Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

We report 60 cases of chronic and subacute myelomonocytic leukaemias (CMML and SMML) in the adult, using the FAB group criteria. The M/F sex ratio was 3.3 and the mean age 67.5 years. Splenomegaly was found in 32% of cases, hyperleucocytosis in 52% of cases and mean blood monocytosis was 4.3 X 10(9)/l. Marrow smears showed an excess of blasts in 57% of patients, a moderate increase in monocytes in most cases and frequent myelodysplastic features. An increase in serum lysozyme and polyclonal hypergammaglobulinaemia were usual and clonal cytogenetic anomalies found in about half of the patients tested. Treatment was usually palliative and the median survival was 28 months, a blastic transformation being responsible for a third of the deaths. Prognostic factors at diagnosis were analysed retrospectively in the 46 patients who had sufficient follow up. Percentage of marrow blasts haemoglobin level and blood monocytosis at diagnosis, were subject to multivariate analysis, resulting in a discriminant 'score'. This allowed assignment of each patient into one of two prognostic subgroups (10.9% probability of error): a poor prognosis one, with a life expectancy of less than 1 year and a high risk of acute transformation (subgroup termed SMML) and a better prognosis subgroup (termed CMML), with some CMML patients surviving over 5 years.
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PMID:Chronic and subacute myelomonocytic leukaemia in the adult: a report of 60 cases with special reference to prognostic factors. 346 95

A 66-year-old man was admitted for shortness of breath and showed fever, abdominal fullness and paraplegia. Monocytosis amounting to 25% and an elevation of serum LDH (4,281 mIu), were remarkable in the laboratory findings. He died of pulmonary insufficiency about a month after admission. On autopsy hepatomegaly (1950 g), splenomegaly (780 g), but no lymphadenopathy and small infarction in the thoracic spinal cord causing paraplegia was noted. Histopathologically, the invasion of the tumor cells into the liver, spleen, lymph nodes, bone marrow and other organs was observed. Malignant histiocytosis was diagnosed by histologic and immunohistochemical studies (lysozyme positive, S-100 protein negative).
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PMID:[A case of malignant histiocytosis with paraplegia]. 362 41

A case of Hodgkin's disease (HD) in a patient with long-standing hairy cell leukemia (HCL) is reported. The diagnosis of HCL was confirmed by clinical features (chronic illness with marked splenomegaly) and hematopathologic findings (increase of characteristic hairy cells with tartrate-resistant acid phosphatase activity in peripheral blood and bone marrow). Cervical lymphadenopathy first appeared 6 years after the diagnosis of HCL, and histologic features of the node were characteristic of HD. As it was possible that the neoplastic cells of both lesions might have originated from a single clone, their phenotypic features were defined. The hairy cells were found to bear surface immunoglobulin, receptors for complement components, leukocyte common antigen, and antigen defined by LN-1 monoclonal antibody, whereas lymph node lesion was characterized as HD because the Reed-Sternberg-like cells were positive for Leu M1 antigen, lysozyme, alpha-1-antitrypsin, and nonspecific cross-reacting antigen. Since there was no evidence indicating a common clonal origin, it is more likely to consider that both lesions are derived from different clones.
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PMID:Hodgkin's disease in hairy cell leukemia. Phenotypic characterization of neoplastic cells. 365 3

To identify adults with acute nonlymphocytic leukemia at risk for the development of central nervous system involvement, we performed periodic cerebrospinal fluid examinations on patients in remission. Among 58 consecutive patients monitored during first remission, central nervous system leukemia developed in nine (16 percent). Four patients, including one who was symptomatic, had central nervous system leukemia detected simultaneously with marrow relapse. Five additional patients were asymptomatic and continue to have bone marrow remission. Following central nervous system and systemic treatment, two of these five patients have never had relapse, and three had relapse in the bone marrow five, 10, and 21 months later. Factors at diagnosis associated with the subsequent development of central nervous system leukemia were elevated leukocyte count, serum lysozyme and lactate dehydrogenase, extramedullary infiltration including splenomegaly, and monocytic (FAB M4 or M5a) morphology. In six of 17 patients (35 percent) with monocytic morphology, central nervous system leukemia developed compared with only three of 41 patients (7 percent) with other subtypes (p = 0.02). Discriminant analysis identified leukocyte count, splenomegaly, and M4 or M5a morphology as the most important risk factors and led to a mathematical formula that correctly identified 90 percent of the patients. Although the risk of central nervous system leukemia in adults with acute nonlymphocytic leukemia is too low to justify routine prophylaxis, those patients recognized to be at a greater risk should receive prophylaxis or be monitored closely with periodic lumbar punctures.
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PMID:Central nervous system involvement in acute nonlymphocytic leukemia. A prospective study of adults in remission. 366 83

