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The Turnover of Blast Cells in Peripheral Blood After in vitro 3 H‐Cytidine Labelling and Retransfusion in Human Acute Leukaemia *
Author(s) -
Hoelzer D.,
Harriss E. B.,
Fliedner T. M.,
Heimpel H.
Publication year - 1972
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1972.tb00653.x
Subject(s) - labelling , population , in vitro , chemistry , bone marrow , andrology , medicine , immunology , pathology , biochemistry , environmental health
. The present study was undertaken to investigate the survival and turnover rate of blast cells in the peripheral blood of patients with acute leukaemia. Results from four cases of acute leukaemia and one blast crisis in chronic myelocytic leukaemia are reported. The method used was to label a random sample of leukaemic blast cells (LBC) representative of the total blood LBC population and to observe their behaviour after retransfusion into the patient. 500 ml blood was incubated with 3 H‐cytidine in vitro (resulting in 87.3 to 99.7% labelling of LBC), retransfused and serial blood samples taken for 10–20 days. The change in labelling index of LBC was evaluated from autoradiographs and the number of labelled LBC was calculated. Mean grain counts were also determined. From the initial dilution after retransfusion, it appears that the cells are rapidly distributed in a pool some 2 to 5 times greater than that calculated from the blood volume and blast count. In analogy with similar studies on granulocytes, and lymphocytes, it is assumed that the circulating LBC exchange with a marginal LBC pool. The disappearance of labelled LBC can be approximated by a double exponential function with T 1/2 values of 1/2 to 2 h and 2.5 to 6 days. Probable reasons for the rapid component are exchange of cells between intravascular and extravascular pools, removal of cells damaged in the labelling process, and sequestration e.g. in the lungs. The slow component is governed largely by the disappearance of LBC from the blood (random loss in addition to senescence) and their replacement by newly produced unlabelled cells. The blood transit times for LBC of 3.7 to 8.5 days, calculated from the slow component, are long compared with those of normal granulocytes and the corresponding turnover rates of LBC are slower than that of normal granulocytes. The blood transit times calculated from the slow component are minimal values since, as a result of cell metabolism, label i8 lost from the LBC so that some cells fall below the threshold of autoradiographic detectability and the curve does not represent only the disappearance of cells. A comparison of the labelling index and number of labelled LBC curves and their changes during the course of the leukaemia and its treatment gives information on the flux changes of LBC since the slope of labelling index depends upon the inflow and outflow of LBC, while the slope of the number of labelled LBC is dependent only on the outflow of cells from the peripheral blood.