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)

Enzymatically homogeneous populations of lymphocytes, monocytes, and neutrophils were isolated by zonal centrifugation from 5 untreated patients with chronic lymphocytic leukemia (CLL) and 2 patients with CLL in full remission. The cells were then quantitatively analyzed for six leukocytic enzymes and compared with cells from normal subjects. CLL monocytes were deficient in beta-glucuronidase (0.06 units; normal, 0.16), myeloperoxidase (0.07 mg; normal, 0.5 mg), and lysozyme (0.7 mg; normal, 3.3 mg). In 2 cases, CLL neutrophils were severely deficient in lysozyme (1 to 2 mg; normal, 7 mg) and myeloperoxidase (2 to 3 mg; normal, 7 mg). Neutrophil alkaline phosphatase and neutral protease were unaffected. CLL lymphocytes shared with the monocytes the deficiency of beta-glucuronidase (0.03 units; normal, 0.09 units). The 2 CLL patients in full remission carried normal enzyme levels in leukocytes of all three cell lines. The CLL lymphocytes of untreated patients were unresponsive to mitogens but became responsive in remission. The CLL monocytes from both untreated and treated patients transformed into macrophages. The pattern of shared enzyme deficiency among lymphocytes, monocytes, and neutrophils of CLL patients and its normalization in all three cell types under remission suggest that the differentiation of the three leukocytic cell lines may be an enzymatically interlinked process and that the deficiency of these enzymes in leukemia may reflect an interrelated aberrant differentiation of the leukemic cells.
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PMID:Monocyte and granulocyte defect in chronic lymphocytic leukemia. 21 99

Electrolyte disturbances in leukemia can be the result of the disease process or drug therapy. One group of electrolyte abnormalities is related to the stage of the leukemic process. Included in this group are newly diagnosed patients who may show elevated serum potassium, phosphorus, and magnesium--a result of their release from malignant cells after cytotoxic therapy or their accumulation due to urate nephropathy. Patients in remission usually have normal serum electrolyte concentrations, but acute leukemia patients during relapse may have hypokalemia, hypophosphatemia, and hypomagnesemia. This imbalance may be related to cellular uptake of these electrolytes in the presence of inadequate dietary intake. Other factors contributing to electrolyte derangements, and related to the leukemic process, include hyponatremia and hypochloremia secondary to the SIADH, hypokalemia in acute monocytic or acute myelomonocytic leukemia due to lysozyme-induced tubular damage, hypercalcemia possibly secondary to leukemic infiltration of bone or parathyroid glands (with PTH release), or production of a PTH-like substance by leukemic cells. Nonspecific factors related to the disease process which may aggravate the electrolyte imbalance include gastrointestinal loss through nausea, vomiting, and malnutrition. The drug-related electrolyte abnormalities include cyclophosphamide- and vincristine-induced SIADH; decreased serum sodium, chloride, potassium, and calcium concentrations as a result of polymyxin B nephrotoxicity; hypokalemia and hypomagnesemia secondary to amphotericin B; hypocalcemia, hypophosphatemia, and hyperphosphaturia due to L-asparaginase-induced hypoparathyroidism; hypokalemia due to a nonreabsorbable anion effect of antibiotics in the distal tubule or changes in membrane ionic transport of all cells by large doses of antibiotics. Electrolyte disturbance in leukemia thus have a multifactorial pathogenesis which can best be delineated according to the stage of the leukemic process and the drugs being used. Recognition of the cause or causes in a particular patient is essential for an effective approach to management. This review emphasizes the need for routine measurement of serum electrolytes during all phases of the leukemic process.
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PMID:Electrolyte and acid-base disturbances in the management of leukemia. 26 90

A simple cytochemical and cytobacterial method for the simultaneous demonstration of peroxidase and lysozyme (muramidase) activities in individual cells was devised. In characterization of myeloid and monocyte series, the combination of these myeloid- and monocyte-specific enzymes not only was more informative than a single enzyme but made it easier to differentiate acute myelomonocytic leukemia, with higher lysozyme activity, from acute myeloid leukemia, with higher peroxidase activity. Acute lymphocytic leukemia had no lysozyme or peroxidase activity.
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PMID:Simultaneous demonstration of peroxidase and lysozyme activities in leukemic cells. 26 61

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

Serum lysozyme activity was measured in samples from children with acute leukemia, malignant tumours, and in normal children. All children with acute lymphatic leukemia (ALL) had significantly reduced levels of lysozyme at diagnosis, and none of the children fell within the normal range. Children with ALL in complete remission had lysozyme levels comparable to normal chidren, while children with ALL in relapse also had pathological low levels. Children with ALL in remission and off therapy also had normal levels of lysozyme. Children with acute myelogenous leukemia had normal lysozyme levels, while children with monomyelocytic leukemia had substantially elevated lysozyme levels before treatment. Determination of serum lysozyme activity in children with acute leukemia is of value both for diagnosis and for evaluating the effect of therapy.
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PMID:Serum lysozyme activity in children with acute leukemia. 27 70

