Efficacy of rhesus antibodies (anti-Rh0 (D)) in autoimmune thrombocytopenia: Correlation with response to high dose IgG and the degree of haemolysis

Panzer, Simon; Grümayer, E. R.; Haas, Oskar A.; Niessner, H; Graninger, W

doi:10.1007/bf00321074

Cited by 20 publications

(9 citation statements)

References 7 publications

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“…In 1986, Panzer et al compared the effi cacy of IVIg (0.4 g/kg × 5 days) with anti-D (11-20 μg/kg × 5 days) in 5 patients with ITP, 2 of whom were children. 11 The one child with acute ITP who received anti-D had a platelet increase of 11 × 10 9 /L while the child with chronic ITP had a platelet increase of 22 × 10 9 /L. Neither child had a signifi cant decrease in their hemoglobin levels.…”

Section: Anti-d Treatment In Childrenmentioning

confidence: 94%

Anti-RhD immunoglobulin in the treatment of immune thrombocytopenia

Liebman¹

2009

BTT

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Immune thrombocytopenia (ITP) is an acquired bleeding autoimmune disorder characterized by a markedly decreased blood platelet count. The disorder is variable, frequently having an acute onset of limited duration in children and a more chronic course in adults. A number of therapeutic agents have demonstrated effi cacy in increasing the platelet counts in both children and adults. Anti-RhD immunoglobulin (anti-D) is one such agent, and has been successfully used in the setting of both acute and chronic immune thrombocytopenia. In this report we review the use of anti-D in the management of ITP. While the FDA-approved dose of 50 mg/kg has documented effi cacy in increasing platelet counts in approximately 80% of children and 70% of adults, a higher dose of 75 μg/kg has been shown to result in a more rapid increase in platelet count without a greater reduction in hemoglobin. Anti-D is generally ineffective in patients who have failed splenectomy. Anti-RhD therapy has been shown capable of delaying splenectomy in adult patients, but does not signifi cantly increase the total number of patients in whom the procedure can be avoided. Anti-D therapy appears to inhibit macrophage phagocytosis by a combination of both FcR blockade and infl ammatory cytokine inhibition of platelet phagocytosis within the spleen. Anti-RhD treatment is associated with mild to moderate infusion toxicities. Rare life-threatening toxicities such as hemoglobinuria, acute renal failure and disseminated intravascular coagulation have been reported. Recommendations have been proposed to reduce the risk of these complications. Anti-D immunoglobulin can be an effective option for rapidly increasing platelet counts in patients with symptomatic ITP.

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Section: Anti-d Treatment In Childrenmentioning

confidence: 94%

Anti-RhD immunoglobulin in the treatment of immune thrombocytopenia

Liebman¹

2009

BTT

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“…These studies provide valuable information about RhIG in mismatched transfusion inasmuch as they illustrate treatment tolerability. The early studies involved a wide range of doses and administration regimens 48‐53 . Based on earlier work to establish PLT‐sparing efficacy, the total RhIG doses given in these studies were relatively high compared to those used in D‐mismatched transfusion.…”

Section: Lessons From Immune Thrombocytopenic Purpuramentioning

confidence: 99%

“…The early studies involved a wide range of doses and administration regimens. [48][49][50][51][52][53] Based on earlier work to establish PLTsparing efficacy, the total RhIG doses given in these studies were relatively high compared to those used in D-mismatched transfusion. Experiences with these doses are therefore likely to exaggerate the adverse events associated with RhIG administration.…”

Section: Lessons From Immune Thrombocytopenic Purpuramentioning

confidence: 99%

Prevention of D sensitization after mismatched transfusion of blood components: toward optimal use of RhIG

Ayache

Herman

2008

Transfusion

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Transfusion of D+ red blood cells (RBCs) into D- recipients, whether through whole blood, RBC, or platelet (PLT) transfusion, can lead to alloimmunization with associated risks of hemolytic reactions from subsequent mismatched transfusion. The incidence of D alloimmunization in various transfused patient populations may be different from that reported in normal subjects or in pregnancy, but prevention of D alloimmunization after mismatched transfusion can be achieved using RhIG. An optimal approach to the use of RhIG, however, has not been identified for the United States. Case histories and studies of volunteers reported over the past 40 years have established that alloimmunization to mismatched RBC transfusion can be successfully prevented with a dose of 20 microg of RhIG per 1 mL of D+ RBCs (per 2 mL of whole blood) when given within a window of opportunity that extends to at least 72 hours. Evidence from prospective studies of RhIG as a therapy for immune thrombocytopenic purpura suggests that such doses can be tolerably given by intravenous injections over short periods, with adverse event rates minimized when pretransfusion medication is given. For mismatched PLT transfusions, the lowest dose of standard preparations of RhIG (e.g., 125 or 300 microg) should be sufficient to prevent alloimmunization given the small D+ RBC volumes involved. This article reviews how our understanding of prevention of alloimmunization in mismatched transfusion has progressed over the years and outlines some practical considerations based on the currently available evidence.

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“…1,6 This hypothesis is supported by studies where anti-D was inefficacious in ITP patients lacking the RhD antigen. 7,8 Interestingly, despite the ability of anti-D to lower hemoglobin values in some patients, no relationship is apparent between hemoglobin decreases and responses in ITP [9][10][11] or between erythrocyte sensitization by different doses of anti-D and responses in ITP. 9,10 To add to the complexity, we have recently shown that the TER119 antibody, which mimics the action of anti-D in murine ITP amelioration, [12][13][14] has anti-inflammatory effects in murine arthritis and can prevent disease activity in a murine model of transfusionrelated acute lung injury.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of platelet phagocytosis as an in vitro predictor for therapeutic potential of RBC antibodies in murine ITP

Khan

Menard

Jen

et al. 2020

Blood

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Polyclonal anti-D is a first-line therapy for immune thrombocytopenia (ITP). Monoclonal antibodies are desirable alternatives, but none have yet proven successful despite their ability to opsonize erythrocytes (or red blood cells, RBCs) and cause anemia. Here, we examined 12 murine erythrocyte–specific antibodies of different specificity and subtypes and found that 8 of these antibodies could induce anemia in antigen-positive mice. Of these 8 antibodies, only 5 ameliorated ITP. All antibodies were examined for their in vitro ability to support macrophage-mediated phagocytosis of erythrocytes. Antibodies which supported erythrocyte phagocytosis in vitro successfully ameliorated ITP in vivo. To examine the ability of each antibody to inhibit phagocytosis of platelets, the antibodies were used to sensitize erythrocytes in vitro and these were added to a platelet phagocytosis assay. Antibodies that inhibited platelet phagocytosis in vitro also all ameliorated ITP in vivo. We conclude that inducing anemia is not a sufficient condition for amelioration of ITP but that the antibody’s ability to prevent platelet phagocytosis in vitro predicted its ability to ameliorate ITP. We suggest that inhibition of in vitro platelet phagocytosis may prove to be a valuable tool for determining which erythrocyte antibodies would likely be candidates for clinical use in ITP.

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Efficacy of rhesus antibodies (anti-Rh0 (D)) in autoimmune thrombocytopenia: Correlation with response to high dose IgG and the degree of haemolysis

Cited by 20 publications

References 7 publications

Anti-RhD immunoglobulin in the treatment of immune thrombocytopenia

Anti-RhD immunoglobulin in the treatment of immune thrombocytopenia

Prevention of D sensitization after mismatched transfusion of blood components: toward optimal use of RhIG

Inhibition of platelet phagocytosis as an in vitro predictor for therapeutic potential of RBC antibodies in murine ITP

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