Aims-To investigate and characterise the appearance of non-transferrin bound iron (NTBI) in the serum ofpatients after cytotoxic chemotherapy and to compare this with the onset and duration of neutropenia. Method-Non-transferrin bound iron was measured by a bleomycin assay in patients undergoing intensive chemotherapy for treatment of acute leukaemia or lymphoma. Results-NTBI was detected after 26 of 27 courses of chemotherapy and lasted for a mean of 14-5 days. The presence of NTBI correlated with the serum iron binding saturation, but not with serum ferritin. Neutropenia occurred after all courses of chemotherapy and lasted for a mean of 20-0 days. NTBI and neutropenia occurred concurrently after 23 courses of chemotherapy, and had a mean joint duration of 9'5 days. Conclusions-NTBI is consistently present in the serum of patients after cytotoxic chemotherapy, often at the same time as the patient is neutropenic. This may be an additional risk factor for the development of infective episodes after chemotherapy.

Aims-To determine whether nontransferrin bound iron is present in the serum of long term survivors of acute leukaemia and bone marrow transplantation who have liver dysfunction as indicated by consistently raised serum aspartate aminotransferase (AST) activities. Methods-Thirty eight patients, who were at least three years from the end of treatment, were studied. Serum samples were analysed for hepatitis C, hepatitis B, AST, ferritin, and non-transferrin bound iron. A bleomycin based assay was used to detect non-transferrin bound iron. Patient and blood bank records were examined to determine the number of units of transfused blood received by each patient.

Possible pathogenetic processes in sickle cell disease include antioxidants, endothelial and platelet changes, and hypercoagulability. Hypothesizing relationships between these processes, we recruited 47 young adult patients (mean age 19 years) with homozygous sickle cell disease and 40 age-, race- and sex-matched healthy controls and measured plasma markers representative of these processes. We found raised plasma von Willebrand factor (P = 0.001) and intercellular adhesion molecule (P = 0.016, both marking endothelial perturbation, but the latter also marking inflammation), raised soluble P selectin (P = 0.002) (marking platelet activation) and inflammation marker C reactive protein (P = 0.021), but reduced antioxidant capacity (P = 0.002) in patients compared with controls. There was no difference in fibrinogen and there was no significant correlation between any of the indices. Our data suggest that changes in endothelial and platelet function in sickle cell disease are unrelated to reduced antioxidant capacity.

We have examined the filterability of sickle erythrocytes, using an initial-flow-rate method, to determine whether sufficient hemoglobin S polymer forms at arterial oxygen saturation to adversely affect erythrocyte deformability. The amount of intracellular polymer was calculated as a function of oxygen saturation to estimate the polymerization tendency for each of eight patients with sickle cell anemia (SCA). Progressive reduction of oxygen tension within the arterial range caused a sudden loss of filterability of SCA erythrocytes through 5-,nmdiam pores at a critical P02 between 110 and 190 mmHg. This loss of filterability occurred at a higher P02 than did morphological sickling, and the critical Po2 correlated significantly (r = 0.844-0.881, P < 0.01) with the polymerization tendency for each patient. Study of density-gradient fractionated cells from four SCA patients indicated that the critical P02 of dense cells was reached when only a small amount of polymer had formed, indicating the influence of this subpopulation on the results obtained for unfractionated cells. Impairment of erythrocyte filterability at high oxygen saturation (> 90%) suggests that small changes in oxygen saturation within the arterial circulation cause Theological impairment of sickle cells.

In homozygous sickle cell disease (SCD), decreased serum Vitamin E is present. Excessive transfusions may lead to iron overload. We hypothesised a relationship between the two and found that Vitamin E type antioxidant capacity was significantly lower in 30 SCD patients than in 30 age‐ and sex‐matched controls (P < 0.001). Antioxidant capacity was lower in 10 transfused patients compared with 20 non‐transfused patients (P < 0.001). Transfusional iron overload in SCD may increase the potential for oxidative damage, and low antioxidant capacity may compound this effect. Am. J. Hematol. 69: 144–146, 2002. © 2002 Wiley‐Liss, Inc.