Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society最新文献

Immunophenotypes and genotypes were analyzed for a case of chronic myelocytic leukemia in blast crisis (BC). In the early stage of BC (early BC), the blasts consisted of lymphoid-myeloid cells, but in the later stage of BC (late BC), they were myeloid cells, morphologically and phenotypically. On Southern blot of DNAs in early BC, a single rearranged fragment of immunoglobulin heavy chain (IgH) genes was detected, whereas IgH genes were in germline configuration in both initial chronic phase and late BC. A clone which had a rearranged IgH gene in early BC, was considered to have co-existed with a clone which had the germline IgH gene. Analysis for bcr genes confirmed that the chronic phase as well as early and late BC were of the same clonal origin. Phenotypic and immunogenotypic analyses, however, revealed that at least two secondary clones emerged from the primary clone. The therapeutic effect against lymphoid population among mixed crisis cells could be evuluated not only phenotypically but also genotypically.

Fifty one patients with myelodysplastic syndromes (MDS) treated between September, 1985 and October, 1988 were retrospectively studied. The incidence of cancer was compared with that in the Cancer Registry population of Japan for the same age and sex distribution. In this series, 4 cancers were observed. The risk of cancers developing in patients with MDS was 4.65 times that for an age- and sex-matched population.

This experiment was undertaken to study the possible difference in the intestinal iron absorption efficiency among iron compounds with different electric charges. Observation of rats given oral administration of 59Fe-labeled cationic cacodylate ferric (59Fe-Cac) colloid, anionic citrate ferric (59Fe-Cit) colloid, cationic 59Fe-Cac complex and anionic 59Fe-Cit complex revealed that iron absorption was more efficient in the 59Fe-Cac colloid, moderate in the 59Fe-Cac complex, low in the 59Fe-Cit colloid, and lowest in the 59Fe- cases given 59Fe-Cac colloid and 59Fe-Cac complex, a very high ratio activity was found in the liver and in the erythrocyte or hemoglobin in circulating blood, while the blood plasma, bone marrow, and spleen were low in activity. Histochemical observations of rat jejunal mucosa exposed independently for 10 min to the Fe-Cac colloid, anionic Fe-Cit colloid, and Fe-Cac and Fe-Cit complexes revealed that the cationic Fe-Cac colloid and Fe-Cac complex adhered to the luminal surface of the mucosa covering the apical area of villi with some ferric iron in the capillaries, while the anionic Fe-Cit colloid and complex did not adhere to the epithelial cells and were found free in the jejunal lumen. Electron microscopy revealed that Fe-Cac colloid particles were taken into epithelial cells by pinocytosis at the webs of microvilli, moved to the Golgi area, exocytosed to the intercellular spaces, and then translocated into the basement membrane toward blood capillaries.

A human cell line, designated as NISI, was established from a patient with erythroleukemia (FAB M6). The presence of a chromosome marker in NISI line indicates that it is derived from the leukemic clone which bears the common marker. The cell line shows morphology of immature erythroblast and has myelocytic properties from surface immunophenotyping. The differentiation capacities of NISI cells by three inducers (hemin, phorbor 12-myristate 13-acetate and 1-25-(OH)2D3) were evaluated. Hemin treated cells showed a significant increase in erythroid antigen expression as well as an increase in number of benzidine positive cells. Phorbor 12-myristate 13-acetate treated cells demonstrated a significant increase in megakaryocytic antigen expression, and a slightly diminished CD36 antigen expression. The surface markers of 1-25-(OH)2D3 treated cells did not demonstrate significant changes. NISI cell line, a human erythroleukemia cell line, still retained the tendency for differentiation to megakaryocytic lineage.

Urokinase type plasminogen activator (u-PA) was purified from three different chest fluids obtained from patients with liver cirrhosis and pleuritis, aplastic anemia and pneumonia, and lung tumor, and the relationship between molecular weight and plasminogen activator (PA) activity was examined by zymography. The molecular weights of u-PAs from the chest fluids were 200 Kd, 150-180 Kd, 95 Kd, 55 Kd, 44 Kd, 33 Kd and 14 Kd, and PA activity was observed at molecular weights of 95 Kd, 55 Kd and 33 Kd. Fibrin binding of u-PA was observed at molecular weights of 55 Kd and 33 Kd.

