Human platelet antigen‐specific alloantibodies implicated in 1162 cases of neonatal alloimmune thrombocytopenia
A Davoren, BR Curtis, RH Aster, JG McFarland - Transfusion, 2004 - Wiley Online Library
A Davoren, BR Curtis, RH Aster, JG McFarland
Transfusion, 2004•Wiley Online LibraryBACKGROUND: Neonatal alloimmune thrombocytopenia (NATP) caused by fetomaternal
mismatch for human platelet (PLT) alloantigens (HPAs) complicates approximately 1 in 1000
to 1 in 2000 pregnancies and can lead to a serious bleeding diathesis, intracranial
hemorrhage, and sometimes death of the fetus or neonate. As a national reference center for
NATP investigations, our experience with this entity over a 12‐year period was reviewed.
STUDY DESIGN AND METHODS: The laboratory records of all cases of suspected NATP …
mismatch for human platelet (PLT) alloantigens (HPAs) complicates approximately 1 in 1000
to 1 in 2000 pregnancies and can lead to a serious bleeding diathesis, intracranial
hemorrhage, and sometimes death of the fetus or neonate. As a national reference center for
NATP investigations, our experience with this entity over a 12‐year period was reviewed.
STUDY DESIGN AND METHODS: The laboratory records of all cases of suspected NATP …
BACKGROUND: Neonatal alloimmune thrombocytopenia (NATP) caused by fetomaternal mismatch for human platelet (PLT) alloantigens (HPAs) complicates approximately 1 in 1000 to 1 in 2000 pregnancies and can lead to a serious bleeding diathesis, intracranial hemorrhage, and sometimes death of the fetus or neonate. As a national reference center for NATP investigations, our experience with this entity over a 12‐year period was reviewed.
STUDY DESIGN AND METHODS: The laboratory records of all cases of suspected NATP referred for evaluation from January 1, 1990, to December 31, 2002, were analyzed. The spectrum of PLT alloantibody specificities identified was compared with an earlier reported series of serologically verified NATP cases.
RESULTS: HPA‐specific alloantibodies were identified in 1162 (31%) of 3743 sera of mothers of infants with clinically suspected NATP. Maternal HPA‐1a (PlA1) alloimmunization accounted for the majority (79%) of confirmed NATP cases, with HPA‐5b (Bra), HPA‐3a (Baka), and HPA‐1b (PLA2) alloantibodies accounting for 9, 2, and 4 percent of cases, respectively. In addition, an increase in the number of cases in which multiple HPA‐specific alloantibodies were present in maternal sera was observed during the study period.
CONCLUSION: Although, as with the earlier series, maternal HPA‐1a alloimmunization was the dominant cause of NATP, the identification of an increasing number of cases due to alternative HPA polymorphisms suggests that investigation for HPA‐1 incompatibility alone is no longer sufficient to fully evaluate clinically suspect NATP cases.
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