Red blood cells of a type B patient became polyagglutinable eight years ago and have remained so to the present. No infection or other cause for the phenomenon has been discovered and laboratory studies have established conclusively that the polyagglutinability is distinguishable from T‐antigen activation and from the effect of periodate treatment in vitro. Combined 51Cr and Ashby differential agglutination studies of the survival in vivo of normal type B donor blood demonstrated that the transfused cells did not become polyagglutinable during more than four months in the patient's circulation. It is concluded that the underlying abnormality of the patient's red blood cells originates during their formative stage in the bone marrow. The clinical implications of these findings and their possible relationship to the patient's accompanying leukopenia and thrombocytopenia are discussed briefly.
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Haynes et al. (1970) studied this question.
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