Management of alloimmune thrombocytopenia

• DOI: 10.1111/j.1423-0410.2007.00980.x
• Publication Date: 2007-09-22T07:24:49Z
• Authors: H. H. H. Kanhai; L. Porcelijn; C. P. Engelfriet; H. W. Reesink; S. Panzer; B. Ulm; M. Goldman; I. Bonacossa; L. Richard; M. David; E. Taaning; M. Hedegaard; C. Kaplan; V. Kiefel; O. Meyer; A. Salama; F. Morelati; N. Greppi; M. Marconi; B. Tassis; N. H. Tsuno; K. Takahashi; D. Oepkes; L. Porcelijn; H. Kanhai; L. T. N. Osnes; A. Husebekk; M. K. Killie; J. Kjeldsen‐Kragh; B. Zupanska; E. Muñiz‐Diaz; N. Nogués; J. Parra; S. J. Urbaniak; A. Cameron
• Keywords: Infant, Newborn; Integrin beta3; Immunoglobulins, Intravenous; Prenatal Care; Platelet Transfusion; 3. Good health; Thrombocytopenia, Neonatal Alloimmune; 03 medical and health sciences; Phenotype; 0302 clinical medicine; Pregnancy; Practice Guidelines as Topic; Humans; Antigens, Human Platelet; Female

Fetal alloimmune thrombocytopenia is caused by maternal sensitization to paternally-derived antigens on fetal platelets, most commonly HPA-1a.1 It occurs in approximately 1 in 1000 live births and is the commonest cause of severe fetal and neonatal thrombocytopenia, and of intracranial hemorrhage in neonates born at term.2 Since there is currently no routine screening, first-time cases of fetal alloimmune thrombocytopenia are generally identified following the birth of a markedly thrombocytopenic neonate. Antenatal management is thus only possible in subsequent pregnancies. Intracranial hemorrhage is the most devastating complication of fetal alloimmune thrombocytopenia and often occurs antenatally. Assessment of projected clinical severity is thus based on the development of intracranial hemorrhage in a previous sibling. If there is such a history of intracranial hemorrhage, the chance of this complication occurring again in the next pregnancy is extremely high in an untreated, antigen-positive sibling.3 Administration of intravenous immunoglobulin (IVIG) to the mother, initially given in conjunction with dexamethasone, was first used to prevent recurrence of antenatal intracranial hemorrhage in 1988.4 This approach of providing IVIG-based medical therapy administered to the mother to increase the fetal platelet count has since been extensively investigated in hundreds of maternal-fetal pairs.5 The efficacy of IVIG-based therapy has been supported by numerous studies6–16 (Table 1A) but not by others17–19 (Table 1B). The studies presented in Tables 1A and 1B surprisingly report virtually identical percentages of cases of intracranial hemorrhage: 2.7% versus 2.9%, respectively. However, overall mean birth platelet counts differed markedly between the two groups. While platelet counts are considered to be surrogate markers of intracranial hemorrhage, fortunately, the likelihood of fetal and neonatal intracranial hemorrhage, in the absence of this complication having occurred in a previous sibling, is relatively low.