Incompatibility of Mother and Foetus with respect to the Iso-Agglutinogen A and its Antibody

Abstract

Recent research on the Rh antigen discovered by Landsteiner and Wiener (1940) has provided conclusive evidence pointing to the occurrence of maternal iso-immunization-i.e. the production of antibodies by the mother in response to the presence of corpuscular antigens in the foetus. Maternal iso-imlunization throws new light on the occurrence of neonatal haemolytic anaemias, of stillbirths, and of abortions in sibships containing members so affected. The importance of its contribution to neonatal and foetal death naturally prompts us to ask to what extent: (a) other foetal antigens evoke the production of maternal antibodies; (b) other maternal antibodies may penetrate the placental barrier with lethal or semi-lethal consequences to the foetus or newly born. These issues had in fact provoked attention before work on the Rhesus antigen clarified current views. Diamond, Blackfan, and Baty (1932) and independently Parsons, Hawksley, and Gittins (1933) suggested that hydrops foetalis, icterus gravis neonatorum, and anaemia of the newborn are different manifestations of the same disease, which they called erythroblastosis foetalis. As the name suggests, its characteristic feature is excess of immature red blood cells in the blood of the foetus. The reason for this remained unexplained until 1940. In 1939 Levine and Stetson described an unusual case of intra-group agglutination in which a woman just delivered of a macerated stillborn foetus was transfused with blood from her husband of the same iso-agglutinogen group (0). Shortly after this she showed all symptoms of incompatible transfusion. Other tests subsequently proved that her serum agglutinated her husband's cells, though she was later transfused with blood from donors of group 0 whose cells did not agglutinate in this way. Tests on a number of group 0 donors, to find a miscible blood, showed that only 20 % were indeed compatible. Levine and Stetson made further tests, and showed that such agglutination was due to an irregular isoagglutinin independent of the factors M, N, or P, but were unable to obtain a

ABO Blood Groups and Toxaemia of Pregnancy

“…If proved typical it must be remembered when considering stabilizing mechanisms for maintaining the distribution of blood groups. It might prove to account in part for the shortage of A children from the mating of 0 mothers with A fathers, shown by Waterhouse and Hogben (1947).…”

“…Aird, Bentall, and Roberts (1953) have shown the disadvantage of group A in cancer of the stomach, and Aird et al (1954) that of group 0 for peptic ulcers. There was an excess of group A children dying under 2 years of age from bronchopneumonia (Struthers, 1951); and fertility and abortions (Waterhouse and Hogben, 1947; also show differing incidence in the various blood groups. It occurred to one of us (L. A. P.) that toxaemic and non-toxaemic patients could be compared in this respect in relatively large numbers from existing obstetric records.…”

Distribution of Abo Isohaemagglutinins Among Fertile and Infertile Women

“…A deficiency of blood type A and/or children among ABO-incompatible matings in which the father is type A or and the mother type O has been 460 George I. Solish reported by numerous authors (Waterhouse & Hogben, 1947;Matsunaga, 1953Matsunaga, , 1955Matsunaga & Itoh, 1953 Reepmaker, 1955;Levene & Rosenfield, 1961). The precise magnitude of this deficit varies from study to study, but in general is considered to be 25%, with a lower limit of 8% and an upper limit of 35% (Levene & Rosenfield, 1961).…”

Acuity of selective mechanisms operating on ABO, Rh, and MN blood groups

“…Compatible '0' children in- creased with increasing parity in other studies (Waterhouse and Hogben, 1947;Kircher, 1972). Livingstone (1978) has suggested that frequency-dependent selection may play a role in maintaining the ABO polymorphism.…”