Transfusion only occasionally gives rise to antibody production, because blood cells per se are not markedly immunogenic. However, the immunological changes that occur during pregnancy increase the risk of alloimmunization against red blood cells, platelets, and/or leukocytes. Fetal-maternal bleeding during pregnancy or in relation to delivery is the antigenic stimuli for immunization against red blood cells, whereas other mechanisms, such as trophoblast-derived microparticles, may also play a role in the production of antibodies against platelets. Antibody-mediated immune suppression has for 4 decades successfully been used for prevention of RhD immunization. Result from a mouse model of fetal and neonatal alloimmune thrombocytopenia (FNAIT) suggests that the same principle may be applied for the prevention of FNAIT. A European Union–funded consortium is presently in the process of developing a hyperimmune anti–human platelet antigen 1a (HPA-1a) immunoglobulin G. The idea is to prevent HPA-1a immunization by administering the drug to nonimmunized HPA-1a–negative women after delivery of an HPA-1a–positive child. The anti–HPA-1a will be purified from plasma collected from women who previously have given birth to a child with FNAIT caused by anti–HPA-1a. If the results of the planned phase III trial are favorable, it is possible that a product for prevention of FNAIT will be available within this decade.
Target Audience: Obstetricians and gynecologists, family physicians
Learning Objectives: After completing this CME activity, physicians should be better able to evaluate the immunological principles behind alloimmunization in pregnancy, compare the attributes of the 3 major hypotheses regarding how Rh prophylaxis works, and explain the most recent endeavors to develop a prophylaxis against fetal and neonatal alloimmune thrombocytopenia.
*Senior Consultant Physician, Department of Clinical Immunology and Transfusion Medicine, University and Regional Laboratories Region Skåne, Lund, Sweden; †Senior Consultant Physician, Department of Laboratory Medicine, University Hospital of North Norway, and ‡Professor, Institute of Medical Biology, University of Tromsø, Tromsø, Norway
The authors have disclosed that they are among the founders of the Norwegian biotech company Prophylix Pharma AS, which leads the European Union–funded consortium developing a hyperimmune anti–human platelet antigen 1a immunoglobulin G for clinical usage. The authors have disclosed that they own stocks in this company and have part-time jobs as chief executive officer (B.S.) and chief scientific officer (J.K.-K.); and their spouses/life partners (if any) have disclosed that they have no financial relationships with, or financial interests in, any commercial organizations pertaining to this educational activity.
This work was supported by a grant from the European Union’s 7th Framework Program (grant agreement no. 305986).
All staff in a position to control the content of this CME activity and their spouses/life partners (if any) have disclosed that they have no financial relationships with, or financial interests in, any commercial organizations pertaining to this educational activity.
Lippincott CME Institute has identified and resolved all conflicts of interest concerning this educational activity.
Correspondence requests to: Jens Kjeldsen-Kragh, MD, PhD, Department of Clinical Immunology and Transfusion Medicine, University and Regional Laboratories Region Skåne, Akutgatan 8, 221 85 Lund, Sweden. E-mail: Jens.Kjeldsen-Kragh@skane.se.