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)

Lysozyme activity was determined in the serum, urine and leukocytes of 53 patients with immunocytoma and 24 patients with lymphoproliferative syndromes without associated monoclonal gammapathy. In patients with multiple myeloma the frequency of low serum lysozyme activity and high leukocyte lysozyme activity was higher. In the cases with renal failure, lysozyme activity was raised in serum and urine, and the 24-hour urinary lysozyme excretion was increased. In 7 patients with increased urinary lysozyme excretion no clinical or laboratory evidence of renal complications was found. Relative monocytosis in peripheral blood was observed in half of the cases of multiple myeloma, and in these patients also in about half of the cases the lysozyme activity was raised in the leukocytes and urine, and the 24-hour urinary lysozyme excretion was increased. In patients with Hodgkin's disease, lymphosarcoma and chronic lymphatic leukemia the frequency of low serum lysozyme activity was increased.
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PMID:Lysozyme in the serum, urine and peripheral blood leukocytes in patients with immunocytoma. 12 34

Measurements of urinary lysozyme were used to evaluate renal tubular integrity in 34 patients with cirrhosis or fulminant hepatic failure who had developed renal impairment. In 18 of the patients the lysozyme values were normal but in the remaining 16 were increased, supporting previous concepts that renal failure complicating hepatocellular disease may occur both without and with tubular necrosis. The lysozyme values were inversely related to the creatinine clearance, suggesting that the development of tubular necrosis may be determined by the level of renal perfusion. The validity of simpler laboratory tests often used to assess renal tubular integrity--namely, the urine sodium concentration, the urine:plasma osmolality ratio, and casts in the urine sediment--was evaluated by comparison with the lysozyme measurements. The urine sodium concentration was of most value and the findings in the sediment were of no value at all.
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PMID:Spectrum of renal tubular damage in renal failure secondary to cirrhosis and fulminant hepatic failure. 63 52

We have examined sixty-seven surgically removed allograft kidneys to identify the different leukocyte subsets of interstitial infiltration and the early vascular lesions which characterize renal allograft rejection. Histochemical and immunohistochemical results (mouse monoclonal antibodies anti: Leu 1, Leu 3a-3b, Leu 7, Leu 2a, OK Ia-Dr, OKB2, Leu M1, Leu M3; rabbit heteroclonal antibodies anti -: IgA, IgG, IgM, C3, fibrinogen, lysozyme; lectins-ABC: RCA, WGA, UEA) and routine histochemical staining have shown an increase of T-helper and T-activated lymphocyte subsets in acute rejection. Neutrophilic leucocytes were present in hyperacute rejection; macrophages were also noted. In chronic rejection, several lymphocyte subsets, in different ratios, were identified. Monocyte/macrophage leukocytes were the most abundant cell population. IgA deposits were noted on tubular epithelia in hyperacute and chronic rejections. IgM deposits were observed in vascular walls in chronic rejection. C3 and fibrinogen deposits were seen in glomerular capillaries and in arterial walls, although in different ratios, in all cases of renal allograft rejections. We have generally seen weak reactions to IgG deposits. Histochemical analysis of lectin receptors has given different results according to the type of rejection considered. In hyperacute rejection, receptors for WGA were found both on glomerular endothelial cells and on the tubular brush border. In the latter, receptors for RCA were also found. In acute rejection, receptors for UEA and WGA were found in a lower number of cases of acute vascular rejection. In acute cellular rejection, receptors for RCA, UEA and WGA were recognized in tubular epithelia. In acute vascular rejection, as well as in chronic rejection, only receptors for WGA were present on tubular epithelia and on capillary loop endothelium. The use of anti-human lysozyme antibodies has yielded the following results: in acute and hyperacute rejection, when renal failure occurred, we saw a high ratio of lysozyme, either coarsely granular or diffuse in the proximal tubular epithelia. Lysozyme was found in myelocyte/macrophage cells within capillary loops and arterial walls, when acute necrotizing vasculitis was present. In acute rejection, proximal tubular cells were lysozyme-negative or lysozyme-positive only segmentally, especially when obliterative vasculitis by fibrointimal proliferation was present and renal function progressively failed. In most of the chronic rejections, tubular cells were lysozyme-negative.
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PMID:Renal allograft rejection: immunohistochemistry of inflammatory cellular subsets and vascular lesions. 242 64

