[Prolonged erythrocytic T activation, depression of blood group A and increase of fetal hemoglobin in a myelodysplastic syndrome evolving into erythroleukemia].

T cryptantigen can be exposed on the red cell membrane as a result of removal of terminal glycosides, either by bacterial enzymes or by incomplete synthesis of the cell membrane due to somatic mutation, usually caused by a neoplasm. T-activated erythrocytes have been observed in different pathologies, but they have not been seen associated with other abnormalities of red blood cell proteins described in myelodysplastic syndromes or acute leukaemias. A patient with initial diagnosis of refractory anaemia that evolved into erythroleukaemia showed prolonged T-activation, a depressed A blood-group antigen and an increase of foetal haemoglobin, simultaneously. The evolutive pattern of T-activation suggests more an abnormal erythropoiesis than an enzymatic effect and a certain relationship with the haemolytic syndrome.