Serum lysozyme activity has been determined in patients suffering from myeloproliferative diseases, chronic myelogenous leukaemia (CML), acute myelogenous leukaemia (AML), chronic lymphatic leukaemia (CLL) and pancytopenia (P). Lysozyme activity was tested in undiluted and tenfold diluted sera. Increased lysozyme activity was found in patients with CML and CLI, whereas there was no change in patients with AML and P. Dilution of sera enhanced lysozyme activity. These data may indicate the presence of inhibitor in the sera tested. The diagnostic significance of the presented findings is discussed.
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PMID:Serum lysozyme activity in some myeloproliferative diseases. 27 10

A case of Schilling type pure acute monocytic leukaemia (M5 variety of the FAB classification) in a 38-year-old man is presented. The initial predominant clinical manifestation was an increase hypertrophic gingivitis. The cytological type was established according to the morphologic and cytochemical criteria currently in use. The patient was treated with daunomycin (60 mg/m2 one day) and ARA-C (100 mg/m2/12 hours for 7 days) in a 2-week interval cycles. Total remission was achieved after the fifth series. The series have been repeated over 4 years with intervals of up to 6 or 8 weeks. Complete haematologic remission has been constant, with normalization of the serum muramidase levels. A gingival biopsy taken at the same time has shown no evidence of leukaemic infiltration. The high incidence of malignancy in this cytological variety of acute leukaemia is pointed out; it is normally less sensitive to chemotherapy than the myeloid types. Remission has been total over a long period of time, which is exceptional in this type of leukaemia. The mean survival rate as recorded in the literature is only a little over 3 months.
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PMID:[Complete clinical remission over 50 months of a patient with acute monocytic leukaemia (author's transl)]. 28 62

Serum lysozyme activity was measured in samples from adult patients with acute leukemia, malignant tumors, and in normal adults. Twenty-eight adult patients with acute myelogenous leukemia (AML) had significantly elevated levels of lysozyme at diagnosis, and none of the adults fell within the normal range. Thirty-two patients with AML in complete remission had lysozyme levels comparable to normal adults, whereas patients with AML in relapse (eight cases) also had abnormally high levels of lysozyme activity. Ten patients with AML in remission and off therapy also had normal lysozyme levels. Three patients with acute lymphatic leukemia had normal lysozyme levels, while one child with monomyelocytic leukemia had substantially elevated lysozyme levels before treatment. It seems that in patients in remission and with normal blood values, the serum lysozyme activity is valuable for monitoring the remission.
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PMID:The prognostic value of serum lysozyme activity in acute myelogenous leukemia. 28 68

12-O-Tetradecanoylphorbol-13-acetate, a potent promoter of carcinogenesis in mouse skin, enhanced differentiation of cultured mouse myeloid leukemia cells (M1) induced by human urinary protein or by lipopolysaccharide from Salmonella typhosa. 12-O-Tetradecanoylphorbol-13-acetate enhanced differentiation of all the markers tested, such as phagocytosis, Fc rosette formation, lysozyme activity, and morphological change. Other potent tumor-promoting macrocyclic plant diterpenes also enhanced the induction of differentiation, but no-tumor-promoting diterpenes did not. These findings were in marked contrast with generally accepted findings on the inhibitory effect of 12-O-tetradecanoylphorbol-13-acetate on terminal differentiation observed in other cell culture systems but consistent with the observations with some kinds of leukemia cells.
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PMID:Enhancing effect of phorbol esters on induction of differentiation of mouse myeloid leukemia cells by human urinary protein and lipopolysaccharide. 29 79

Leukaemic cells taken from the blood of patients with acute myelogenous leukaemia (AML) frequently proliferate in suspension culture without the addition of growth factors for a limited period only. After a 6--10-fold increase in total cells, cell numbers remain constant for a time and finally decline. The main cause for this limited growth in vitro is not, initially at least, cell death leading to a steady state, but maturation associated in its final stages with cessation of DNA synthesis. Two populations of AML cells from Patients St and Wi respectively were studied, and progressive maturation towards mature leucocytes was demonstrated by the gradual acquisition in culture by the growing blast cells of intracellular enzymes (lysozyme, arginase, acid phosphatase and esterase being measured), surface markers (Fc and C3 receptors), of lactoferrin by Wi cells and of colony-stimulating activity by St cells, as well as changes in Ia antigens, phagocytic properties, morphology and adhesiveness to plastic. With St cells, which carried a characteristic chromosome marker, maturation terminated in cells with the characteristic properties of macrophages. At an intermediate stage, non-adherent and still-dividing St cells acquired Fc and C3 receptors and enzymes characteristic of monocytes. Wi cells progressively became neutrophil-like, and again there was an intermediate population of dividing cells which had Fc and C3 receptors and proteins such as lactoferrin and esterases. characteristic of neutrophils.
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PMID:Patterns of maturation in short-term culture of human acute myeloid leukaemic cells. 29 51


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