There have been many reports of cases in which chronic increases in the numbers of natural killer (NK) cells have been reported. Whether this is reactive or neoplastic in nature has been debated. We report the first case of an aggressive NK cell leukemia in an adult with establishment of an NK cell line. A 70-year-old man had two spontaneous episodes of jejunal perforation and one month later developed a severe febrile illness with moderate splenomegaly. Hemoglobin was 13.1 g/L, and WBC count was 1.8 X 10(9)/L with 2% large granular lymphocytes (LGLs). Platelet count was 143 X 10(9)/L; prothrombin time (PT) and partial thromboplastin time (PTT) were normal. Bone marrow was infiltrated with 25% to 30% LGLs; serum lysozyme was normal. Serum LDH was initially 1,191 U/L and rose to 6,408 (normal 240 to 525 U/L). Ten days later, the WBC count increased to 99.9 X 10(9)/L with 70% LGL cells; the PT and PTT increased, and the platelet count dropped. No bacterial or viral cause of fever was identified. The cells from peripheral blood were LGLs that stained positively for acid phosphatase. All of the LGLs reacted with a monoclonal antibody reactive with NK cells (LEU-11b). Functionally, the patient's peripheral blood mononuclear cells (PBMs) demonstrated 100 times more lytic activity against K562 tumor cell lines than did normal PBMs. The patient's PBMs were propagated in vitro. The cultured cells showed the morphological, cytochemical, immunological, and functional characteristics of NK cells. In addition, partial trisomy involving chromosome 1 q with duplication in regions of q21 through q31 was observed in all metaphases analyzed. The extra chromosome 1q with duplication in regions q21 through q31 was translocated to the p-terminal of chromosome 5. One percent to 5% of normal PBMs comprise NK cells; in most cases, leukemias arise from normal phenotypic counterparts. This case demonstrated that aggressive NK cell leukemia may occur in adults. In addition, the chromosomal abnormalities suggest that this is not a reactive process but a malignancy.
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PMID:Aggressive natural killer cell leukemia in an adult with establishment of an NK cell line. 395 37

The kinetics of blood neutrophils was investigated by means of the in vitro radioactive diisopropyl fluorophosphate method in 35 patients with a chronic, steady-state neutropenia. There were 17 patients in whom the half disappearance time of neutrophils was normal. In 10 of these patients, the production of neutrophils was low and in 7, production was normal. In 18 patients the half disappearance time of neutrophilic granulocytes was shorter than normal. The production of neutrophilic granulocytes was low in five of these patients, normal in eight patients, and increased in five. An attempt was made to correlate other laboratory measurements with the kinetic picture, but no relationship was found; the marrow neutrophil reserve as measured by endotoxin or cortisol injection; marrow cellularity on aspiration or biopsy; in vitro-labeling index with (3)HTdR; or serum lysozyme concentration proved of no value in identifying the various kinetic groups. The only finding that seemed to correlate with the kinetic picture was the presence or absence of splenomegaly. In 12 of the 18 patients with a short half disappearance time, splenomegaly was present whereas in 15 of 17 patients with a normal half disappearance time, there was no splenomegaly. Of 20 patients with greater than 1000 neutrophils per mm(3), 17 were found to have a normal total-blood neutrophil pool. Thus these patients, with many of their cells marginated, agree to have a "shift neutropenia."Myelocyte to blood transit time and myelocyte generation time, as measured in seven patients by in vivo labeling with diisopropy fluorophosphate, proved to be essentially normal. Thus, it appears that in chronic neutropenia, increased or decreased production of neutrophils is accomplished by increasing or decreasing early precursor input into the system.
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PMID:Leukokinetic studies. XIV. Blood neutrophil kinetics in chronic, steady-state neutropenia. 509 74