Diagnostic features (cytochemistry, immunophenotyping and serum biochemistry) were examined in 51 cases of acute monocytic leukaemia (AMoL). Peroxidase, Sudan black B and alpha naphthyl acetate esterase (ANAE) cytochemical reactions were unrelated to morphological (FAB groups M5a and M5b) or immunological subtype. ANAE cytochemistry, however, indicated that AMoL cases could be subdivided into those with typical (M-type) reactions and those with insignificant staining or monocytic ANAE isoenzymes (defined by IEF). All cases were phenotypically CD13/CD33 positive and, with one exception, had greater than 30% HLA-DR positive cells. Membrane CD14 expression was insignificant or variable in 33% of M5a cases in contrast to 23/24 M5b cases which showed high proportions of CD14-staining cells with at least two monoclonal antibodies. Serum lysozyme, LDH and beta-2 microglobulin (beta 2m) were increased in 88%, 68% and 81% of cases respectively but, with the exception of statistically higher lysozyme levels in CD14+ cases, were unrelated to the morphological, cytochemical or immunological diagnostic subgroups. Clinical and diagnostic features were also examined as possible prognostic indicators. The morphological, cytochemical and immunological subgroups of AMoL were not found to be of prognostic relevance but age (P = 0.004), renal failure (P = 0.005) and serum beta 2m levels (P = 0.002) were related to patient survival. Moreover, renal failure and serum beta 2m remained significant (P = 0.012 respectively) when age was taken into account and were shown to be independent prognostic variables.
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PMID:Diagnostic and prognostic factors in acute monocytic leukaemia: an analysis of 51 cases. 329 31

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

Seventy-four cases of pure acute monoblastic leukemia (AMol) have been retrospectively studied. All patients were treated at Hospital Saint-Louis between 1970 and 1978. Diagnosis was based on morphological and cytochemical features according to the FAB classification. This type of leukemia occurred at any age and in both sexes, with a high frequency of extramedullary involvements. Hyperleukocytosis was very frequent and was significantly correlated with increased blood and urine levels of lysozyme, with renal failure and hypokalemia, and with coagulation abnormalities. AMol still has a poor prognosis, despite a best remission rate (75%) obtained with rubidazone, since the duration of complete remission was short. Central nervous irradiation prolonged remission and prevented meningeal relapses, while 6 meningeal relapses occurred in the patients not irradiated. The high frequency of the extramedullary relapses, including gum and skin, emphasized the question of persistant blast cell sanctuaries after achievement of bone marrow remissions. A more intensive induction with several drugs active against monoblasts could be more efficient and prolong the duration of complete remissions.
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PMID:Acute monoblastic leukemia: a clinical and biologic study of 74 cases. 692 57

In two patients who had malignant histiocytosis, renal involvement was present at an early stage of their diseases and consisted clinically of proteinuria and renal failure. The associated renal lesion was characterized by a diffuse and global endocapillary hypercellularity of the glomeruli imputable to atypical cells occluding the capillary loops. Immunoglobulins were absent from this lesion. The atypical cells were positively identified by lysozyme immunoperoxidase study as malignant histiocytes. It is suggested that renal biopsy complemented by marker study could play a role in the diagnosis of malignant histiocytosis.
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PMID:Renal involvement in malignant histiocytosis. An immunoperoxidase marker study. 702 27

