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)

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

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

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

Hen egg white lysozyme (Fleming's lysozyme) prevented the thrombocytopenia provoked by carrageenan injected intravenously into rabbits but not that provoked by an anaphylactic shock. Lysozyme was given intravenously at 25, 50, 100 mg/kg 30 sec before carrageenan. Platelets were counted 15 and 60 min after carrageenan. Lysozyme was given intravenously to immunized animals at the dose of 100 mg/kg 5 min before a challenging dose of the antigens (horse serum-ovalbumin). Platelets were counted 5 min after challenge. The results are discussed in the light of the intervention of platelets and prostaglandins into tumour spread and metastases dissemination.
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PMID:Thrombocytopenia provoked by carrageenan in rabbits and the inhibitory effect of lysozyme. 716 37

Although prolonged Gram-negative sepsis with high permeability alveolar edema, a well documented cause of adult respiratory distress syndrome, has been shown to result in surfactant alterations, the effects of acute endotoxemia on the lung surfactant system are largely unknown. In this study, lethal endotoxemia (> 80% mortality at 24 h) resulting in severe, rapid leukopenia with progressive thrombocytopenia was achieved through intraperitoneal injection of adult Fischer 344 rats with 3.5 mg of Escherichia coli endotoxin/kg. After assessment of pulmonary mechanics under general anesthesia, endotoxin-injected rats and appropriate controls were killed at 4, 8, and 12 h for morphological and biochemical analyses. Morphometric estimation of surfactant membrane subtypes in bronchoalveolar lavage fluid revealed prominent alterations including significant decrease (45%) in tubular myelin 12 h post-endotoxin, with a threefold increase in lamellar body-like forms at 8 and 12 h. Acute endotoxicosis resulted in decrease of total dynamic compliance, whereas pulmonary resistance remained unchanged. These changes were associated with margination of polymorphonuclear leukocytes in lung microcirculation, multifocal septal edema, and decrease in lamellar body lysozyme specific activity at 12 h. Alveolar edema, as determined by measurement of total protein in cell-free bronchoalveolar lavage fluid, was absent in both controls and endotoxin-injected rats. The results indicate that bloodborne lung injury induced by lethal endotoxicosis initiates acute perturbation of secreted surfactant membranes with pulmonary dysfunction in the absence of high protein alveolar edema.
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PMID:Depletion of surfactant tubular myelin with pulmonary dysfunction in a rat model for acute endotoxemia. 774 73

Fifty-three children, aged 7 months to 14.4 years and with typical acute immune thrombocytopenic purpura and platelet counts < or = 20 10(9)/L, were randomly assigned to receive intravenously administered immune globulin G (IVIG), 1 gm/kg per day for 2 consecutive days (n = 19); orally administered prednisone, starting at a dose of 4 mg/kg per day, with tapering and discontinuation of corticosteroids by day 21 (n = 18); or no therapy (n = 16). Both IVIG and prednisone resulted in significantly fewer days with platelet counts < or = 20 x 10(9)/L in comparison with no therapy (median, 1 and 2 days vs 4 days; corresponding ranges, 1 to 20 and 1 to 11 days vs 1 to 132 days; p < 0.01). Reversal of clinically important thrombocytopenia assessed by the number of days taken to achieve a platelet count of > or = 50 x 10(9)/L was significantly faster in children randomly assigned to receive IVIG (median, 2 days; range, 1 to 34 days) than in those receiving prednisone (median, 4 days; range, 2 to 13 days; p < 0.001) or no therapy (median, 16 days; range, 2 to 132 days; p < 0.001). Because the risk of intracranial hemorrhage in children with acute immune thrombocytopenic purpura is highest in the group with severe thrombocytopenia, and appears to be restricted to children with platelet counts < or = 20 x 10(9)/L, these results support the use of IVIG or high doses of prednisone as initial therapy in children with acute immune thrombocytopenic purpura and severe thrombocytopenia (platelet counts < or = 20 x 10(9)/L).
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PMID:A prospective, randomized trial of high-dose intravenous immune globulin G therapy, oral prednisone therapy, and no therapy in childhood acute immune thrombocytopenic purpura. 781 11

