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X Yataganas

Publications and source records attributed to X Yataganas.

12 recordsLinked to original sources
PubMed1991

The effect of recombinant alpha-interferon on natural killer cell activity and clinical course in patients with myelodysplastic syndrome.

Thirteen patients with myelodysplastic syndrome (MDS) were included in this study and consented to treatment with recombinant alpha-interferon (a-IFN). These patients were subclassified: six as RAEB, one as RAEB-T and six as CMML. T-cell subsets and natural killer cells were identified in the peripheral blood with the use of monoclonal antibodies and natural killer cell activity (NKa) was assayed before, during and after a-INF treatment. The treatment schedule consisted of 2.0 MU/m2 sc t.i.w. continuously for the three months. Prior to treatment, NKa was found decreased in 11 of 13 patients as compared to that of normal individuals. Following a-IFN administration, a rise of NKa was observed in eight of the eleven patients. In those who responded, a-IFN was continued for 1 to 21 months. Alpha-IFN treatment was myelosuppressive for most of the patients, but transient increase of the number of neutrophils and platelets was observed in 3 and of the reticulocytes in one patient. Disease progression was recorded in 9/13 patients (69%) at a median time of 17.3 months. The median overall survival was 30.5 months (range 7.5 to 65+ months). No evidence of a relationship was found between the rise in Nka and the limited clinical improvement observed. Two NKa responders under continuous a-IFN treatment are in stable clinical condition for 36+ and 65+ months. The study provides only limited evidence that a-IFN may improve the clinical course of patients with MDS.

Aged↗
PubMed1991

alpha Interferon treatment of essential thrombocythaemia and other myeloproliferative disorders with excessive thrombocytosis.

The effect of recombinant interferon alfa-2b on platelet count, thrombocytosis-associated symptoms and marrow fibrosis was studied in 18 patients with myeloproliferative diseases and associated thrombocytosis (nine with essential thrombocythaemia, three with polycythaemia vera, three with myelofibrosis and three with chronic myelogenous leukaemia). A reduction of the platelet count below 600 x 10(9)/L was achieved in 94%, and below 400 x 10(9)/L in 77% of the patients within 8 to 330 days of treatment. The selective thrombocytosis-reducing effect of alpha interferon was maintained for long periods of time in most patients without serious side effects. Thrombocytosis-associated symptoms were relieved once the number of platelets was reduced to near normal levels. Marrow reticulin content was found to be reduced after treatment in two of the seven patients studied. Side effects of alpha interferon were flu-like symptoms, which usually subsided within 7 days of treatment.

Adult↗
PubMed1991

Randomized clinical trial comparing ceftriaxone/amikacin versus ceftazidime/amikacin as initial therapy of febrile episodes in neutropenic patients.

Neutropenic patients with underlying hematologic (usually malignant) diseases were randomized to receive either 2 g ceftriaxone once daily +0.5 g amikacin or 2 g ceftazidime twice daily +0.5 g amikacin b.i.d. when fever was higher than 38 degrees C and granulocyte counts less than 0.5 x 10(9)/l. 25 patients were included in each treatment group. Successful outcome of treatment was observed in 28 (13/15) and in an additional 5 (2/3) patients after modification of the therapy. Tolerability was excellent in both groups.

Adolescent↗
PubMed1991

Effect of recombinant alpha-interferon administration on peripheral blood lymphocyte subpopulations and natural killer cell activity in patients with refractory anemia with excess of blasts.

Peripheral blood lymphocyte subpopulations and natural killer cell activity (NKa) were determined in 7 patients with refractory anemia with excess of blasts (RAEB) subjected to alpha-interferon (alpha-IFN) administration. Patients received subcutaneously 3 MU alpha-IFN three times a week for 3 consecutive months, and studies were done just before and one month after the cessation of alpha-IFN administration. Before starting alpha-IFN, the patients NKa was severely reduced in relation to control (p less than 0.001), natural killer (NK) cells (CD16+ cells) and suppressor/cytolytic T-lymphocytes (CD8+ cells) were within normal range, while helper/inducer T-lymphocytes (CD4+ cells), as well CD4+/CD8+ cell ratio, were significantly reduced (p less than 0.001 and p less than 0.001, respectively). Significant diminution was also noted in B-lymphocyte numbers (CD19+ cells) (p less than 0.05). Following alpha-IFN administration, NKa values increased significantly in comparison to pre-IFN values (p less than 0.05), but failed to reach normal range. CD3+ cells and CD8+ cells decreased (p less than 0.05 and p less than 0.02), while CD4+ cells and CD4+/CD8+ cell ratio did not change significantly. A statistically significant rise was observed in CD16+ cells (p less than 0.05). The sensitivity of NK-cells against alpha-IFN and interleukin-2 (IL-2) added in vitro, was also significantly increased (p less than 0.05). The findings indicate that alpha-IFN administration may affect some disturbed immunologic functions in patients with RAEB, but further studies are needed to elucidate the mechanism and the extent of this action.

