This sequential scheme with intensified and high-dose chemotherapy with ASCT is feasible with moderate toxicity and may improve the outcome in high-risk DLCL.
The capacity of blood mononuclear cells to produce procoagulant activity upon stimulation with bacterial endotoxin in vitro was studied in 21 untreated patients with chronic myeloid leukaemia (CML). Procoagulant activity developed by patients' cells after prolonged incubation with endotoxin was significantly lower than that produced by cells from a matched control group (P less than 0.001). Reduced activity was seen in all patients when each of them was compared to a matched control studied simultaneously. It was below 50% of the control in 19 patients, and in eight of these it was less than 10%. These findings suggest that qualitative abnormalities in mononuclear cell function may exist in CML and might explain why these patients are less prone to thrombotic complications than those with other myeloproliferative diseases.
Platelets of patients with myeloproliferative disorders (MD) such as polycythaemia vera (PV), chronic myelogenous leukaemia (CML), idiopathic myelofibrosis (IM) and essential thrombocythaemia (ET) have been found to have low 5HT levels measured both by a fluorimetric and a liquid chromatographic assay. Km and Vmax for platelet active uptake of 3H‐5HT were not significantly different in controls and patients. Inhibition of 5HT reuptake by imipramine or induction of moderate release by fenfluramine were not sufficient to distinguish the group of MD platelets from controls, although some patients had less of a tendency to retain intraplatelet amine. The low platelet 5HT content found in our patients seems not to be the consequence of disturbed active transport of 5HT across platelet membrane. Although defective storage of this amine within the cell is probable, the results of the present study do not rule out the possibility that platelets from MD patients undergo in vivo activation by endogenous stimuli not inhibited by aspirin. 10 d treatment with aspirin did not result in any significant rise in intraplatelet 5HT concentration.
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