A 57-year-old man was admitted with massive nasal bleeding and blurred vision in January, 1991. Laboratory examination showed a prominent decrease of platelet number (1,000/microliters) and a marked elevation of PAIgG (4,025 ng/10(7) cells). Serological test revealed positive antinuclear factor, low concentration of C3 and C4, high level of immune complex and polyclonal hypergammaglobulinemia. The patient had uveitis and bilateral hilar lymphadenopathy with a high level of serum lysozyme and negative PPD skin test. The diagnosis of SLE complicated with thrombocytopenia and sarcoidosis was made. In spite of the various trials of treatment, such as oral prednisolone (PSL), methyl-PSL pulse therapy, plasma exchange, high-dose intravenous gammaglobulin, cyclophosphamide, azathioprine, vincristine, colchicine, cyclosporine-A, mizoribine, danazol, ascorbic acid and interferon alpha 2b, the platelet number could not be raised enough to keep more than 10,000/microliters, though the level of PAIgG decreased to 200 ng/10(7) cells. Finally, the administration of 75 mg/day of dapsone brought about a significant rise in platelet number within 2 weeks. The maximum number of 6.2 x 10(4)/microliters was obtained after 2 months. Then the patient stopped himself to take the drug, but the platelet number remained around 4-5 x 10(4)/microliters. Same dose of the drug was again prescribed to confirm the effect of dapsone. The platelet number increased to 7.9 x 10(4)/microliters in 2 weeks, and gradually returned to 5 x 10(4)/microliters after cessation of the drug. Thus being certainly effective against thrombocytopenia, dapsone should be considered as one of the therapeutic choice for refractory autoimmune thrombocytopenia.
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PMID:[Effectiveness of dapsone on refractory immune thrombocytopenia in a patient with systemic lupus erythematosus associated with sarcoidosis]. 836 Sep 92

We have encountered a 49-year-old female with persistent proteinuria and hematuria. Blood pressure, renal function, physical findings and chest X-p showed no abnormality, but blood tests disclosed mild thrombocytopenia, elevated serum ACE activity, serum lysozyme activity and serum IgA concentration. Abdominal echography and CT revealed multiple nodules in her spleen. In order to make a definite diagnosis and exclude the possibilities of malignant lymphoma or metastatic malignant tumor, splenectomy, and open renal biopsy were performed at the same time. On histological examinations, light microscopic appearance of the spleen was characterized by non-caseating granulomas compatible with sarcoidosis. Renal biopsy specimen showed diffuse proliferative glomerulonephritis with positive staining of IgA predominantly located in the mesangial area, compatible with IgA nephropathy. The present case may provide suggestive evidence for a link between sarcoidosis and IgA nephropathy in the pathogenesis. IgA nephropathy complicated by sarcoidosis is rare, and thus is of particular interest because common immunological abnormalities might be considered in the disease process of both diseases. We feel that despite a low index of suspicion, physicians must be alert to the possibility of IgA nephritis associated with sarcoidosis. The literature is reviewed regarding the relationship between IgA nephropathy and sarcoidosis.
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PMID:[Sarcoidosis representing multiple splenic nodules in a patient with IgA nephropathy]. 885 36

A 68 year-old-man was first found to have CLL with IgG, kappa monoclonal gammopathy 6 years ago. Bestrabucil (total dose 35,150 mg) was taken orally from August 1989 to December 1989. Etoposide (total dose 23,100 mg) was then orally administered from January 1990 to December 1995. He was then referred to our hospital in January 1996 because of progressive anemia and thrombocytopenia. Peripheral blood showed a WBC of 21,200/microliter with 4% myeloblasts and 79% lymphocytes, Hb 7.9 g/dl and Plt 5 x 10(4)/microliter. The serum level of lysozyme was increased (75.6 micrograms/ml). Bone marrow aspiration disclosed hyper-cellularity with proliferation of the blasts and a monocytoid cell population, which cytochemical studies demonstrated to be of the myelo-monocytic series, thus indicating acute myelogenous leukemia (AML-M4) superimposed on CLL. Surface marker analysis of bone marrow mononuclear cells revealed reactivity for CD 11c, CD13, CD15, CD33, HLA-DR. The karyotype was normal. Southern blot analysis and reverse transcriptase-polymerase chain reaction did not reveal rearrangement of the MLL gene. Complete remission was achieved by chemotherapy consisted of BHAC, idarubicine, 6MP, vincristine and predonisolone. Long-term treatment with oral etoposide may contribute to secondary AML.
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PMID:[Acute myelogenous leukemia (M4) occurring during chronic lymphocytic leukemia]. 942 40

Recombinant human interleukin-11 (rHu-IL-11) is a multifunctional cytokine with thrombopoietic activity and demonstrated clinical efficacy in treating chemotherapy-induced thrombocytopenia. rHu-IL-11 also exhibits anti-inflammatory activity and is currently in clinical trials for the treatment of several inflammatory diseases. As neutrophils are involved in both innate immunity and an acute inflammatory response, the effect of rHU-IL-11 on the function of human peripheral blood neutrophils in vitro was examined. rHu-IL-11 was not cytotoxic and did not induce superoxide anion production or the release of granular enzymes from resting neutrophils. Phagocytosis and chemotaxis were unaffected. rHu-IL-11 treatment did not block the response of neutrophils to stimulation. Pretreatment with rHu-IL-11 did not reduce production of IL-8 following activation with lipopolysaccharide (LPS) or zymosan A particles. Pretreatment with rHu-IL-11 did not affect the release of lysozyme and beta-glucuronidase in response to A23187 or PMA-stimulated production of superoxide anion. These results indicate that rHu-IL-11 does not directly modulate key functions of neutrophils in vitro.
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PMID:Recombinant human interleukin-11 does not affect functions of purified human neutrophils in vitro. 980 25


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