R. R. Race

DETECTION OF WEAK AND "INCOMPLETE" Rh AGGLUTININS: A NEW TEST

In most cases of haemolytic disease of the newborn, and of transfusion reactions due to Rh incompatibility, agglutinins can be detected by direct microscopic agglutination tests. The “incomplete” Rh antibody (see Race1 and Wiener2) differs from the true Rh agglutinin in that it fails to agglutinate the red blood-cells which it sensitises; nevertheless, it is probably just as important in the causation of the disease (Wiener2). Until recently, its presence has only been detected by an inhibition test, in which appropriate cells treated with this antibody do not agglutinate when subsequently exposed to the action of homologous agglutinating serum. Also in a number of cases of haemolytic disease and transfusion reaction, when the history and Rh groups strongly suggest immunisation, antibodies either cannot be detected or are present in such small amount as to leave their existence in doubt.

An ‘Incomplete’ Antibody in Human Serum

A study of the properties of mixtures of different types of human anti-Rh sera has led to the recognition of what appears to be an incomplete antibody. The research arose out of a suggestion by Prof. R. A. Fisher that this technique might throw some light on the problem of antibody absorption.

The Rh Factor and Erythroblastosis Foetalis.

The part played by iso-immunization in this condition has been described at length by Levine, Burnham, Katzin, and Vogel (1941) and by Boorman, Dodd, and Mollison (1942). In their view, erythroblastosis foetalis results from isoimmunization of the mother to a red-blood-cell antigen present in the foetus, inherited from the father but absent in the mother herself, and the subsequent passage of the mothers immune agglutinins through the placenta to act on the susceptible blood of the foetus. In most cases described by the above authors iso-immunization to the Rh blood-group factor appeared to be responsible, as more than 90% of the mothers were Rh-negative and an antibody to the Rh factor was found in the serum of many of them. The Rh factor is inherited as a dominant character. Whenever it was possible to examine the blood of an erythroblastotic baby of an Rhnegative mother it proved to be Rh-positive. The finding that more than 90% of mothers of erythroblastotic children are Rh-negative when only 15% of the normal population are Rhnegative is in itself so overwhelmingly significant statistically that a connexion between the Rh groups and this disease can hardly be doubted, even apart from the evidence provided by the detection of the antibody in many of the cases. It can be shown that in one pregnancy in ten the mother is Rh-negative and the baby Rh-positive, and that in one pregnancy in five the mother has an agglutinin for an antigen of the A-B-system of groups present in her foetus. Haemolytic disease of the newborn is, however, much rarer than would be expected if iso-immunization and placental transmission of harmful agglutinins from mother to foetus occurred in every instance in which the possibility exists. It is obvious, therefore, that there is yet much to be learned about the way in which iso-immunization operates in such families. The subject is undoubtedly of importance in obstetrics and in paediatrics, and while at the moment it is not clear whiat facts may prove of importance in extending our knowledge, it .s essential that no opportunity of making serological investigations should be lost. The object of the present paper is to put on record our findings in the examination of 50 families in which erythroblastosis foetalis has been diagnosed, and a list of their pedigrees forms the main part of this communication. The cases have been sent to us by practitioners and pathologists from many parts of the United Kingdom and from Northern Ireland, and in those reported it seems reasonably certain that the diagnosis of erythroblastosis foetalis was correct. The material is far from complete, for the great difficulties always present in the