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Neonatal Alloimmune Thrombocytopenia
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Basics
Description
Neonatal alloimmune thrombocytopenia (NAIT) is one of the major causes of severe thrombocytopenia in the newborn.
- Analogous to ABO/Rh incompatibility but involves platelets instead of RBCs
- Presents with bleeding complications including petechiae, bruising, mucosal bleeding, and/or intracranial hemorrhage (ICH) that can occur in utero
Epidemiology
- Incidence is ∼1:1,000 to 1:2,000 live births.
General Prevention
The disease cannot be prevented.
Pathophysiology
Antibody-mediated platelet destruction
Etiology
Maternal IgG antibodies (Ab), directed against paternally inherited platelet-specific antigens in the fetus, cross the placenta, enter the fetal circulation, and attack fetal platelets.
- HPA-1a (formerly PLA-1) incompatibility is by far the most common cause of NAIT in those of Caucasian ancestry, accounting for ∼75% of cases. The disease happens when the mother is HPA-1a negative (HPA 1b/1b) and father is HPA-1a positive (HPA 1a/1a or 1a/1b). If the fetus inherits HPA-1a from father, maternal exposure to HPA-1a–positive fetal platelets during pregnancy causes mother to generate anti–HPA-1a IgG Ab. Anti–HPA-1a Ab crosses the placenta and causes platelet destruction.
- Other common antigens implicated in NAIT include HPA-2, HPA-3, HPA-5, HPA-9, and HPA-15.
- HPA-4 incompatibility accounts for the majority of cases in Asian populations.
- At least 23 other low-frequency antigens have been reported in a small fraction of cases.
- HPA-1a–negative mothers who are HLA-DRB3*0101 positive are far more likely to develop Ab than those who are DRB3 negative.
- The role of HLA platelet antigens in NAIT is unclear.
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Basics
Description
Neonatal alloimmune thrombocytopenia (NAIT) is one of the major causes of severe thrombocytopenia in the newborn.
- Analogous to ABO/Rh incompatibility but involves platelets instead of RBCs
- Presents with bleeding complications including petechiae, bruising, mucosal bleeding, and/or intracranial hemorrhage (ICH) that can occur in utero
Epidemiology
- Incidence is ∼1:1,000 to 1:2,000 live births.
General Prevention
The disease cannot be prevented.
Pathophysiology
Antibody-mediated platelet destruction
Etiology
Maternal IgG antibodies (Ab), directed against paternally inherited platelet-specific antigens in the fetus, cross the placenta, enter the fetal circulation, and attack fetal platelets.
- HPA-1a (formerly PLA-1) incompatibility is by far the most common cause of NAIT in those of Caucasian ancestry, accounting for ∼75% of cases. The disease happens when the mother is HPA-1a negative (HPA 1b/1b) and father is HPA-1a positive (HPA 1a/1a or 1a/1b). If the fetus inherits HPA-1a from father, maternal exposure to HPA-1a–positive fetal platelets during pregnancy causes mother to generate anti–HPA-1a IgG Ab. Anti–HPA-1a Ab crosses the placenta and causes platelet destruction.
- Other common antigens implicated in NAIT include HPA-2, HPA-3, HPA-5, HPA-9, and HPA-15.
- HPA-4 incompatibility accounts for the majority of cases in Asian populations.
- At least 23 other low-frequency antigens have been reported in a small fraction of cases.
- HPA-1a–negative mothers who are HLA-DRB3*0101 positive are far more likely to develop Ab than those who are DRB3 negative.
- The role of HLA platelet antigens in NAIT is unclear.
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