Blood groups in man / R.R. Race and Ruth Sanger.

  • R.R. Race
Date:
1975
Catalogue details

Licence: Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)

Credit: Blood groups in man / R.R. Race and Ruth Sanger. Source: Wellcome Collection.

    53/688 page 29
    THE ABO BLOOD GROUPS 29 Prokop, Simon and Rackwitz^® recorded an interesting family: father A3 (weak), mother O, two children A3 (weak), two О and one Aj. There is no reason to think that the A2 child is extra-marital: his other groups fit and anatomical tests, measurements, finger-prints etc., are in favour of his being a full sib. A Greek family in which an A^-like condition is present was described by Jakobowicz, Simmons, Graydon, Constantoulakis and Ehrlich^^'*'. However, the serum of the propositus contained anti-Le'' and not anti-H : she was a non-secretor and her red cells gave the reactions Le(a—b—). There was a hint that the condition could only be expressed in females and a possible explanation involving an X- linked gene was put forward. A peculiar form of Aj, was described by Voak et Two English sisters react as A2 but do not react with anti-H, their serum contains a 'cold' anti-H ; one of the sisters has transmitted an allele to her child, Hrubisko and his colleagues^'^^ • describe dominant depression of red cell H, A and Al in three Czechoslovak families whose salivary antigens were normal. How this ties up with the elaborate study by Voak et of H, A and В strengths in Sheffield families is a question for more robust brains than remain to us. 3. Variations due to the action of the environment Until 1957 blood group antigens were thought to be independent of the environ¬ ment : it then emerged that they could on rare occasions be modified by disease. Leukaemia and the antigen A An extremely weak A antigen was found in a patient suffering from myeloblastic leukaemia who, a year before, had been grouped as A without difficulty or com¬ ment (van Loghem, Dorfmeier and van der Hart®^, 1957). It seemed possible that the change in the A antigen of his cells was associated in some way with his disease. A similar change was observed by Stratton, Renton and Hancock^®^ in a patient suffering from hypoplastic anaemia : he was proved to be Ai by previous grouping and by family tests but his cells became inagglutinable by anti-A though they did not lose their power to adsorb anti-A. After the publication of the paper it was stated^°^ that the patient had died of leukaemia. An even more striking case was then reported by Gold, Tovey, Benney and Lewis^°^'^°^. The cells of a patient, suffering from acute monoblastic leukaemia^ gave a very feeble reaction with anti-A (2 per cent only were agglutinated) but the inagglutinable cells when separated were capable of adsorbing anti-A. During a remission of the disease the number of agglutinable cells rose to 35 % only to fall again, just before death, to 8 %. The 'inagglutinable' cells reacted more strongly with anti-H {Ulex) than did the cells which were agglutinable by anti-A. Family tests made it probable that the patient was Ai rather than A2. Further cases were reported by Bhatia and Sanghvi^®'^, by Salmon and his colleagues^°^~^°^, by Gandini and CeppelHni^^'*', by Hoogstraten, Rosenfield and
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