Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pattern of changes in neutrophil myeloperoxidase (MPO) before, during and after bacteraemia was studied in 34 patients recovering from autologous bone marrow transplantation for relapsed Hodgkin's disease and non Hodgkin's lymphomas. Thirteen patients received haemopoietic growth factors (7 received M-CSF, 3 received G-CSF and 3 GM-CSF). The mean peroxidase index (MPXI) produced as part of a routine FBC performed by a flow cytochemistry blood autoanalyser (Technicon H*1) was used as a parameter to assess the MPO and subsequently the azurophil degranulation. The manufacturer's normal values for MPXI range from -10 to +10. Median MPXI on the day of documented bacteraemia was just below normal in the control and M-CSF groups (-10.8 and -8.9 respectively), but it was much below normal in the G-CSF (-16.5, P < 0.05) and even lower in the GM-CSF group (-39.6, P < 0.02); this correlated well with the decreased bacteraemia incidence in the last two groups. Although contact of neutrophils with bacterial chemoattractants resulted in primary degranulation in all groups, the pattern of changes in MPO content was different, suggesting that neutrophils primed in vivo with various haemopoietins respond to the challenge of microbial agents via different pathways.
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PMID:Patterns of primary degranulation as indicated by the mean myeloperoxidase index (MPXI) during bacteraemia in lymphoma transplants treated with growth factors. 128 46

Neutrophil myeloperoxidase activity has been studied in twenty one patients diagnosed with Hodgkin's disease. The presented data indicate no differences in total MPO activity, whereas we observed some differences in the percentage of granulocytes with different degree of scores. Changes in the intensity of reaction may indicate the possibility of exocytosis as a mechanism releasing MPO from the cell to the surrounding area. In peripheral, circulating neutrophils, such a phenomenon seems to be of no avail and may disorganise anti-cancer defence.
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PMID:The activity of neutrophil myeloperoxidase in patients with Hodgkin's disease. 171 88

Immunohistochemical detection of intracellular myeloperoxidase, a major constituent of primary granules of neutrophilic myeloid cells, was determined in paraffin sections of 161 specimens using a rabbit polyclonal antibody to human myeloperoxidase and an indirect immunoperoxidase technique. In normal tissues and in a variety of myeloproliferative disorders, myeloid cells of both neutrophilic and eosinophilic types, at all stages of maturation, exhibited strong cytoplasmic reactivity for myeloperoxidase. Myeloperoxidase was readily detected in myeloblasts and immature myeloid cells of acute myelogenous leukemia, progranulocytic leukemia, monomyelocytic leukemia, erythroleukemia, myeloblastomas, and other hematopoietic disorders. Erythroid precursors, megakaryocytes. other hematopoietic disorders. Erythroid precursors, megakaryocytes, lymphoid cells, mast cells, and plasma cells were nonreactive. Cells of monocytic derivation revealed variable reactivity and were typically weakly positive or nonreactive. In a few specimens, rare histiocytes were reactive, some possibly due to phagocytosed material. Cells comprising the infiltrate of a spectrum of lymphoid malignancies, e.q., lymphoblastic lymphoma or leukemia, chronic lymphocytic leukemia, hairy cell leukemia, non-Hodgkin's lymphomas of T- or B-cell type, and Hodgkin's disease, were nonreactive, as were the non-neoplastic tissues present in these specimens, except for occasional cells of myeloid derivation. Myeloperoxidase was not observed in the neoplastic cells of a wide variety of epithelial tumors and sarcomas, or in the contiguous non-neoplastic tissues. Immunoreactivity for myeloperoxidase was well preserved following fixation in a variety of fixatives, including Zenker's-acetic acid solution (employed for processing bone marrow biopsies), B5 solution, and formalin. Immunohistochemical detection of myeloperoxidase represents a sensitive and highly specific technique for identification of mature and immature myeloid cells in paraffin-embedded tissue.
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PMID:Myeloperoxidase: a specific marker for myeloid cells in paraffin sections. 172 87

