Erythroblastosis fetalis

Rh incompatibility may occur when an Rh negative mother carries an Rh-positive fetus. At the time of delivery, a small amount of the baby s Rh-positive blood may gain access to the maternal circulation. In response, the immune system of the mother produces anti-Rh antibodies. During the subsequent pregnancy, the fetus is exposed to these antibodies as they cross the placenta. If this fetus is also Rh-positive, then the anti-Rh antibodies attack the fetal erythrocytes and cause hemolytic disease of the newborn (erythroblastosis fetalis). This may occur in about 3% of second Rh-positive babies and about 10% of third Rh-positive babies. The incidence continues to increase with subsequent pregnancies. 

Al. Abelson, N. M., and Boggs, T. R., Plasma pigments in erythroblastosis fetalis. I. Spectrophotometric absorption patterns. Pediatrics 17, 452-460 (1956). 

The homozygous state of a-thalassemia type-1 (a-Thi) leads to a form of erythroblastosis fetalis and intrauterine death [ (K2, L18, L20, L21, L22, L23, L24, L26, P4, T6, T7, T8) and others]. This form of hydrops fetalis is found in Chinese from various countries, in Filippinos, and in Thais. All children are either stillborn or die within hours after birth. The hematological observations usually include anemia with reticulo-cytosis, hypochromia with macrocytosis, aniso- and poikilocytosis, and many erythroblasts. The red cells sickle rather easily. Most fetuses are hydropic (but not all). 

A major complicating factor can be hemolytic anemia such as that of erythroblastosis fetalis caused by Rh incompatibility between mother and child. The hemolysis increases the rate of bilimbin formation, which soon overwhelms the liver and produces severe jaundice and ker-nicterus. Sickle cell anemia has a similar effect. Congenital absence of bilimbin UDP-glucuronyltransferase (Crigler-Najjar syndrome type 1) usually causes a kemictems that is fatal shortly afterbirth. Inhibition of glucuronyltransferase... 

Normal serum albumin (5% containing 130 to 160 mEq/L sodium) may be used in the treatment of a patient in shock with greatly reduced blood volume, after a bum injury, and in acute but not chronic hypoproteinemia. The use of albumin in transfusion (1 g/kg 1 to 2 hours before transfusion) is effective in hyperbilimbinemia and erythroblastosis fetalis, increasing the amount of bilimbin removed with each transfusion. 

Aldesleukin (IL-2) and several other interleukins activate natural killer cells (NK cells) and lymphokine-activated killer cells (LAK cells promiscuous killers ). The investigational use of aldesleukin in AIDS patients is partly based on the fact that lymphocytes from such individuals produce significantly less IL-2 than lymphocytes from healthy controls. The answer is (A). RhJD) immune globulin contains antibodies against Rh (D) antigens. Administration to an Rh-negative mother within 72 hours after the birth of an Rh-positive baby prevents Rh hemolytic disease of the newborn (erythroblastosis fetalis) in subsequent pregnancies. The answer is (D). 

In erythroblastosis fetalis resulting from isoimmunization, the blood bilirubin glucuronide levels reach values comparable to those observed in obstructive jaundice. Again, it is not known if this results from occlusion of the biliary tract by inspissated bile or from hepatocellular damage. 

Hyperinsulinemia occur in insulinomas, erythroblastosis fetalis and diabetes. The causes of hyperinsulinemia in erythroblastosis fetalis are unknown. 

RH Factor Incompatibility. This problem, which is also known as erythroblastosis fetalis, has little to do with nutrition, but it is presented here so that it will not be overlooked by prospective parents. (All obstetricians are well aware of this problem and the appropriate preventive measures, but some American women may have their babies with little or no prenatal advice from a doctor.)... 

Hemolytic Disease of the Newborn Disease in which a baby is born with enlarged liver and spleen caused by efforts of these organs to destroy red blood cells damaged by maternal antibodies mother is Rh-negative and baby is Rh-positive. Known also as Erythroblastosis Fetalis. 

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