Alloimmune hemolytic disease of the fetus and newborn: genetics, structure, and function of the commonly involved erythrocyte antigens.

Hemolytic disease of the fetus and newborn (HDFN) can occur when a pregnant woman has antibody directed against an erythrocyte surface antigen expressed by her fetus. This alloimmune disorder is restricted to situations where transplacental transfer of maternal antibody to the fetus occurs, and binds to fetal erythrocytes, and significantly shortens the red cell lifespan. The pathogenesis of HDFN involves maternal sensitization to erythrocyte "non-self" antigens (those she does not express). Exposure of a woman to a non-self-erythrocyte antigen principally occurs through either a blood transfusion or a pregnancy where paternally derived erythrocyte antigens, expressed by her fetus, enter her circulation, and are immunologically recognized as foreign. This review focuses on the genetics, structure, and function of the erythrocyte antigens that are most frequently involved in the pathogenesis of alloimmune HDFN. By providing this information we aim to convey useful insights to clinicians caring for patients with this condition.

Cerebral perfusion pressure, and not cerebral blood flow, may be the critical determinant of intracranial injury in preeclampsia: a new hypothesis.

OBJECTIVE: The relationship between cerebral perfusion pressure (CPP) and cerebral blood flow is unclear in preeclampsia. Our objective was to clarify this issue by comparing normal pregnant women to those with mild and severe preeclampsia. STUDY DESIGN: Patients with mild (n = 72) and severe (n = 120) preeclampsia underwent transcranial Doppler (TCD) imaging of the maternal middle cerebral artery (MCA). At the same time, blood pressure was taken with a Dinamap monitor (Dinamap; Criticon Inc, Tampa, Fla). CPP, resistance area product (RAP), and the cerebral flow index (CFI) were calculated by standard formulas. Data were plotted on normative curves for pregnancy (5% and 95%) and compared by chi(2) and Mann-Whitney U tests. RESULTS: CFI is usually normal in both severe (75%) and mild (72%) cases. If CFI is abnormal in severe cases, it may be either increased (14%) or decreased (10%), although in mild cases almost all abnormal CFI (25%) is lower than normal. In those cases with low or normal CFI, severe cases are associated with a significantly higher CPP, RAP, and MAP than mild cases (P <.05), although the CFI is not significantly different. A significant proportion of severe cases have high CPP (52%), whereas in mild cases the CPP is almost always normal (87%). Overall, in severe cases the RAP is abnormally high, although it is within the normal range in mild cases. CONCLUSIONS: One of the fundamental differences between mild and severe cases relates to the degree of cerebral perfusion pressure that the MCAs are subjected to. Because most preeclamptic women, regardless of degree of severity, have a normal CFI, it appears that autoregulation is generally intact. Because women with severe cases are more prone to cerebral catastrophe than those with mild preeclampsia, uncontrolled CPP may cause barotrauma and vessel damage, leading to hypertensive encephalopathy and overperfusion injury. Therapeutic strategies that ensure reduction of the CPP with maintenance of the CFI seem most likely to prevent the cerebral injuries (overperfusion or underperfusion) that cause seizures or death in women with preeclampsia.