Thirty-five patients who fulfilled the FAB diagnosis criteria of chronic myelomonocytic leukemia (CMML), i.e., myelodysplastic features, monocytosis over 10(9)/liter, bone marrow monocyte infiltration, blast cells less than 5% in the peripheral blood and less than 30% in the bone marrow, are analyzed. CMML appears as an entity distinct from myelodysplastic and myeloproliferative disorders. Splenomegaly, anemia, thrombocytopenia, leukocytosis with monocytes and granulocytic cells in all stages of development, increased blood and urine lysozyme levels without renal failure, and polyclonal hyperimmunoglobulinemia are its main clinical and biologic features. With conventional cytotoxic drugs (6-mercaptopurine, hydroxyurea), the prognosis of CMML appears poor (median survival 475 days). None of the clinical hematologic or biologic parameters tested had a significant effect on prognosis. As other chemotherapy trials seemed necessary, we recently administered small doses of cytosine-arabinoside (ARA-C) to six patients over several consecutive days and obtained a complete remission in four. These preliminary results must be confirmed by larger series using the diagnostic criteria proposed by the FAB cooperative group.
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PMID:Chronic myelomonocytic leukemia according to FAB classification: analysis of 35 cases. 658 39

Fifteen of 73 newly diagnosed patients with acute myeloid leukemia (AML), admitted to Mount Sinai Hospital between July 1977 and October 1979, presented with leukocyte counts greater than 100,000/microliter. Eleven of these 15 patients with hyperleukocytosis had myelomonocytic (AMML-M4) or monocytic (AMOL-M5) leukemia compared to 15 of 58 patients with lower white cell counts (p < 0.001). Identification of type of leukemia, using the FAB classification, was based on morphology and special stains, including myeloperoxidase, Sudan black B, periodic acid-Schiff and nonspecific esterase with and without inhibition by fluoride. The proportion of patients with splenomegaly is higher in those with hyperleukocytosis (73 percent) than in those with lower white blood cell counts (p < 0.001) regardless of cell type. Leukemic infiltration of the skin, gums and central nervous system was seen exclusively in patients with AMML and AMOL. The serum lysozyme levels were significantly higher for all patients with AMML and AMOL regardless of the white blood cell count. The mean serum lysozyme for M-4, M-5 patients was 59.7 microgram/ml compared to 18.9 microgram/ml in patients with other cell types (p < 0.0001). Patients with a white blood cell count less than or equal to 100,000/microliter had a complete remission rate of 69 percent compared to 47 percent for patients with higher white blood cell counts.
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PMID:Association of monocytic leukemia in patients with extreme leukocytosis. 693 15

Myelomonocytic myeloproliferative disease in a horse was diagnosed on the basis of hematologic, enzymatic, and histopathologic findings. It was characterized clinically by depression, weight loss splenomegaly, lymphadenopathy, coagulopathy, and bacteremia. Hematologic findings included severe refractory anemia, thrombocytopenia, monocytosis, and pleomorphic leukocytes, with a left shift of the myeloid series. The serum lysozyme concentration was 14.5 microgram/ml (normal, less than 5 microgram/ml). The bone marrow contained many immature cells of the myeloid series and had a myeloid-to-erythroid ratio of 30.5 to 1. The horse died after brief hospitalization. Necropsy revealed generalized lymphadenopathy and hemorrhages throughout the body. Histopathologically, primitive cells were seen in several tissues. Cells that proliferated in the bone marrow were primarily myeloblastic, with some additional erythropoietic cells. Myeloblastic cells with evidence of normal erythropoiesis were seen in numerous lymph nodes and in the spleen, whereas primarily normal erythropoietic cells proliferated in the adrenal glands. Myeloid blast-type cells predominated in the lungs, myocardium, liver, and kidneys.
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PMID:Myelomonocytic myeloproliferative diseases in a horse. 705 85

A 53-year-old male patient was admitted to our hospital with painful splenomegaly. He was diagnosed as having chronic myelomonocytic leukemia (CMML) with leukocytosis, monocytosis, increased lysozyme concentrations in serum und urine, and lack of the Philadelphia chromosome. The clinical course of the disease was characterized by rapidly rising leukocyte counts, cutaneous infiltrates, respiratory insufficiency and neurological symptoms. Excessive hyperleukocytosis with a significant increase in monocytic cells led to microcirculatory obstruction, vascular endothelial damage and organ malfunction. This complication could not be prevented by low-dose chemotherapy with cytosine arabinoside. The patient finally died from pulmonary and cerebral hyperleukocytic syndrome.
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PMID:Fatal hyperleukocytic syndrome in a patient with chronic myelomonocytic leukemia. 911 Nov 70


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