A Technicon H-1 hematologic analyzer was used to measure the mean leukocyte myeloperoxidase (MPX) in 160 patients seen in a hematology clinic. The normal range was -15 to +10, which included 95% of 300 consecutive hospitalized patients. No abnormalities in the MPX were found in 35 patients with beta-thalassemia minor, 8 with iron deficiency, 14 with myeloproliferative disorders, 17 with autoimmune disorders, and 37 patients with lymphoma in complete remission. On the other hand 36% (10/28) of lymphoma patients with active disease either at diagnosis or relapse had a MPX of greater than 10 compared to only 2.3% (7/300) in hospitalized patients (P less than 0.001). Increased levels of MPX were found primarily in patients with non-Hodgkin's lymphoma (NHL) of intermediate or high grades, or Hodgkin's disease [56% (9/16) compared to only 8.3% (1/12) in those with low grade NHLs, P less than 0.05]. The MPX levels returned to normal after successful treatment. Of the various chemotherapeutic agents used, only hydroxyurea led to a consistent elevation of the MPX. The authors conclude that MPX is commonly increased in patients with lymphoma and in those receiving hydroxyurea. Further studies are required to determine if the MPX is a sensitive test for relapse in patients with lymphomas who had an elevated pretreatment value.
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PMID:The mean leukocyte myeloperoxidase index in hematological patients. 255 19

This thesis is a survey of nine previously published articles on MPO deficient PMN. The incidences in leukaemia and allied disorders of the presence of this abnormal subpopulation of mature neutrophils and the relationship to clinical course in AML, susceptibility to infections in AML, FAB classification in AML and MDS, cytogenetically defined aberrations in MDS and morphometrical characteristics were investigated. The aims of the studies were to examine the diagnostic as well as the prognostic value of the parameter, to examine the usefulness of the parameter as an predictive indicator of CR and relapse in AML and to examine the concept that MPO deficient PMN may originate from leukaemic precursors. MPO deficient PMN were found to occur in a minor number (less than 4% of the total number of PMN) in normal humans and the incidences of an abnormal number (greater than 4%) were found to be about 40% in AML (I, II, III, IV, VIII), 60% in CML (I, VII), 30% in MPD other than CML (VII) and 30% in MDS (V). The highest incidences in AML were found in the FAB subtypes possessing the most myeloid differentiation potential i.e. FAB M2 and FAB M4 (IV). In ALL, CLL, HCL, Hodgkin's disease, anaemia not related to leukaemia and leukaemoid reactions the incidences all were 0% (I, unpublished data). The abnormal MPO deficient PMN subpopulation, if present, disappeared when CR was achieved and reappeared when relapse eventually was developed (II, VIII). In both situations serial determinations showed that the change occurred before the usual routine blood examinations predicted CR and relapse; several days and several months prior, respectively (VIII). The probability of obtaining CR was lower in the AML patients with the abnormal subpopulation and the risk of developing relapse higher than in AML patients without the anomaly (II, VIII). These differences were not statistically significant, however. AML patients, showing an increased number of MPO deficient PMN, revealed a statistically significant increased susceptibility to infections (P less than 0.01) during the preremission phase accounting for 18% to 67% of the total number of infections in this period (III). This increase was positively correlated to the extent of the anomaly (P less than 0.002). The spontaneous occurrence of a subpopulation of MPO deficient PMN in MDS went together with a simultaneous progression in cytogenetically determined clonal chromosomal aberrations and were related to progression in FAB subtype as well (VI). Morphometrically MPO deficient PMN were characterized by a decreased total cell size and an increased nucleus size of the projected images (IX).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Myeloperoxidase deficient polymorphonuclear leucocytes in leukaemia and allied disorders. 285 15

Phagocytosis and lysis of C. pseudotropicalis by peripheral blood monocytes from Hodgkin's and non-Hodgkin's lymphoma were analysed. In Hodgkin's disease, there was a decrease in the phagocytic activity of blood monocytes; moreover, the candidacidal activity was significantly decreased as compared with normal controls. Although monocytes from non-Hodgkin's patients presented normal phagocytic function, the ability to kill C. pseudotropicalis was impaired. In both groups of lymphomas, the data showed that the abnormal findings were not related to treatment. These results indicate that monocytes from Hodgkin's and non-Hodgkin's lymphoma posses a deficiency in killing C. pseudotropicalis, which could be due to an intrinsic macrophage defect in the myeloperoxidase-independent mechanisms and which may be responsible for the predisposition of the se patients to candida infections.
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PMID:Defective function of peripheral blood monocytes in patients with Hodgkin's and non-Hodgkin's lymphomas. 738 72

