Erythrocyte acetylcholinesterase activity in ABO hemolytic disease of the newborn

A Review: Human Erythrocyte Acetylcholinesterase

“…In infants with ABO disease, the activities of glucose 6-phosphate dehydrogenase and of inorganic pyrophosphatase [44] were higher than in normal neonates, reflecting the presence of more young erythrocytes in the peripheral blood. The characteristic reduction of acetylcholinesterase activity in ABO disease is transient, since by the 4th month of life normal adult levels are found [60].…”

“…During an investigation to establish correlation between erythrocyte survival and erythrocyte enzyme activity in the first days of life, Kaplan et al [60] found a consistent reduction in acetylcholinesterase activity in newborn infants affected with ABO hemolytic disease. No decrease in enzyme activity was noted in infants with Rh hemolytic disease, in infants with congenital spherocytosis, or in infants with unexplained neonatal hyperbilirubinemia.…”

“…Others have not found any association between the levels of acetylcholinesterase activity and severity of clinical disease [36,60].…”

“…Since ABO hemolytic disease of the neonate does not represent a clearly defined clinical entity, but a loose complex of clinical, hematologic, and immunologic abnormalities [60,80], a continuous spectrum of levels of acetylcholinesterase activity in offsprings from ABO incompatible matings is to be expected. The comparison between full term infants of ABO-compatible pregnancy and infants of ABO-incompatible pregnancy but without signs of hemolytic disease reveals that acetylcholinesterase activity is somewhat lower in the latter group of children (98 ± 16 versus 91 ± 12).…”

“…Because acetylcholinesterase activity also seems to be reduced in bone marrow aspirates it has been suggested that the reduction is the result of defective cell membrane synthesis [3]. In both paroxysmal nocturnal hemoglobinuria [107] and ABO disease of the neonate [60], the activities of other membrane enzymes do not seem to be affected. One family in which several members had reduced acetylcholinesterase activity without apparent disease has been described by Johns [57].…”