We administered low-dose cytosine arabinoside (Ara-C) to 32 newly diagnosed acute non-lymphocytic leukemia (ANLL) patients, 10 mg/m2 twice a day for 14-21 days, by subcutaneous injection or continuous intravenous infusion. CFU-GM of bone marrow cells were performed before low-dose Ara-C in some patients. Patients ranged in age from 21 to 78 years old. Ten showed complete remission and 16 partial response. The pretreatment CFU-GM pattern did not reflect the response to low-dose Ara-C. The major hematological effect of the treatment was myelosuppression, and most patients required platelet transfusion and the administration of antibiotics. Our study suggested that low-dose Ara-C treatment benefits some ANLL patients.

We report a case of acute promyelocytic leukemia (APL) coexisting with insulinoma in a 61-year-old female. Two years before the onset of APL, she was diagnosed as having insulinoma and underwent resection of the body and tail of the pancreas, but no insulinoma was found in the resected pancreas. The clinical symptoms of hyperinsulinism, however, continued after the operation and were treated with diazoxide (100 mg daily, 37 g in total) for about two years until the onset of APL. During the induction therapy for APL, she died of hemorrhage and infection; autopsy revealed the presence of insulinoma (13 X 9 mm in size) in the residual pancreas head. This is the first case report of coexistence of APL and insulinoma.

We treated a patient with chronic granulocytic leukemia (CGL), in the accelerated phase by intensive chemotherapy followed by the infusion of cryopreserved peripheral blood buffy-coat cells. The cells had been stored for 32 months. The chemotherapy consisted of daunorubicin 40 mg X 2 days, vincristine 2 mg X 1 day, cytosine arabinoside (Ara-C) 200 mg X 6 days and prednisolone 30 mg X 7 days in the first week, then Ara-C 3 g/m2 X 3 days and cyclophosphamide 60 mg/kg X 2 days in the second week, but reversion to the chronic phase was not achieved. Therefore, total body irradiation (TBI) was added to repeated intensive chemotherapy followed by infusion of the remaining cells. Marrow recovery was good. The patient is currently alive and has been in the chronic phase for 22 months. This preliminary result indicates that this therapy may be tried soon after transformation in CGL and that TBI is an important part of therapy in BMT in the accelerated or blastic phase of CGL.

Gamma interferon (gamma-INF) production was studied and two-color fluorescence flow cytometry analysis was done on the peripheral blood mononuclear cells (PBMC) in allogeneic bone marrow transplant recipients. Gamma INF was not detected in any patients within a year after transplantation whether PBMC was stimulated with PHA or not. A year after transplantation, gamma-INF was produced in the normal level in the stimulated and unstimulated PBMC. The number of suppressor-inducer T cells (CD4+2H4+) was decreased and that of suppressor T cells (CD11+CD8+) was normal. The numbers of helper-inducer T cells (CD4+4B4+) and helper T cells (CD4+2H4-) were normal. The numbers of activated helper-inducer T cells (CD4+HLA-DR+) and suppressor-cytotoxic T cells (CD8+HLA-DR+) were elevated. In the NK cells, Leu7+ CD16-cells were elevated, whereas Leu7+CD16+ cells and Leu7-CD16+ cells were normal. Leu7+CD8+ cells were elevated. These results indicated immunodeficiency after transplantation.

To determine the mechanism by which haematopoiesis is suppressed in aplastic anaemia, the effect of the sera from 6 patients on the granulopoietic precursors (colony-forming units in culture; CFU-C) was studied in vitro. Addition of the sera from 2 patients significantly suppressed CFU-C. The suppressive effect of the sera on CFU-C was inhibited by the addition of 1.5 NU/ml of anti-gamma-IFN antibody. In another patient, anti-gamma-IFN antibody increased autologous CFU-C although the serum of the patient did not suppress CFU-C. Serum gamma-IFN levels of all patients were under 2 IU/ml. The above findings suggest that humoral factors inhibit haematopoiesis in some patients with aplastic anaemia, and that gamma-IFN plays a role as an inhibitor even at a low concentration.