The association of Tn transformation with leukemia or preleukemic states, is a well-known, though very rare phenomenon [l]. It has been shown in 1978 [2] that Tn cryptantigen exposure results from a deficiency of a 3-P-D-galactosyltransferase, an enzyme involved in the biosynthesis of the alkali-labile tetrasaccharides, linked mainly to glycophorin A. Th was first described in 1978 [3] in 2 patients as a new form of acquired polyagglutination, probably induced by a bacterial enzyme. Th red cells, which are agglutinated by Arachis hypogaea, can be distinguished from T and Tk red cells by their negative reactions with Gfycine soja and BS I1 lectins and the susceptibility of the exposed receptor to protease treatment. Recently [4], Th activation could be reproduced in vitro with a neuraminidase from a strain of Corynebacrerium aquaticum. It was also shown that the neuraminidase from Vibrio choferae, known to induce a typical T transformation, was able to expose the Th cryptantigen, when used at very low concentrations. As previously suggested [l], Th exposure can be considered as an intermediate stage of T transformation. We report here the association between Tn and Th activations in a patient with myelodysplasia.
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