Recent advances in immunology have clarified the cellular origin of hematopoietic neoplasms. Blast cells with a CD7+ CD4- CD8- phenotype are demonstrated to originate from malignant pluripotent hematopoietic stem cells. In this article, the authors describe three rare cases, designated as a lymphoma type of CD7+ stem cell leukemia/lymphoma, with clinical features described below. All three patients were admitted with non-Hodgkin lymphoma with a 2-month to 4-month history of lymphadenopathy. Histologic examination of lymph nodes showed lymphoblastic lymphoma (LBL) in all patients. Bone marrow blast cells had an immunophenotype consistent with CD7+ CD4- CD8- acute leukemia, although abnormal cells were not observed in the peripheral blood during the course of the disease. One patient had a recurrence in the bone marrow, with myeloperoxidase-positive blast cells expressing myeloid differentiation antigens. Chromosomal analysis detected a common abnormal karyotype initially and at relapse. Furthermore, the same T-cell receptor gene rearrangement was found initially and at relapse, suggesting that these blast cells originated from the same pluripotent leukemic clone. Additional studies on more patients are required to determine the clinical significance of this group, including the difference from CD7+ stem cell leukemia/lymphoma with circulating blast cells (leukemic type) or LBL.
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PMID:CD7+ stem cell leukemia/lymphoma. Features of a subgroup without circulating blast cells. 768 44

Luminol-enhanced whole blood chemiluminescence of human neutrophils was studied using opsonized zymosan as a stimulus. Heparinized blood (0.5 microliters) was used, and the chemiluminescence signals were recorded by a very sensitive, automated, and computer-assisted luminometer (LB 950, Berthold, Wildbad, Germany). The following parameters were provided: integral values over the total measuring time, peak values, the time to reach maximum value, and the time to reach half maximum value. Normal subjects, neutropenic patients, subjects with total or partial myeloperoxidase deficiency, patients with recurrent infections, phagocytic defects, thrombocythemic patients and those with non-Hodgkin's lymphomas undergoing therapy with recombinant human granulocyte colony-stimulating factor were studied. The integral response of chemiluminescence and the time of reach half maximal value were useful indicators of chemiluminescence defects; the assay, was able to detect chemiluminescence responses in neutropenic subjects with neutrophil levels as low as 0.6 x 10(9)/l; differences between cellular and plasma defects could be identified; the quenching effect exerted by erythrocytes was negligible.
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PMID:Luminol-enhanced, whole blood chemiluminescence of human neutrophils evaluated by means of an automated, computer-assisted, and high-sensitivity luminescence analyzer. 878 51

Sclerosing extramedullary hematopoietic tumor (SEMHT) occasionally may arise in patients with chronic myeloproliferative disorders (CMPDs). Morphologically, these tumors may be mistaken for sarcomas or other neoplasms, especially if the clinical history is unknown. We analyzed four cases to identify features to aid in this differential diagnosis. Clinically, there were four men (mean age, 64.5 years), each with a history of CMPD. Grossly, the SEMHTs formed solitary renal or perirenal masses or multiple mesenteric or omental nodules. Morphologically, each SEMHT had a sclerotic to myxoid background with thick collagen strands and trapped fat. Atypical megakaryocytes, maturing granulocytic and erythroid precursors, and few to no blasts were identified in all cases. The megakaryocytes, granulocytic precursors, and erythroid precursors reacted strongly with antibodies to factor VIII, myeloperoxidase, and hemoglobin, respectively, in immunohistochemical studies performed in selected cases. SEMHT is a rare manifestation of CMPD that may be mistaken for a sarcoma, especially sclerosing liposarcoma, Hodgkin's disease, especially lymphocyte depletion type, or a myelolipoma. In a myxoid tumor with trapped fat and atypical cells, morphologic and immunohistochemical identification of maturing hematopoietic precursors helps distinguish SEMHT from sarcoma or Hodgkin's disease. The presence of sclerosis and atypical megakaryocytes helps distinguish SEMHT from myelolipoma.
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PMID:Sclerosing extramedullary hematopoietic tumor in chronic myeloproliferative disorders. 1102 9

Intravascular large B-cell lymphoma (IVLBL) is an uncommon form of non-Hodgkin lymphoma that is also known as malignant angioendotheliosis, intravascular lymphomatosis, and angiotropic large-cell lymphoma. The disease is characterized by a bizarre population of neoplastic cells, which are found systemically within vascular lumina. Although originally thought to be a neoplastic process of the endothelial cells, it has since been demonstrated, by molecular techniques and immunohistochemistry, that the neoplastic cells are of lymphoid origin. The differential diagnosis of these lesions includes granulocytic sarcomas that can be distinguished from IVLBL or other lymphomas by the presence of immunohistochemical positivity for myeloperoxidase. We describe a patient with a history of a myelodysplastic syndrome who subsequently developed IVLBL, which demonstrated immunohistochemical positivity for myeloperoxidase. To our knowledge, this represents the first case of a malignant lymphoma to demonstrate such findings.
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PMID:Myeloperoxidase-positive intravascular large B-cell lymphoma. 1141 84


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