Platelets have many proteins on their surface. Each person has a different set of proteins, which are inherited from their parents. These different platelet proteins make different platelet groups, just like different proteins on red blood cells make different blood groups. These differences do not affect how the platelets work. However, if a baby inherits a protein that is found on the father's platelets but is absent from the mother's platelets, the mother may respond to this foreign protein by developing an antibody that fights against it. This antibody may pass from the mother's blood into the baby's blood and attach to the baby's platelets. This antibody destroys the baby's platelets and suppresses production of fetal platelets, they are also thought to weaken the blood vessel walls (vascular integrity) and affect production of new blood vessels (angiogenesis). This results in an increased risk of bleeding for the baby, and this can lead to the baby's death. The mother's antibodies can remain in the baby's bloodstream for weeks, and bleeding can occur in the baby before birth (fetal), during birth or after birth<unk> . A number of different proteins can cause<unk> , about 80% of cases are caused by antibodies against platelet antigen -1a, 15% by anti--5b, and 5% by other antibodies (e.g. -1b, -15, -3 and -9b). -1a is present in 98% of the population of the United States, suggesting that approximately 2% of women who are -1a negative may be at risk for during pregnancy. Of course, the antigen expression of the father must also be taken into account - in most cases the father is -1a/1a or 1a/1b and the mother is -1b/1b with anti--1a antibodies. In women of Asian descent, -4 antigens are the most frequently implicated. Studies have shown a relationship between maternal type DRw52a (DRB3* 0101) and the development of anti--1a. The offending antibodies are IgG subtype and therefore capable of crossing the placenta and entering the fetal circulation. Unlike hemolytic disease of the fetus and newborn, occurs during the first pregnancy in up to 50% of cases, and the affected fetuses may develop severe thrombocytopenia (−1) very early during pregnancy (as early as 20 weeks gestation, consistent with the development of platelet antigens, and the majority of the time in utero). Usually, the thrombocytopenia increases as gestation progresses. During the first pregnancy, is often not detected until birth when the newborn presents with classic symptoms of thrombocytopenia including petechiae, bruising or intracranial hemorrhage. In utero intracranial hemorrhage occurs in about 10% to 30% of affected cases (and is thought to be the underlying cause in the majority of cases of intracranial hemorrhage due to thrombocytopenia- greater than all other causes of thrombocytopenia combined). The risk of hemorrhage is inversely related to the platelet count with the greatest risk when the platelet count is below 100,000 μL−1. The recurrence of has been estimated to be more than 80% in subsequent pregnancies in which the fetus also carries the target platelet antigen. Subsequent cases of may be equivalent or more severe. The fetal response to is variable and may include compensatory extramedullary hematopoiesis. Rarely, fetal hydrops may develop. Fetal anemia (in presence of red cell incompatibility) may also occur.
Neonatal alloimmune thrombocytopenia
Gestational thrombocytopenia
X linked thrombocytopenia
Quebec platelet disorder
Congenital amegakaryocytic thrombocytopenia
Gray platelet syndrome
Severe fever with thrombocytopenia syndrome
Harris platelet syndrome