Aged↗
PubMed1977

Angio-immunoblastic lymphadenopathy terminating as Hodgkin's disease.

The clinical course of a 33-year-old man with generalized lymphadenopathy bearing all physical, laboratory and histologic characteristics of "angio-immunoblastic lymphadenopathy with dysproteinemia" (AILD) is described. Therapy was without significant benefit and the patient died 22 months after initial diagnosis. At autopsy in addition to the characteristic cellular polymorphism of AILD, numerous Hodgkin's cells and Sternberg-Reed cells were identified in the lymph nodes and spleen. Pleomorphic cellular infiltrates containing an increased number of immunoblasts and some giant cells were found also in the portal spaces of the liver. The evolution of Hodgkin's disease (H.D.) from AILD suggests that the latter may have represented a reaction to the agent which causes H.D..

Abdomen↗
PubMed1977

Beta-glucuronidase activity of lymph node imprints from malignant lymphomas and chronic lymphocytic leukaemia.

beta-Glucuronidase activity was semiquantitatively estimated in the cells of lymph node (LN) imprints from patients with Hodgkin's disease (HD), diffuse non-Hodgkin's lymphomas, chronic lymphocytic leukaemia (CLL), normal lymph nodes, and benign lymphadenopathies. In addition, in some of these cases beta-glucuronidase activity was semiquantitatively determined in peripheral blood smear lymphocytes. The beta-glucuronidase score (betaGS) was very low in the cells of the LN imprints from patients with diffuse non-Hodgkin's lymphomas. The LN lymphocytes of HD had a normal betaGS independently of the histological subtype of the disease, while in the LN imprint of CLL the enzyme activity was low, normal, or high. The betaGS of the lymphocytes in LN imprints of normal controls and HD were in general significantly lower compared with he lymphocytes of the peripheral blood smears in the same cases. The relation of our findings to the B and T cell origin of malignant lymphomas and chronic lymphocytic leukaemia is discussed.

Acid Phosphatase↗
PubMed1976

Cell kill kinetics with hydroxyurea.

The effects of various concentrations of hydroxyurea (HU) on a human lymphoid cell line in exponential growth phase have been studied using a combination of methods, including determination of the total and viable cell counts; the cells relative DNA content, measured in a flow microfluorimeter after staining with a fluorescent Feulgen technique; the mitotic index; and the percentage of cells incorporating thymidine-3H (TdR-3H) during brief and continuous exposure to the isotope both in the presence and absence of colcemid. A significant redistribution of the cells in the various phases of the cell cycle occurred during the first 24 hr of continuous treatment with 10(-3) M and 10(-2) M HU as follows: (1) division of cells in G2; (2) depletion of mid and late S phase cells due to early cell death; (3) movement of most G1 cells at a normal rate into early S phase where they accumulate; and (4) arrest of the remaining cells in G1, which represented the surviving population after treatment for 96 hr or longer. After removal of the drug, the cell fraction blocked in early S phase progressed semisynchronously through S, but many of the cells were unable to complete division. Their capacity to recover depended on the drug concentration and duration of exposure, but in general the cellular injury caused by HU was more reversible than that caused by "equivalent" concentrations of arabinosylcytosine.

Cell Count↗
PubMed1976

Quantitative cytochemistry of glycogen in blood cells. Methods and clinical application.

