Secondary cutaneous plasmacytoma.
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Biomedical subjects
Publications and source records attributed to M Cavo.
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The glucocorticoid receptor (GR) quantitation by a whole-cell assay and/or cytosol technique and the in vitro sensitivity to steroids have been assessed in peripheral blood cells from normal donors and patients with chronic lymphatic leukemia (CLL), acute lymphoblastic leukemia (ALL), lymphosarcoma cell leukemia (LSCL), acute nonlymphatic leukemia (ANLL), and chronic myeloid leukemia (CML). Within the lymphoproliferative diseases, ALL cells exhibited the highest GR concentration (regardless of the method used) and the highest in vitro inhibition of spontaneous [3H]thymidine ([3H]TdR) uptake by glucocorticoids. A significant relationship between GR concentration (whole-cell assay) and in vitro sensitivity to dexamethasone was also found. On the contrary, CLL cells presented the highest sensitivity to glucocorticoids in PHA-stimulated cell cultures. Cells from the only two ALL patients who did not undergo a remission after glucocorticoid-inclusive chemotherapy had both the lowest in vitro sensitivity to dexamethasone and the lowest GR concentration with whole-cell assay. Concerning myeloid leukemia, ANLL patients had GR concentrations slightly higher than those found in the ALL group but exhibited the lowest degree of inhibition of spontaneous [3H]TdR uptake by dexamethasone (stimulatory effects occurred in some cases). CML cells exhibited an inhibition degree by in vitro glucocorticoids significantly higher than that of ANLL cells but not different from that of lymphoproliferative diseases. No clear relationship among GR pattern, in vitro cell sensitivity to glucocorticoids, and clinicohematologic parameters was observed in myeloid leukemia-bearing patients.
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One-hundred and eighty-eight patients with chronic lymphocytic leukemia were analyzed for prognosis based on Rai's staging system. It was found that stages I and II were not homogeneous as to prognosis. Stage II patients presenting with isolated splenomegaly had a long survival and were pooled with stage 0 patients (low risk group, 30% of cases, relative death rate 0.24, median survival greater than 10 yr). Stages I and II patients with a lymphocyte count higher than 40 x 10(9)/liter had a short survival and were pooled with stages III and IV patients (high risk group, 39% of cases, relative death rate 1.91, median survival 3.3 yr). Stages I and II patients with a lymphocyte count lower than 40 x 10(9)/liter made up an intermediate or standard risk group (31% of cases, relative death rate 1.00, median survival 6.2 yr). This modified staging system applied successfully to both old and young patients (more and less than 60 yr old, respectively).
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Human recombinant granulocyte-macrophage colony-stimulating-factor has been employed, on a compassionate basis, in 14 hematological patients in order to reduce the duration of the neutropenic period after high-dose chemotherapy for the treatment of hematological malignancies (7 traditional CHT courses, 7 autologous bone marrow transplantations). The compound was administered intravenously by 6-hour infusion at a dose of 5 microgram/kg/day until the patient reached at least 1000 PMN in the peripheral blood. Eleven out of the 13 evaluable patients showed a significative improvement in hemopoietic recovery, even though in CHT patients hematological reconstitution was higher in terms of PMN counts. The ABMT patients, however, showed a faster myeloid recovery than that obtained both in a group of 14 NHL and in a series of 8 MM previously submitted to ABMT in our Institution. Moreover the increase in peripheral neutrophils appeared to be stable, since it was maintained throughout one month after the end of rhGM-CSF therapy. We did not observe effects on platelet or erythrocyte recovery. We conclude that rhGM-CSF is active in accelerating the recovery of myelopoiesis, without significant toxic or collateral effects.
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BACKGROUND: Vincristine and anthracyclines are first-line agents for the treatment of multiple myeloma (MM). P170-related multidrug resistance (MDR) may influence the response to these drugs. MATERIALS AND METHODS: P170 expression of bone marrow plasma cells was assayed by immunocytochemistry (alkaline phosphatase anti-alkaline phosphatase technique) with the MRK-16 monoclonal antibody. A case was considered positive if one per cent or more of plasma cells stained as strongly as positive controls. RESULTS: Six of 17 (35%) cases in relapse and 18/72 (25%) at diagnosis were MDR positive. MDR positivity was not found in micromolecular MM and was significantly associated with the serum beta 2-microglobulin level. Response to treatments including dexamethasone, vincristine and doxorubicin, or idarubicin, or mitoxantrone was independent of MDR positivity (50% in positive cases vs. 56% in negative ones). CONCLUSIONS: The detection of P170 in bone marrow plasma cells with the currently available methodology is not likely to predict response to treatments that include vincristine, anthracyclines or mitoxantrone. Further studies are required to evaluate the relevance of P170-related MDR to the development of MM therapy.
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We report on two patients with Ph+ chronic myeloid leukemia (CML) in chronic phase who developed severe thrombocytopenia during treatment with interferon-alpha 2A (IFN-alpha 2A). In both cases, we detected the presence of platelet-associated antibodies (PAIg) by autoimmune flow cytometry. We postulated an immune mediated platelet destruction mechanism; corticosteroid therapy was employed and interferon therapy was withdrawn, resulting in an increase in platelet count and a reduction of PAIg. Our observation reports the detection of PAIg associated with IFN-alpha 2A therapy in CML and suggests that this immunomodulant drug could induce thrombocytopenia through a mechanism other than antiproliferation.