Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.17 (lysozyme)
 21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The levels of haptoglobin, alpha1 antitrypsin and alpha1 acid glycoprotein are moderately raised in chronic leukaemias. In CGL the level of haptoglobin and acid glycoprotein show the highest correlation with cell number, whilst no such correlations occur in CLL or CMML. There does not appear to be a relation between blood lysozyme levels and the levels of antiprotease (alpha1 antitrypsin and alpha2 macroglobulin).
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PMID:Acute phase reactant proteins in chronic leukaemia. 7 70

44 patients suffering from myelomonocytic leukemia (MML) have been observed over the last four years. They have been subclassified in acute myelomonocytic and acute monoblastic leukemias (AMML, n = 12; AMoL, n = 10), subacute myelomonocytic leukemias (SMML, n = 13), and chronic myelomonocytic leukemias (CMML, n = 9) on the basis of bone marrow cytology(blast and promonocyte counts, maturation of granulopoesis) and cytochemical findings (peroxydase and unspecific esterase reaction). This subclassification has been proved to be of prognostic relevance by its good correlation with the mean survival times (AMML : 4.5 months, AMoL : 2.4 months, SMML : 8 months, CMML : 18 months). The acute forms have been treated in general with combined cytostatic chemotherapy, whereas SMML and CMML have been treated this way only in case of progression to an acute phase. These progressions to an AMML have been observed more often and earlier in subacute forms than in chronic forms. The diagnosis of SMML and CMML is supported by the finding of sea-blue histiocytes in the bone marrow, increased lysozyme levels in serum and urine and by the absence of the Philadelphia-Chromosome.
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PMID:[Myelomonocytic leukemia: clinical, cytological, and cytogenetic studies of acute, subacute, and chronic forms (author's transl)]. 26 23

The clinical and laboratory features of nine patients with chronic myelomonocytic leukemia are described. Hepatic or splenic enlargement accompanied by an absolute monocytosis in an older patient with an elevated serum or urine lysozyme and serum vitamin B12 levels were characteristic of the majority of patients in this series. No single clinical or laboratory finding was diagnostic for the disease. Most importantly, seven of nine patients had abnormal coagulation values; in two cases the abnormalities were consistent with disseminated intravascular coagulation and correlated with a hemorrhagic diathesis. It is concluded that patients with chronic myelomonocytic leukemia who have thrombocytopenia or a bleeding tendency should be evaluated for evidence of disseminated intravascular coagulation.
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PMID:Disseminated coagulopathy in chronic myelomonocytic leukemia. 29 10

The authors report on 16 cases of either subacute (SMML) or chronic (CMML) myelomonocytic leukemia as well as chronic monocytic leukemia (CMoL). All these cases were oligoblastic and, according to their clinical course, they could be termed as smouldering leukemias. The chronic types affected mainly males. The diagnostic cytomorphological and cytochemical criteria are discussed. Erythro- and thrombocytopoiesis were distinctly less impaired than in acute leukemias (AL). The leucocyte count in the peripheral blood of the SMML cases was within the normal range. Hepato- and splenomegaly were markedly increased as compared to AL. According to our materials leukemic skin infiltrations were less frequent in CMoL, CMML and SMML than in acute monocytic leukemias. In each of the three types of leukemia discussed monocytic leukemic cells could be readily identified by cytochemical tests and usually showed fairly normal maturation. In accordance with these observations lysozyme levels in urine and serum usually were strongly increased. The patients in the CMML and CMoL groups showed a mean survival of more than 13 months (2 out of 7 are still alive), whereas the SMML patients survived an average of 8 months. Deaths were frequently due to advanced age rather than to leukemia. In other cases a terminal accumulation of blasts marked a transition to acute leukemia. During the smouldering phase of the disease no beneficial effect of combined chemotherapy could be noted. Supportive and symptomatic therapy might improve length and quality of survival.
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PMID:[Subacute and chronic monocytic leukemia: diagnostic and clinical problems]. 29 89

The classification of acute leukemia has almost invariably been based on the morphologic diagnosis into two broad categories: acute lymphocytic and acute myeloid leukemia. Despite the wide range of morphologic variation in both groups, strict criteria to define the subgroups have only recently been proposed. The conventional markers for B and T cells are now being applied to leukemic cells as are cytochemistry and electron microscopy, terminal deoxynucleotidyl transferase, serum lysozyme, and surface markers, E-rosettes, membrane immunoglobulin, antinull acute lymphocytic leukemia antiserum, and Fc and C3 receptors. The myelodysplastic syndromes may mimic acute leukemia and it is important that they be identified and treated appropriately. The high incidence with which chronic myelomonocytic leukemia terminates in acute leukemia suggests that it is a preleukemic condition, whereas refractory anemia with excess blasts and acquired idiopathic sideroblastic anemia may have long, drawn-out courses. Only a small population of patients with the latter conditions develop acute leukemia.
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PMID:Classification of acute leukemia. 33 70

