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A case of disseminated infection with Trichosporon capitatum is reported in a 23-year-old patient with acute myeloid leukemia undergoing HLA-mismatched bone marrow transplantation. He was receiving immunosuppressive therapy with cyclosporine and corticosteroids for acute graft-versus-host disease and he was severely neutropenic. While being treated with fluconazole for 28 days for an oropharyngeal candidiasis the patient developed a T. capitatum septicemia. He died despite receiving amphotericin B therapy. Autopsy revealed widespread infection with T. capitatum. The portal of entry was probably the digestive tract in this patient as T. capitatum had been first isolated in the stools.

The frequency of sister chromatid exchange (SCE) was analyzed in bone marrow cells of 16 patients with chronic myeloid leukemia. We have compared the SCE frequency in these patients, in both chronic and blastic phases of the disease, to that of normal individuals. The frequency of SCE in blastic-phase chronic myeloid leukemia patients (mean, 1.86/cell) was significantly lower than that in chronic phase (mean, 2.96/cell), which was in turn lower than that in normal individuals (mean, 4.108/cell). We have used the SCE data to compare the rates of division of the bone marrow cells. Cells from chronic myeloid leukemia patients divided more slowly than did those from normal individuals, those from blastic-phase patients being slowest.

Origin and spread of the chromosomally abnormal cells that appear in chronic myeloid leukemia (CML) after transformation are unknown. Spleen and lymph node may be involved. In 16 patients with CML splenectomy and/or adenectomy were performed before or during the blastic crisis of the disease, followed by a chromosomal analysis of the cells from the removed organ. At the same time, the chromosomes of the blood cell and of the bone marrow were also analyzed. Analyses were done with R banding. The results show that an extramedullary clonal development with duplication of the Ph1 chromosome and other features occurred. From a cytogenetic standpoint, acute blastic phase of CML is frequently characterized by an increased number of chromosomes owing to preferential gain of additional chromosomes. This, then, would clearly point to extamedullary acute transition in CML.

Y chromosome duplication appeared in a patient with chronic myeloid leukaemia (CML) during blastic crisis. Additional chromosome changes were present. Y chromosome duplication may be a minor route of karyotype evolution in CML.

In 4 cases, the probable diagnosis was that of a chronic myeloid leukaemia (CML) in a blast crisis, because of the sudden acute onset and the presence of the Ph 1 chromosome. In each case, however, there were Auer bodies in the blasts, an unusual finding in CML. Cytological and cytochemical examination led respectively to the diagnosis of an M2 acute myeloblastic leukaemia (AML), according to the FAB classification, to that of a pre-leukaemia progressing to an M2 AML, to that of a M3 promyelocyte leukaemia, with numerous monocytes and finally, in one case, the diagnosis lay between a possible acute crisis of CML with Auer bodies or an acute myelo-monocyte leukaemia. These atypical findings did not conform to the classic picture of CML and cannot be classified as such in spite of the presence of the Ph 1 chromosome. To consider them as true CML would be to run a risk of distorting the haematological evolutive and therapeutic aspects of this disease.

We saw bone marrow necrosis in a case of acute myelomonocytic leukemia. The diagnosis was made during the patinet's life, and the bone marrow microcirculation was studied immediately postmortem. Histology and injection of the bone marrow arteries showed an acute microcirculation failure. The pathogenesis and possible relationship with soluble immune complexes was studied.