Successful treatment of invasive pulmonary aspergillosis in a patient with acute leukaemia.
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Biomedical subjects
Publications and source records attributed to S R McCann.
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A red-cell pyruvate kinase (PK) variant from an individual with congenital non-spherocytic haemolytic anaemia was characterized according to the procedure recommended by the International Committee for Standardization in Haematology (ICSH 1979). Activity of the mutant enzyme in haemolysates was one fifth of that found in normal control subjects. The electrophoretic mobility and thermostability of the mutant enzyme were lower than those of the normal enzyme and its apparent affinity for phosphoenolpyruvate was higher.
27 patients with B-CLL were evaluated before treatment. All patients were staged according to the 'Rai' classification and the following cell populations were studied B cells, surface immunoglobulin characteristics, mouse red cell rosettes, T cells (E+) and T cell subsets (TG and TM). Serum immunoglobulins were measured in all patients. The relationship between the clinical stage and the above immunological parameters was studied and the possible role of splenic involvement in the finding of abnormal ratios of T cell subsets in the peripheral blood of patients with B-Cell is discussed.
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Four patients in a leukaemic ward were infected with multi-resistant Pseudomonas aeruginosa. Similar organisms were found in the environment and it appeared that lapses in aseptic routine contributed to the outbreak. Serological, bacteriophage and pyocin-typing revealed that a fifth patient was infected with a distinct strain, but agarose gel electrophoresis indicated that all patient and environmental strains carried the same plasmid. The plasmid had a molecular weight of 47 (s.d. +/- 2) X 10(6) dal and was transfer deficient. It conferred resistance to carbenicillin, gentamicin, kanamycin, streptomycin, sulphonamide, tetracycline and tobramycin and determined an aminoglycoside adenylyltransferase active against amikacin in-vitro and not in-vivo. Spread of this non-transferable plasmid to a different Ps. aeruginosa strain and dissemination of multi-resistant organisms led to serious infections.
Fifteen patients with chronic lymphocytic leukaemia (CLL) were studied. The diagnosis was made by a combination of clinical findings, peripheral blood morphology and cell surface markers. The Rai clinical staging (Rai et al, 1975) was used to classify all patients. Serum immunoglobins, B and T cell lymphocytes, TG and TM cell populations were evaluated in all patients before commencing treatment. No correlation was found between clinical staging and the presence or absence of hypogammaglobulinaemia. The ratios of TG to TM cells were abnormal in all patients and this abnormality paralleled the stage of the disease. While there was significant difference in the proliferative responses of highly purified T cells from patients and controls at 1 micrograms and 2 micrograms/ml of Concanavalin A (Con A) (P values = P less than 0.005 and P less than 0.01 respectively). There was no significant difference at dose 5 micrograms/ml. The ability of T cells to suppress allogeneic PBMC responses to Con A was dependent on T cell purification procedures. The significance of the results and the possible role of T cells in the pathogenesis of CLL is discussed.
Four patients with chronic lymphocytic leukaemia were treated with splenic irradiation, 100 rads per week for 10 weeks. No patient had received prior therapy of any kind. All patients showed an excellent clinical response in terms of decrease in lymphocyte count in blood and bone marrow and decrease in lymph node and spleen size. B and T cell populations returned to normal in all patients as did the ratio of TG to TM cells. Two patients showed an increase in IgM levels, but the overall pattern of immunoglobulins showed no consistent change following treatment. No toxicity was incurred during treatment. We conclude that splenic irradiation is a safe and effective treatment of previously untreated patients with CLL and is associated with a return to normal of lymphocyte sub-populations. The role of the abnormal T cell population in the pathogenesis of the hypoimmunoglobulinaemia remains unclear.
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Acute myelofibrosis (AM) or malignant myelosclerosis is a myeloprofilerative syndrome in which bone marrow fibrosis is associated with a proliferation of immature myeloid cells. In four patients with typical AM, investigated by the platelet-peroxidase reaction at ultrastructural level, the blast cells were found to be megakaryoblasts. One patient, treated with the drug combination DAT, achieved a complete remission of 5 mo duration. This study supports the view that megakaryoblastic leukemia is the most frequent underlying cause of AM and proposes that it should be classified as a form of acute myeloid leukemia.