The term "plasmacytoid T-zone cells" has been used to describe distinctive cells that occur in clusters in the paracortex of some reactive lymph nodes. Recently, tumorous proliferations of these cells have been described in several patients with myelomonocytic leukemias. Neither the nature of these cells nor their relationship to myeloid leukemia has been conclusively established. We report the case of a 64-year-old woman with chronic myelomonocytic leukemia who developed lymphadenopathy that proved to be due to tumorous accumulation of plasmacytoid T-zone cells in the interfollicular regions of the lymph nodes. She underwent splenectomy because of symptomatic splenomegaly; the resected spleen also contained aggregates of plasmacytoid T-zone cells, in addition to extramedullary hematopoiesis. On treatment with busulphan and prednisone, the lymphadenopathy resolved and did not recur. The patient died 7 years later with blast transformation of her myelomonocytic leukemia and no recurrence of lymphadenopathy. The aggregates of plasmacytoid T-zone cells were architecturally and cytologically distinct from the leukemic infiltrates of myeloid cells in the spleen, and there was no evidence of differentiation of these cells into myeloid or monocytic cells. A panel of monoclonal antibodies on paraffin sections revealed no lineage-specific T- or B-cell markers (UCHL1-, L26-), and the plasmacytoid cells were positive for CD68 (KP1) and L60 (CD43), as well as faintly positive for 4KB5 (CD45RA) and MB1 (CD45R). They did not stain with antibodies to myeloid lineage antigens CD15, lysozyme, or myeloperoxidase. The combination of clinical, morphologic, and immunologic features of plasmacytoid T-zone cells in this case suggests that these cells may be of monocytic lineage but are not direct precursors of mature monocytic or granulocytic cells, and may not be part of the neoplastic clone in patients with myelomonocytic leukemia.
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PMID:Plasmacytoid T-zone cell proliferation in a patient with chronic myelomonocytic leukemia. Histologic and immunohistologic characterization. 184 25

We examined fourteen patients with chronic myelomonocytic leukemia (CMMoL) according to the following staging criteria at diagnosis; Group A: bone marrow (BM) blast less than 5% (eight cases), Group B; BM blast more than 5% and less than 30% (five cases), Group C; BM blast more than 30% (one case). Compared with Group A, Group B patients have much more peripheral blood leukocyte, granulocyte and monocyte counts, LDH level, and serum and urine lysozyme levels. Two of the five Group B cases transformed to acute leukemia (BC) within one and a half year, and other three patients died of infection and hemorrhage within a year. On the contrary, three of the eight Group A patients survived four years, and transformation to acute leukemia occurred in only one case after four years. Autopsy revealed multiple organ infiltration of monocytoid granulocytes on the patients with advanced stage and more bone marrow blasts. Two cases have coexistence of myeloproliferative disorders, one with essential thrombocythemia, and another with myelofibrosis, which, later, transformed to acute leukemia. And a Group C patient transformed to chronic phase with chemotherapy, and maintained the state for six years, but at the end stage, mature monocytes increased and pancytopenia developed. These findings indicate the heterogeneity of CMMoL in respect of the disease stage and the coexistence of other myeloproliferative disorders.
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PMID:[Clinical study on heterogeneity of chronic myelomonocytic leukemia]. 207 27

A 65-year-old woman had chronic myelomonocytic leukemia with peripheral neuropathy and IgA paraprotein with kappa type light chain. Plasma cells with "flaming" cytoplasma were seen in the bone marrow specimens. The findings suggest that chronic myelomonocytic leukemia may involve B-lymphocytes in the proliferative process and that it may be a clonal disease. Moreover, this case was associated with peripheral sensori-motor polyneuropathy. The disorder was responsive to prednisolone, as oral administration of prednisolone improved not only the peripheral polyneuropathy, but also the hematological findings. Serum vitamin B12 and lysozyme in the serum and urine were decreased by the steroid therapy. The administration of prednisolone is effective not only for polyneuropathy but also chronic myelomonocytic leukemia.
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PMID:Chronic myelomonocytic leukemia with polyneuropathy and IgA-paraprotein. 256 Dec 95

A 37-year-old male was diagnosed as having chronic myelomonocytic leukemia (CMMoL) with chief complaint of systemic lymph node swelling. On admission, his peripheral blood revealed mild anemia and mild thrombocytopenia with giant platelets, and monocytosis (1480/microliters). NAP score was low. Serum lysozyme increased. The bone marrow showed normal cellularity consisting of 4% myeloblasts and 14.4% promyelocytes, and a few myeloid cells were positive for double staining by alpha-naphthyl butyrate and naphthol ASD chloroacetate esterase. Biopsied specimens of the cervical lymph node showed infiltration of monocytoid cells, which were positive for lysozyme staining, into interfollicular tissue. As for chromosome variation, 21 large satellite was observed in all dividing cells from his bone marrow and peripheral blood. Furthermore, hemolytic anemia with hemoglobinuria developed during his course. Sugar water test was positive, but Ham test negative. Coombs test and Donath-Landsteiner reaction were negative. Abnormal hemoglobin, spherocyte and fragmentation were not found. Hemolysis disappeared about two months later. However, blastic crisis appeared and he died. We showed a case of CMMoL with 21 large satellite and paroxysmal nocturnal hemoglobinuria (PNH)-like complication. Satellite have usually been reported as asymptomatic, and thus this chromosome variant and CMMoL may have been coincidentally observed.
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PMID:[Chronic myelomonocytic leukemia (CMMoL) with systemic lymph node swelling and paroxysmal nocturnal hemoglobinuria (PNH)-like complication]. 260 15

Two cases of Ph1-negative chronic myelogenous leukemia (CML) are described, they were 66-year-old female and 73-year-old male. Both patients shared all of the following features: presence of anemia, thrombocytopenia and leukocytosis with every stage of neutrophilic differentiation, hypercellular bone marrow with hyperplasia of the degranulated neutrophilic series, diminished neutrophilic alkaline phosphatase, elevated serum lysozyme and vitamin B12 level, mosaic pattern of trisomy 8 and normal karyotypes in chromosome analysis, and markedly increased number of CFU-GM. In addition, bcr rearrangement by Southern blot hybridization was not demonstrated in these patients. The diagnosis of chronic myelomonocytic leukemia was not verified, however, because of the absence of monocytosis in peripheral blood. The existence of so-called Ph1-negative CML like these two cases as a diagnostic entity must be further studied.
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PMID:[So-called Ph1-negative chronic myelogenous leukemia with a mosaic pattern of trisomy 8 and normal karyotypes--report of 2 cases]. 276 71


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