Abnormalities of the immune response can be secondary to old age, to several pathologic conditions (i.e. diabetes mellitus, renal failure, solid and lymphohematologic neoplasias, leukopenia, malnutrition, autoimmune diseases, AIDS), to surgical stress or to burns, and to immunosuppressive therapies, both medical (corticosteroids, cytotoxic agents, antilymphocytic globulins) and surgical (splenectomy) as well as radiant (extensive radiotherapy). Old age can affect both humoral (reduced antibody synthesis) and cell-mediated (thymus involution, diminished ratio Th/Ts, depression of both delayed hypersensitivity reactions and cytotoxic activity of K cells) immune response. Hyponutrition, often observed in the elderly, adds a reduced production of secretory IgA, lysozyme and interferon, diminished complementary activity, phagocytosis defects, and vitamin deficits. Furthermore, in some chronic diseases we can observe reduced primary antibody response or depression of delayed hypersensitivity reactions (renal failure, neoplasias), changes in leukocyte functions (diabetes mellitus, leukemias and lymphomas) and, in particular in solid neoplasias, increased activity of Ts lymphocytes and the presence of circulating immunocomplexes. Changes in phagocytosis, opsonization and chemotaxis are typically seen in burns, whereas surgical stress can cause some inhibition of cell-mediated immunity. Finally, after splenectomy it is possible to observe an increased synthesis of IgA and IgG and, on the contrary, reduced production of IgM and properdin.
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PMID:[Pathogenetic mechanisms responsible for producing a secondary immunodeficiency state]. 786 Dec 9

The leukemias have long been associated, albeit rarely, with the development of renal failure and several metabolic perturbations. While renal insufficiency may result from a variety of mechanisms in the setting of leukemia, severe leukostasis with microvascular insufficiency and renal parenchymal infiltration by blast cells are rare and infrequently described etiologies. In addition, hypokalemia can occur from lysozyme-induced renal tubular injury with inappropriate kaliuresis. We present a case of acute myelomonocytic leukemia that was complicated by renal failure and severe hypokalemia and discuss the probable mechanisms.
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PMID:Renal failure and severe hypokalemia associated with acute myelomonocytic leukemia. 837 46

A 39-year-old woman was consulted to our hospital because of renal failure on October 1992. A chest X-ray showed no abnormal shadow. Subsequently, she was under conservative treatment until December 1993, when she began to notice clouded vision. The iridocyclitis in both eyes was diagnosed by a ophthalmologist. She was admitted to our hospital for the purpose of a renal biopsy. Laboratory tests revealed renal failure: a creatinine clearance of 24.5 ml/min, a serum level of creatinine of 3.2 mg/ml and blood urea nitrogen of 38.7 mg/dl. The angiotensin converting enzyme was 17.6 IU/ml (normal 8.3 approximately 21.4 IU/ml), but lysozyme was 49.5 micrograms/ml (normal 5.0 approximately 10.2). Mantoux's reaction was negative. 57Ga scintigram showed abnormal uptakes on eyes, bilateral salivary gland, both thighs, both kidneys, and in a part of lung field. A percutaneous renal biopsy revealed non-caseating histiocytic granulomas with diffuse infiltration of lymphocytes and neutrophils into interstitium. Glomeruli were ischemic and mild endocapillary proliferations with pericapsular fibrosis were seen. Both of transbronchial lung biopsy (TBLB) and skin biopsy also revealed non-caseating histiocytic granulomas. Oral administration of prednisolone, 40 mg/day, improved the level of serum creatinine and lysozyme. Sarcoidosis is a granulomatous disease of unknown etiology that may involve any organ or tissue of the body. The clinical picture dominating in adults is the one with pulmonary and mediastinal lymph node involvement, eye and skin lesions. Although the renal involvement were rarely encountered, the present case showed that the renal failure was one of the most important clinical feature in patient with sarcoidosis.
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PMID:[A case of sarcoidosis with renal failure as the main manifestation in granulomatous interstitial nephritis]. 856 2


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