HPA-1a is present in 98% of the population of the United States, suggesting that approximately 2% of women who are HPA-1a negative may be at risk for NAIT during pregnancy. Of course, the antigen expression of the father must also be taken into account - in most cases the father is HPA-1a/1a or 1a/1b and the mother is HPA-1b/1b with anti-HPA-1a antibodies. In women of Asian descent, HPA-4 antigens are the most frequently implicated.Studies have shown a relationship between maternal HLA type DRw52a (DRB3* 0101) and the development of anti-HPA-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, NAIT occurs during the first pregnancy in up to 50% of cases, and the affected fetuses may develop severe thrombocytopenia (<50,000 μL−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, NAIT 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 NAIT 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).
A double inlet left ventricle (DILV) or "single ventricle", is a congenital heart defect appearing in 5 in 100,000 newborns, where both the left atrium and the right atrium feed into the left ventricle. The right ventricle is hypoplastic or does not exist. Both atria communicate with the ventricle by a single atrio-ventricular valve. There is a big shunt left-right with a quickly evolutive pulmonary hypertension. Without life-prolonging interventions, the condition is fatal, but with intervention, the newborn may survive. Even if there is no foetal sickness, the diagnosis can be made in utero by foetal echocardiography. Presentation
Infants born with DILV cannot feed normally (breathlessness) and have difficulty gaining weight. The mixed blood in systemic circulation leads to hypoxia (lack of oxygen to the body and organs), so infants develop cyanosis and breathlessness early. Diagnosis
Treatment
In the first few days, if there is no pulmonary valve stenosis, a pulmonary valve banding is necessary to prevent pulmonary hypertension and the ductus must be kept open to allow blood-flow using medication containing prostaglandin. At same time, if necessary, the atrial and ventricular septum communications must be enlarged. When possible Glenn procedure is done. Later, surgical options include the Damus–Kaye–Stansel procedure, the Fontan procedure, and the Norwood procedure. The goal of all of these is separating the pulmonary and the systemic circulation.Usually, DILV is associated with other cardiac malformations. Prognosis
Mortality is very high in the first 2 years, 85%,  but after it decreases and between 2 and 15 years old the mortality is only around 9%.