgG1), and NaM10-6G4 (IgG2a), which recognize peptide epitopes on the M and N forms of hGPA, 12 were purchased from EFS (Nantes, France). Hybridomas producing mAb 6A7, an IgG1 specific for a sialic acid-dependent epitope on M-type hGPA, 13-15 10F7, an IgG1 recognizing a nonpolymorphic epitope on hGPA, 13,14 and J11d, a rat IgM recognizing CD24 on mRBCs, 16,17...

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Section: Introductionmentioning

confidence: 99%

Mouse models of IgG- and IgM-mediated hemolysis

Schirmer

Song

Baliff

et al. 2006

Blood

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“…Antibodies are usually IgG isotypes, with some more prone than others to severe delayed reactions and/or waxing and waning expression (e.g. Kidd-Jk a [27], Duffy-Fy a , and Kell-K [28]. After the first confrontation, antibody levels eventually dissipate.…”

Section: Delayed Haemolytic Transfusion Reactionmentioning

confidence: 99%

“…These antibodies bind to the red cell, with haemolysis occasionally following. Frequency is 1 in 2500-11 000 [18,28]. The FDA reported two fatal cases in 2012 -both failed to determine the implicated antibody before transfusion.…”

Section: Delayed Haemolytic Transfusion Reactionmentioning

confidence: 99%

“…To varying degrees, alloantibodies may be adsorbed onto the incompatible subpopulation of red cells. These reactions are usually less severe than an acute reaction, and may be missed entirely, especially with reduced hospital length of stay [28]. Severity depends on antibody quality (subclass, affinity, thermal range), quantity (titre), and target antigen density.…”

Section: Delayed Haemolytic Transfusion Reactionmentioning

confidence: 99%

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Red cell transfusion and the immune system

2014

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SummaryUnderstanding the complex immunological consequences of red cell transfusion is essential if we are to use this valuable resource wisely and safely. The decision to transfuse red cells should be made after serious considerations of the associated risks and benefits. Immunological risks of transfusion include major incompatibility reactions and transfusion-related acute lung injury, while other immunological insults such as transfusion-related immunomodulation are relatively underappreciated. Red cell transfusions should be acknowledged as immunological exposures, with consequences weighed against expected benefits. This article reviews immunological consequences and the emerging evidence that may inform risk-benefit considerations in clinical practice.

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“…Alloimmunization is estimated to occur in as many as 1 in 1612 transfused red blood cell units. 1 However, in heavily transfused subjects, such as those with sickle cell anemia, the alloimmunization rate may approach 50%. [2][3][4][5][6][7] Acute or delayed hemolytic transfusion reactions may occur if an alloimmunized patient is exposed to the same foreign antigen during subsequent transfusion.…”

Section: Arch Intern Med 2001;161:285-290mentioning

confidence: 99%

Autoantibody Formation in the Alloimmunized Red Blood Cell Recipient

et al. 2001

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Alloimmunization to erythrocyte antigens is a well-characterized complication in heavily transfused patients. Less well recognized, however, is the frequency of autoantibody formation in these previously alloimmunized patients. The autoantibodies are heterogeneous and of variable clinical significance. We describe the clinical history, laboratory evaluation, diagnosis, and treatment in 4 patients who developed autoantibodies in temporal association with alloantibody formation. In one case, the autoantibody found on routine screening had no clinical significance. In another case, the autoantibody made accurate blood typing and subsequent transfusion exceedingly difficult. Two patients experienced hemolysis as a consequence of the autoantibody. The management of both patients included supportive measures, while one patient required glucocorticosteroids and red blood cell transfusion. We review the published literature concerning autoimmunization in the transfused alloimmunized host. The spectrum of clinical consequences is important for the general practitioner to recognize, as these complications may occur during routine blood transfusions.

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Trends in the incidence of delayed hemolytic and delayed serologic transfusion reactions

Cited by 85 publications

References 15 publications

Mouse models of IgG- and IgM-mediated hemolysis

Mouse models of IgG- and IgM-mediated hemolysis

Red cell transfusion and the immune system

Autoantibody Formation in the Alloimmunized Red Blood Cell Recipient

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