[Changing complement sensitivity and PNH red cell population during the clinical course in a case of PNH with hypoplastic bone marrow].
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Biomedical subjects
Publications and source records attributed to S Kariyone.
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An 8;21 chromosome translocation was found in cells from myeloblastomas of two acute myeloblastic leukemia (AML) patients. In one patient, a sudden onset of paraplegia, which was caused by an epidural myeloblastoma in the thoracic vertebral canal, was the initial symptom of the disease and that of the first relapse. In the other, myeloblastomas, which occurred in the breasts during a hematologic remission, heralded the first relapse. Karyotypes of tumor cells obtained from both patients showed the t(8;21) and additional chromosome abnormalities. These findings, together with earlier experience and reports in the literature, indicate that myeloblastoma may be unique to the 8;21 translocation, and that certain chromosomal abnormalities additional to the t(8;21) may be necessary for the tumor formation.
A case of promyelocytic crisis of chronic myelogenous leukemia is reported. The amount of promyelocytoid blasts in peripheral blood and bone marrow were 70% and 58%, respectively, at the onset of the blastic phase. Cytogenetic analyses during the blastic phase did not reveal t(15;17); however, t(3;21) in addition to the t(9;22) in the karyotype of bone marrow or peripheral blood cells was observed.
We performed a cytogenetic analysis of eosinophilic colonies grown from bone marrow culture of a patient with acute myelogenous leukemia (FAB-M2) associated with t(8;21). The bone marrow, in which 50.2% myeloblasts and 5.6% eosinophils were observed, gave rise to eosinophilic colonies, as well as colonies consisting of immature myeloid cells. The cytogenetic analyses of the colonies were performed on two occasions. The first study revealed t(8;21) in 15 of 16 metaphases in randomly plucked colonies from a dish, in which 65% of the total colonies were those consisting of immature myeloid cells and 35% were eosinophilic colonies identified by positive staining with Luxol-Fast-Blue. The second study, in which eosinophilic colonies were selectively plucked for cytogenetic analysis, showed Cq- and Gq+ markers, which were considered to be t(8;21), in all metaphases (6/6). Our present study strongly suggests that an involvement of the eosinophilic series in the leukemic process of this patient.
A 46-yr-old woman was diagnosed as having M3 variant leukaemia in FAB subclassification with disseminated intravascular coagulation (DIC) and the 15;17 translocation. Immunologic examinations revealed that the blast cells exhibited monocytic (Ia+, Mo1+, Mo2+, My4+, My7+ and My9+) and T-lymphocytic (OKT11+, Leu4+ and Leu5b+) immunophenotype, with probably a biphenotypic population of cells. Expression of monocytic phenotype on the blast cells suggests that M3 variant includes a subtype with monocytic characteristics, and may be related to the morphologic monocyte-like feature of that of M3 variant.
We identified bone marrow megakaryocytes by an immunocytochemical technique using a monoclonal antibody (TP80) against platelet glycoprotein IIb-IIIa (GPIIb-IIIa). The immunocytochemical technique using TP80, specific to megakaryocytes, enabled us to observe cellular morphology and immunological reaction under light microscopy, and permitted quantitative assessment of megakaryocytes. In normal marrow, TP80 labelled 22 +/- 5 megakaryocytes/10(4) mononuclear cells (mean +/- 1 SD, n = 14). In addition to typical large megakaryocytes, small immature megakaryocytes (less than or equal to 20 micron) were recognized in 10-15% of total megakaryocytes. 4 out of 18 patients with acute myeloblastic leukaemia and 9 of 10 patients with myelodysplastic syndrome showed increased numbers of megakaryocytes. In these patients, cell size distribution was abnormal, i.e., most of the megakaryocytes consisted of small, atypical megakaryocytes. None of the patients with acute lymphoblastic leukaemia showed increased megakaryocytes. Immunocytochemical identification of megakaryocytes using a specific antibody is useful to quantitate the megakaryocytes and to detect the proliferation of atypical megakaryocytes in several leukaemic conditions.
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Cytogenetic analysis was performed on colonies from erythroid burst-forming units (BFU-E) derived from bone marrow (BM) cells of a Ph-positive acute lymphocytic leukemia (Ph+ ALL) patient. A normal diploid karyotype was revealed in all 15 metaphases that could be analyzed in the erythroid colonies. Previous cytogenetic analyses of erythroid colonies obtained from BM cells of patients with Ph+ chronic myelogenous leukemia (CML) revealed that Ph-positive karyotypes were predominant in all 11 cases. Two of them were also examined in blastic phase (BP) and showed 100% Ph+ cells in BFU-E-derived colonies. The present findings suggest that the leukemic process of Ph+ ALL does not involve the erythroid series, which is in contrast to the involvement in CML. This is considered to be a fundamental difference between Ph+ ALL and the blastic phase of CML (BP CML). Clinically, cytogenetic analysis of erythroid colonies from BM cells may constitute a valuable approach for the differential diagnosis between Ph+ ALL and the BP of Ph+ CML.
The kinetics of 111Indium-oxine-labelled autologous blood lymphocytes were studied in normal subjects and 10 patients with chronic lymphocytic leukaemia (CLL). In both normal and leukaemic subjects, intravascular survival of lymphocytes was characterized by two exponential decreases, the first being a rapid one and the second slow phase. T 1/2 of the second phase for normal T lymphocytes (52.0 +/- 3.2 h: mean +/- SEM) was longer than that for B lymphocytes (31.6 +/- 2.8 h). T 1/2 of the second phase in patients with CLL was 15.1 to 192.6 h, which correlated well with the clinical stage of CLL by the Rai classification. Body surface scanning revealed prominent splenic accumulation of labelled cells in normal individuals and patients with CLL. Lymph node visualization was recognized in all patients with T-cell CLL; however, there was no visualization in 8 of the 9 patients with B-cell CLL. The longer survival time and splenic and lymph node visualization suggest that an expansion of the extravascular lymphocyte pool may be important in the pathophysiology of CLL.