Serum thrombopoietin levels in acute myeloid leukaemia.

To improve our understanding of the regulation of circulating platelet counts (PC) by thrombopoietin (TPO), we studied serum TPO levels and PC before and after myelosuppressive chemotherapy in 12 patients with acute myeloid leukaemia (AML). Serum TPO levels were measured by the quantitative sandwich enzyme-linked immunosorbent assay (Quantikine, RD Systems). At the start of the induction chemotherapy, the patients had a median serum TPO level of 199 pg/ml (range 120-2,150 pg/ml), while 10 to 12 days after the end of chemotherapy, their TPO levels were substantially increased, the median value being 1,907 pg/ml (range 1,049-4,194 pg/ml). The correlation between PC and TPO was statistically significant prior to chemotherapy (p < 0.03) and insignificant after chemotherapy. As a result of chemotherapy, the patients developed aplasia; after the administration of platelet transfusions, their median PC increased to 21 x 10(9)/l (range 5-55 x 10(9)/l), while the median TPO value decreased by 300 pg/ml (range 11-1,125 pg/ml). Our results suggest that platelet mass directly regulates serum TPO levels in acute leukaemia patients prior to chemotherapy and after the administration of platelet transfusions. Serum TPO levels may also be influenced by the cytokine response during complicating infections in patients with chemotherapy-induced cytopenia.

Indices of iron status in patients treated by chronic haemodialysis.

Iron deficiency in patients with end stage renal disease (ESRD) treated by haemodialysis (HD) is difficult to diagnose. The reticulocyte hemoglobin content (CHr) and the percentage of hypochromic red cells (%hypo) are sensitive novel assays for the detection of functional iron deficiency in patients treated with erithropoietin (EPO). In our study thirty-nine chronically hemodialyzed patients were evaluated to determine the value of these two parameters in comparison to the conventional biochemical indicators of iron metabolism. There were significant correlations between CHr and transferrin saturation, CHr and weekly dosage of EPO, and also between %hypo and weekly dosage of EPO. Our data represent superior value of %hypo and CHr to the transferrin saturation and ferritin concentration in detecteng of iron deficiency in HD patients.

Effects of molgramostim, filgrastim and lenograstim in the treatment of myelokathexis.

Myelokathexis is a very rare form of chronic hereditary neutropenia resulting from impaired neutrophil releasing mechanism in the bone marrow. The recombinant human granulocyte-macrophage (molgramostim) and granulocyte (filgrastim, lenograstim) colony stimulating factors release the mature granulocytes from the bone marrow. We describe a 43-year-old woman suffering from myelokathexis, with the absolute neutrophil count ranging between 0.03 and 1.35 x 10(9)/L. In the period before the introduction of cytokines, the patient had more than 80 major infectious episodes. Since 1991, infections in this patient have been treated with cytokines, given in conjunction with antibiotics. Initially, she received molgramostim in a daily dose of 5 microg/kg subcutaneously, which stimulated the release of granulocytes from her bone marrow, thereby allowing successful treatment of infection. After the development of hypersensitivity, molgramostim was substituted with filgrastim. Finally, lenograstim was given a trial. With all three cytokines, the patient's neutrophil count always attained normal values already 4 hours after subcutaneous application of the drug in a dose of 5 microg/kg, the highest neutrophil levels were measured at 24 hours post-injection, and the neutrophil count was again close to the baseline value 72 hours after the treatment. A slight neutropenia was present 48 hours after the application of filgrastim. We believe that all three cytokines are equally effective in increasing the neutrophil count in venous blood of patients with myelokathexis.

Cerebral toxoplasmosis - a late complication of allogeneic haematopoietic stem cell transplantation.

Toxoplasma gondii infection reactivation predominantly occurs among patients after allogeneic haematopoietic stem cell transplantation. Mostly, reactivation occurs during first 3 months after transplant, especially when risk factors are present. We report a case of late cerebral toxoplasmosis reactivation, which was probably triggered by a brief course of corticosteroids, administered for chronic graft-versus-host disease (cGVHD). In the presence of risk factors, such as cGVHD, prophylactic treatment for toxoplasmosis should be reinstituted; Trimethoprim-sulfamethoxasole most probably prevented earlier reactivation of toxoplasmosis in our patient.