The presence of co-existing ABO incompatibility decreases the incidence of this hemolytic disease drastically because of the presence of anti-A/anti-B antibodies against the fetus in maternal serum. The risk of death and stillbirths are 24% and 11% respectively among these affected newborns, while 13% of affected neonates develop kernicterus with the highest reported mortality rates in the Eastern Europe/Central Asian region with 38 deaths per 100,000 live births. The southwest United States has a 1.5 times greater incidence rate than the national average, probably due to immigration factors. Despite a remarkable decline in reported cases of Rh-hemolytic disease due to proper prenatal screening and prophylaxis, 276 neonates per 100,000 live births per year are still being affected globally, especially in developing countries. 15% of Whites (North Americans and Europeans) are found to be Rh-negative, while only 4%-8% of Africans and 0.1 to 0.3% of Asians have the Rhesus negative blood group. The varying prevalence of Rhesus negative type individuals around the globe has caused a significant impact on the incidence of disease worldwide. Secondly, a less common cause of Rh incompatibility is the transfusion of an Rh-negative female with Rh-positive blood, especially during an emergency. These IgG antibodies can cross the placenta and cause hemolysis causing severe fetal anemia and hyperbilirubinemia, which can cause neurological damage or death. There are two main causes responsible for Rh Hemolytic disease. The first is the exposure of an Rh-negative pregnant mother to Rh-positive fetal erythrocytes due to fetomaternal hemorrhage during pregnancy secondary to normal delivery, spontaneous or induced abortion, ectopic pregnancy, placenta previa, lack of prenatal care, invasive obstetric procedures (cordocentesis, chorionic villous sampling, amniocentesis), external cephalic version, c-section or trauma.Īfter the sensitization of the mother due to the formation of anti-D IgG immunoglobulins, future pregnancies are at risk for the development of the hemolytic disease of the newborn (HDN) due to Rh incompatibility if the fetus is Rh-positive. Universal parental Rh screening and prophylaxis treatment with Rh immunoglobulin have significantly reduced neonatal mortality rates. If undiagnosed, the mortality rate is high, at 24% in neonates. The severity of illness depends greatly on the number of immunoglobulins, the gestational age, and the enzymatic activity of the fetus. This results in alloimmune hemolytic anemia in the fetus known as erythroblastosis fetalis. After this sensitization, these maternal alloantibodies (IgG immunoglobulins) may persist for life and move freely across the placenta to the fetal circulation during subsequent pregnancies, where they lead to the destruction of fetal erythrocytes after forming antigen-antibody complexes with their surface D antigen. Rh-hemolytic disease, also known as Rh incompatibility, is a condition that occurs when a woman with Rhesus-negative blood type is exposed to Rhesus-positive blood cells, leading to the development of anti-D antibodies by a process called isoimmunization. A person can be Rh-positive or Rh-negative based on the presence or absence of D antigen on the surface of red blood cells, respectively. D antigen is mainly responsible for Rh disease due to its high immunogenicity. The Rh blood group system consists of multiple antigens (over 50), but D, C, c, E, and e are the most common antigens identified. The term "Rhesus" was coined since it was first discovered in Rhesus monkeys. The Rhesus factor (Rh factor) is a surface antigen of erythrocytes.
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