Quantitative glycogen determinations can be made in single blood and bone marrow cells, using microspectrophotometry or microfluorometry after staining with variants of the periodic acid--Schiff (PAS) reaction. These PAS variant reactions generally do not indicate the presence of non-glycogen PAS-positive substances, known to be prevalent in various hematopoietic cells, possibly due to masking of reactive groups. The specificity of the reaction in blood cells was ascertained by alpha-amylase digestion, which removed more than 95% of the PAS-positive material. Calibration of the PAS reaction was undertaken with a microdroplet model of pure leukocyte glycogen. The glycogen amounts in the droplets were determined by microinterferometry, the droplets were stained with a variant PAS reaction, and the total extinction of the reaction product in the stained droplets was determined by microspectrophotometry. The extinction coefficient (k) was obtained from the equation k equals Etot divided by M where (Etot) is the total extinction as determined by microspectrophotometry and (M) the dry glycogen amount as determined by microinterferometry. The microinterferometric dry mass determinations were calibrated by X-ray absorption in order to obtain the absolute amounts of glycogen. For practical purposes a reference system was made of normal neutrophil leukocytes. The glycogen content in the reference neutrophils was first determined with the micromodel. These neutrophils, now with a known glycogen amount, were stained with the PAS reagents and measured microspectrophotometrically in parallel with cells containing an unknown glycogen amount. Alternatively, the staining was made with a fluorescent PAS reaction, and the glycogen content determined by microfluorometry. Both methods appeared suitable for determining the glycogen content of blood cells from patients with various diseases, though the microfluorometric method was preferable for measurements of small amounts of inhomogeneously distributed glycogen. The mean glycogen content of normal neutrophil leukocytes was found to be 13.6 times 10(-12) g. The content was increased in infectious diseases such as pneumonia and tonisillitis, as well as in polycythemia vera and myelofibrosis, while low amounts were found in untreated chronic myelocytic leukemia. In chronic myelocytic leukemia in remission, the glycogen content of mature neutrophils had completely normalized. Erythroblasts normally do not contain detectable amounts of glycogen. However, in certain diseases such as beta-thalassemia and Di Guglielomo's syndrome, appreciable amounts of glycogen accumulate in the erythropoietic precursor cells. In beta-thalassemia this was associated with an arrest in the proliferation of early polychromatic erythroblasts, which accumulate glycogen in the G1 phase of the cell cycle. In all these diseases quantitative glycogen determinations in the blood cells have diagnostic importance.

Autoradiography↗
PubMed1975

Proliferative kinetics of central nervous system (CNS) leukemia.

The proliferative kinetics of the leukemic cells in the cerebrospinal fluid (CSF) were studied in three adults with CNS leukemia after 18 and 8 months while receiving an intensive treatment regimen. One (J.L.) had acute myeloblastic leukemia and developed CNS disease after 5 years' treatment with arabinosylcytosine and 6-thioguanine. All were in marrow remission at the time of study. G.H. had had no therapy for CNS disease, A.K. had had intrathecal methotrexate 2 months previously, and J.L. had recently completed radiotherapy (1900 R) to the head. An Ommaya reservoir was placed in a lateral ventricle and 3H-thymidine was injected into the resrvoir every 12 hours for 10 days; samples of cells were obtained by lumbar puncture periodically for autoradiography. In all patients the flash 3H-thymidine labeling index (LI) of the leukemic cells was less than 2% (determined in vitro) and the mitotic index less than 0.1%. After 10 days of 3H-thymidine injections in vivo, the LIs of the leukemic cells were 55%, 36%, and 21% in G.H., A.K., and J.L., respectively. These findings indicate that leukemic cells may proliferate very slowly in the CNS, and stress the difficulty of eradicating CNS leukemia with chemotherapeutic agents which are only active against proliferating cells.

Acute Disease↗
PubMedDate not supplied

Defective mitogen-induced cellular cytotoxicity in myelodysplastic syndromes. Recovery after alpha-interferon administration.

Peripheral blood mitogen - induced cellular cytotoxicity (MICC) and natural killer- cell cytotoxicity (NKCC) were assessed in 25 patients with myelodysplastic syndromes (MDS). Both MICC and NKCC were examined under the same experimental conditions using the 18 hr chromium release assay, except that cultures for MICC were stimulated in vitro by the addition of phytohemagglutinin (PHA). Patients' MICC was found significantly reduced, in relation to controls (p less than 0.001), but significantly higher than patients' NKCC (p less than 0.001). Furthermore, patients CD3+ cells and CD4+ cells, as well as the CD4+/CD8+ ratio, were significantly decreased (p less than 0.01, p less than 0.001 and p less than 0.001, respectively), while CD8+ cells and CD16+ cells were within normal limits. No relationship was noted between patients' MICC and total lymphocyte count or any lymphocyte subpopulation. In eleven patients who were subsequently subjected to a-interferon (a-IFN) administration, MICC values were found within normal range one month after the cessation of alpha-IFN, while NKCC values were significantly increased (p less than 0.01), but they still remained below the lower limit of the control (p less than 0.001). Percentages of CD3+, CD4+ and CD8+ cells, as well as the CD4+/CD8+ ratio, did not change after alpha-IFN, but the absolute numbers of CD3+ cells and CD8+ cells were significantly reduced. A statistically significant rise was noted in CD16+ cells. Post- IFN rises in MICC did not correlate with lymphocyte subpopulations. The findings indicate that MDS patients display very low MICC, which can be restored by alpha-IFN administration. The cause of this disturbance and the mechanism of its restoration by alpha-IFN remain unclear.

Aged↗