Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.11.1.7 (peroxidase)
 65,474 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper describes the test characteristics and clinical relevance of a newly developed homogeneous enzyme immunoassay IMAC lipase test for the determination of serum pancreatic lipase. The method of determination is based on an immunoactivation technology and utilizes antibody fragments against human pancreatic lipase covalently bound to the marker enzyme horseradish peroxidase. The serum samples of 408 persons were investigated with this new assay. The within-run and day-to-day precision, the linearity, and the recovery of this immunoassay correspond to a very high degree to the requirements made of a modern immunological test. Comparison with an ELISA method resulted in a correlation coefficient of 0.971, whereby the IMAC lipase assay tended to register lower serum values. The serum range for the IMAC lipase test is 0-47 micrograms/L, based on a normal collective of 187 healthy controls. A sensitivity of 95.8% for the diagnosis of acute pancreatitis at a cutoff level of twice the upper normal range and a specificity of 99.3% at an efficiency of 99.8% can be given. The advantage of the IMAC lipase test method is its ability to be adapted to work on automatic laboratory analyzers.
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PMID:Determination of pancreatic lipase by immunoactivation technology. A rapid test system with high sensitivity and specificity. 128 19

Cerulein-induced acute pancreatitis in rats is associated with a reversible lung injury that is characterized by alveolar capillary endothelial-cell injury, increased microvascular permeability, interstitial edema formation, and intraalveolar hemorrhage and fibrin deposition. The role of mediators in this injury was analyzed using gravimetric data, microvascular permeability indices, electron microscopy, and a quantitative morphometric analysis. Neutrophil depletion induced by a specific antibody was highly protective against lung injury. Interruption of the complement pathway (using low dose Naja naja cobra venom factor) also protected against lung injury. Catalase and superoxide dismutase were also protective. The iron chelator deferoxamine and the hydroxyl radical scavenger, dimethylsulfoxide, were not protective against acute lung injury. These data suggest that complement, neutrophils, and neutrophil-derived (H2O2-dependent) oxygen products mediate lung injury that occurs secondary to cerulein-induced pancreatitis. In contrast to other models of neutrophil-dependent, oxygen-radical-mediated lung injury, this lung injury does not appear to be an iron-dependent and hydroxyl-radical mediated injury. We postulate that the process of acute pancreatitis leads to complement activation followed by neutrophil recruitment, sequestration, and adherence to alveolar capillary endothelial cells. Ultimately lung injury appears to result from local endothelial-cell injury secondary to neutrophil-generated oxygen products that may be myeloperoxidase dependent.
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PMID:Neutrophil-dependent, oxygen-radical mediated lung injury associated with acute pancreatitis. 258 87

Phospholipase A2 was localized with peroxidase anti-peroxidase (PAP)-technique in pancreatic tissue resected from normal portions of tumor-bearing glands of 4 patients and from pancreases of 16 patients suffering from either acute or chronic pancreatitis. In acute pancreatitis the enzyme immunoreactivity was detected in the apical zymogen granule portion of acinar cells and in ductal secretory material similarly as in normal tissue. At the border of necrotic and non-necrotic exocrine parenchyma the staining reaction was evenly dispersed throughout the cytoplasm or localized in small cell fragments. There was no reaction in necrotic acinar cell remnants. Some dilated acinar lumina contained intensively stained plugs. Fat necroses were stained but surrounding neutrophil leukocytes were unstained. Thrombosed small vessels were also unstained. In chronic pancreatitis, diminished staining characterized small acinar cells at the border of lobules. Some macrophages stained positively. It was concluded that during acute inflammation in pancreas, localization of phospholipase A2 in pancreatic tissue is abnormal, and that phospholipases A2 of neutrophil leukocytes and platelets are not crossreactive with the secretory enzyme.
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PMID:Immunohistochemical localization of phospholipase A2 in human pancreas in acute and chronic pancreatitis. 634 33

Immunoreactive trypsin was localized with the peroxidase-antiperoxidase technique in normal human pancreatic tissue and in the glands of patients suffering from acute or chronic pancreatitis. In the normal pancreas and in the histologically normal areas of the inflamed pancreas, trypsin was detected in the zymogen granules of acinar cells and in ductal secretory material. During acute pancreatitis, three characteristic changes were observed: (1) separate acinar cell fragments in early lesions; (2) decreased and evenly dispersed staining in necrotic acinar cells, and (3) intensive reaction in plugs in acinar lumina in advanced lesions. In chronic pancreatitis, the localization of trypsin in acinar cells was similar to that in normal pancreas. Some proteinaceous plugs in dilated pancreatic ducts were weakly immunoreactive. The results show that the tissue distribution of immunoreactive trypsin is altered in acute pancreatitis.
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PMID:Immunohistochemical localization of trypsinogen and trypsin in acute and chronic pancreatitis. 635 76

