4.2 Review

Fetal and neonatal alloimmune thrombocytopenia

Journal

SEMINARS IN FETAL & NEONATAL MEDICINE
Volume 21, Issue 1, Pages 19-27

Publisher

ELSEVIER SCI LTD
DOI: 10.1016/j.siny.2015.12.004

Keywords

Platelets; Fetal and neonatal alloimmune thrombocytopenia; beta 3 integrin and GPIb alpha; Intravenous immunoglobulin G; Antibody-induced immune suppression

Categories

Funding

  1. Canadian Institutes of Health Research [MOP 68986, MOP 119540, MOP 119551]
  2. Canada Foundation for Innovation
  3. St Michael's Hospital
  4. Canadian Blood Services
  5. University of Toronto, Department of Laboratory Medicine and Pathobiology
  6. Department of Laboratory Medicine and Pathobiology, University of Toronto
  7. Queen Elizabeth II Ontario Graduate Scholarship
  8. Connaught Scholarship
  9. Laboratory Medicine and Pathobiology Departmental Fellowships, University of Toronto

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Fetal and neonatal alloimmune thrombocytopenia (FNAIT) is an alloimmune disorder resulting from platelet opsonization by maternal antibodies that destroy fetal platelets. The major risk of FNAIT is severe bleeding, particularly intracranial hemorrhage. Miscarriage has also been reported but the incidence requires further study. Analogous to adult autoimmune thrombocytopenia (ITP), the major target antigen in FNAIT is the platelet membrane glycoprotein (GP)IIbIIIa. FNAIT caused by antibodies against platelet GPIb alpha or other antigens has also been reported, but the reported incidence of the anti-GPIb alpha-mediated FNAIT is far lower than in ITP. To date, the maternal immune response to fetal platelet antigens is still not well understood and it is unclear why bleeding is more severe in FNAIT than in ITP. In this review, we introduce the pathogenesis of FNAIT, particularly those new discoveries from animal models, and discuss possible improvements for the diagnosis, therapy, and prevention of this devastating disease. (C) 2015 Elsevier Ltd. All rights reserved.

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