In severe acute pancreatitis (SAP), the mechanisms leading to adult respiratory distress syndrome (ARDS) are usually attributed to the release of active enzymes and vasoactive substances from the pancreas. Thoracic duct drainage has been proposed as a means of removing the portion of these substances that drain through retroperitoneal lymphatics before they reach the systemic circulation. This technique was used in six patients with ARDS complicating SAP. The levels of proinflammatory cytokines (tumor necrosis factor-alpha [TNF alpha], interleukin-1 [IL-1], and interleukin-6 [IL-6]), neutrophil enzymes (myeloperoxidase and lactoferrin), and pancreatic enzymes (amylase, lipase and trypsin) were measured in plasma and lymph in the first 24 h of ARDS and then on Day 2, Day 4, and at the end of the drainage (Day 8). High plasma concentrations of these products were measured. A moderate lymph-to-plasma gradient was observed for IL-6, lipase, and trypsin, while similar levels in plasma and lymph were recorded for the other substances. Plasma levels of pancreatic enzymes were weakly correlated with the lung injury score and lymph level of cytokines. These results suggest that in patients with ARDS due to SAP, cytokines as well as pancreatic enzymes could contribute to the development of the lung injury, and that lymphatics are potential vectors of these mediators.
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PMID:Lymphatic release of cytokines during acute lung injury complicating severe pancreatitis. 758 88

The administration of a high-dose of a serine protease inhibitor is recommended in patients complicated by multiple organ failure (MOF), including adult respiratory distress syndrome (ARDS), induced by acute pancreatitis. The accumulation of polymorphonuclear leukocytes (PMN) in affected organs is considered to be one of the causative factors of MOF. Adhesion to endothelial cells (EC), via adhesion molecules, and the transendothelial migration of PMN is closely associated with the accumulation of PMN. We examined the effects of two serine protease inhibitors, ulinastatin (UT) and gabexate mesilate (GM), on EC-PMN adhesion and transendothelial migration in human umbilical vein EC and 51Cr-labeled PMN in vitro. EC-PMN adhesion, and the expression of intercellular adhesion molecule-1 (ICAM-1) and endothelial cell adhesion molecule-1 (ELAM-1) on EC induced by IL-1 beta and TNF alpha, were reduced by the pretreatment of EC with these inhibitors. The transendothelial migration of PMN stimulated by IL-8 was also inhibited by pretreating PMN with UT or GM. We also examined whether these inhibitors reduced PMN accumulation in the lung in rats with acute pancreatitis induced by a closed duodenal loop. The myeloperoxidase activity in and histological findings of the lung suggested that UT and GM reduced PMN accumulation. In conclusion, serine protease inhibitors may inhibit PMN accumulation in ARDS due to acute pancreatitis.
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PMID:Effects of serine protease inhibitors on accumulation of polymorphonuclear leukocytes in the lung induced by acute pancreatitis in rats. 764 5

We report the evaluation of a new commercial kit for the determination of pancreatic lipase activity. The kit is based on the use of a 1,2-diglyceride as substrate and a specific monoglyceride lipase. The detection step is the continuous colorimetric measurement of hydrogen peroxide produced from glycerol by glycerol kinase, glycerol-3-phosphate oxidase, and peroxidase reactions. The procedure appears to be precise (between-day CV < 9%) and the results show good correlation with those obtained by alternative procedures (vs turbidimetry, r = 0.965; vs ultraviolet absorbance-enzymatic method, r = 0.995; vs Ektachem, r = 0.976; vs immunometry, r = 0.970). However, the method is susceptible to interference by increased concentrations (> 4.5 mmol/L) of serum triglycerides. We estimated the reference interval for healthy adults to be 8-44 U/L. When we evaluated clinical efficacy by using receiver-operating characteristic curves and the overlap index, no significant differences were found between the commercial kit and a common turbidimetric assay for diagnosing patients with acute pancreatitis; both methods performed satisfactorily.
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PMID:Clinical and analytical evaluation of a continuous enzymatic method for measuring pancreatic lipase activity. 838 33

We have described a 45-year-old obese white man found to have myeloperoxidase (MPO) deficiency of the granulocytic and monocytic series. Pancreatic necrosis due to bacterial infection developed as a complication of acute pancreatitis. Subsequently, he died of sepsis. MPO staining of terminal antemortem blood smears and postmortem bone marrow aspirates showed absence of MPO in cells of the myelocytic and monocytic series. Family members' neutrophils and monocytes stained positive for MPO. MPO deficiency associated with severe sepsis is rarely reported. This case serves as a review of the association between hereditary and acquired MPO deficiency and severe infection.
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PMID:Myeloperoxidase deficiency and severe sepsis. 839 23

Hyperstimulation of the exocrine pancreas with cerulein causes acute pancreatitis, characterized by intensive interstitial edema, acinar vacuolization, leukocytic infiltration, and hyperamylasemia. Whereas the pathogenesis of cerulein-induced pancreatitis is not well-defined, a local inflammatory response may contribute to the full expression of acute pancreatitis. Platelet-activating factor (PAF) seems to be an important mediator of the inflammatory response. The present evidence includes: 1) pancreatic PAF levels increased in rats in which cerulein-induced pancreatitis was initiated, concomitant with an increase in calcium concentrations in the pancreatic tissue; 2) treatment of rats exposed to cerulein with WEB2170, a PAF receptor antagonist, was shown to reduce inflammatory injury, as demonstrated by decreases in pancreatic weight, Evan's blue extravasation, and myeloperoxidase activity and an improvement in pancreatic histology. In an idealized in vitro experiment mimicking cerulein-induced acute pancreatitis, in which pancreatic acini were employed, cerulein induced amylase release, an increase in [Ca2+]i, and an increase in PAF synthesis. Whereas amylase release was induced by low concentrations of cerulein (10(-11) mol/L), relatively high concentrations of cerulein (10(-9) mol/L) were required for the observed increases in PAF synthesis and the [Ca2+]i, indicating that these two responses may not occur under physiological conditions. The present study suggests that the pancreatic accumulation of PAF coupled with Ca2+ overload are important biochemical components of the pathophysiology of cerulein-induced acute pancreatitis. In fact, PAF production may serve as a primary mediator of inflammation observed during pancreatic hyperstimulation. This is an important observation that will allow a more detailed characterization of the molecular basis of cerulein-induced acute pancreatitis.
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PMID:Platelet-activating factor: a mediator of pancreatic inflammation during cerulein hyperstimulation. 849 49

We investigated the effects of the xanthine derivative propentofylline on lung injury in rats with cerulein-induced acute pancreatitis and endotoxemia. Pancreatitis was induced by four intramuscular injections of cerulein (50 micrograms/kg at 1-h intervals). Pancreatitis rats were injected intraperitoneally with 30 mg/kg lipopolysaccharide (LPS) 6 h following the first cerulein injection as a septic challenge. Propentofylline (50 mg/kg) was injected intravenously 15 min before the administration of LPS. Rats were divided randomly into five experimental groups: group I, normal rats; group II, pancreatitis; group III, LPS injection; group IV, pancreatitis and LPS injection; and group V, pancreatitis and LPS injection with propentofylline pretreatment. Serum amylase concentrations in groups II, IV, and V increased significantly 8 h after the first cerulein injection compared to those in groups I and III. Serum tumor necrosis factor (TNF)-alpha concentrations, cytokine-induced neutrophil chemoattractant (CINC) concentrations in serum or bronchoalveolar (BAL) fluid, lung myeloperoxidase (MPO) activity, and extent of pulmonary polymorphonuclear cell infiltration in group IV were significantly higher than those observed in group III. Pretreatment with propentofylline inhibited the rise in TNF-alpha levels (group V). However, propentofylline did not prevent the elevation of CINC levels in group V. In contrast, propentofylline reduced lung MPO and pulmonary PMN infiltration in group V. In addition, lung compliance was improved by pretreatment with propentofylline. These results suggest that propentofylline attenuates lung injury in an experimental model of pancreatitis complicated by endotoxemia but has differential effects on cytokine production.
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PMID:Effects of propentofylline on tumor necrosis factor-alpha and cytokine-induced neutrophil chemoattractant production in rats with cerulein-induced pancreatitis and endotoxemia. 909 57


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