Gene/Protein Disease Symptom Drug Enzyme Compound
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42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several aspects of in vitro tests for life-threatening anaphylactoid reactions (AR) to neuromuscular blockers (NMB, muscle relaxants) were addressed and highlighted. They include topics which have been under study in our centre in the past few years. Already available tests and newly developed ones were assessed for diagnostic and predictive value, as well as for usefulness in understanding of mechanism(s) of AR. The theoretical and practical aspects of radioallergosorbent tests (RAST) for antibodies to NMB (particularly IgE), their predictive value and their possible use in "screening" with the hope of preventing AR are discussed. Confirmatory tests after AR include plasma or serum histamine/methylhistamine, tryptase and possibly eosinophil cationic protein (ECP), all of which point to activation of mast cells, basophils, eosinophils and possibly other inflammatory cells. Future anesthetics after AR can be guided by measurement of the in vitro release of histamine, leukotrienes and possibly eosinophil cationic protein (ECP) and serum antibodies. Antibody studies (mainly IgE by RAST) are valuable for diagnosis and, together with other tests, can throw light on cross-reaction and further clarify the mechanisms of AR. In RAST (IgE)-negative cases of AR, which may be due to immune or nonimmune mechanisms, mediator release measurements are particularly useful. Lymphocyte stimulation tests may also be useful in such cases. RASTs cannot be advocated for general preoperative screening, as yet. Further development or selection of potentially "susceptible" subpopulations may improve the predictive value of these tests.
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PMID:Predictive value of in vitro tests for the IgE-dependent and the IgE-independent anaphylactoid reactions to muscle relaxants. 769 Feb 6

By using a microsuction technique, a quantitative determination of chemical mediators in nasal secretions was performed in 18 hay-fever patients and in a control group of 10 healthy volunteers. The authors then compared these quantitative data for mediators with objective nasal findings counting the number of sneezes, passive anterior rhinomanometry (PAR) and nasal inspiratory peak flow. A sampling protocol was designed with a follow-up of 3 days after nasal allergen challenge (NAC) in order to investigate both early and late allergic reactions. Median baseline concentrations of five major mediators were obtained: histamine, 19 ng/g; leukotriene C4 (LTC4), 5.7 ng/g. tryptase, 0; prostaglandin D2 (PGD2), 477 pg/g; eosinophil cationic protein (ECP), 105 ng/g. Significant increases in histamine (214 ng/g), LTC4 (20 ng/g) and tryptase (28 microU/g) were found, but a significant decrease occurred in ECP (47 ng/g) and PGD (226 pg/g) immediately after NAC in the patients studied. Most ECP concentrations (94%) increased slowly 1 h after NAC and reached a significantly higher level 24 h later. In evaluating nasal symptoms, sneezes were present in a high percentage of cases (76%) during the early phase but were uncommon during the late phase (29%). Total nasal obstruction occurred in 94% during the early phase. In contrast, unilateral nasal obstruction presented in 82% during the late phase, whereas total nasal obstruction was present only in 41%. The most common type of late phase nasal obstruction shown by PAR was alternating nasal obstruction.
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PMID:Concentrations of chemical mediators in nasal secretions after nasal allergen challenges in atopic patients. 773 74

By using the microsuction technique, quantitative determination of the chemical mediators in nasal secretions was performed in 40 patients with seasonal allergic rhinitis during the pollen season. The aim of this study was to investigate the actual concentrations of these important mediators in nasal secretions during natural allergen exposure so as to better understand the pathophysiology of allergic rhinitis. The median concentrations of four mediators, were histamine: 51.5 ng/g (range: 4-146 ng/g); tryptase: 0 (range: 0-84 microU/g); leukotriene C4 (LTC4): 23 ng/g (range: 11-77 ng/g); and eosinophil cationic protein (ECP): 410 ng/g (range: 6-2380 ng/g). The authors compared these concentrations with those of the same mediator found in a previous study of seasonal allergic rhinitis patients after nasal challenge outside the pollen season. The present study demonstrates that during the season allergic rhinitis reflects a chronic state of allergic inflammation of the nasal mucosa involving various inflammatory mediators induced by one or more episodes of early type allergic reaction.
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PMID:Concentrations of chemical mediators in nasal secretions of patients with hay fever during natural allergen exposure. 782 40

In the last years, the role of nasal mast cells and the eosinophils in the immediate hypersensitivity reaction of allergic rhinitis has been well documented. Tryptase and the eosinophil cationic protein (ECP) are specific activation markers for mast cells and esosinophils respectively. To determine the possible diagnostic value of these markers in allergic rhinitis we measured the levels in both serum and native nasal fluid using sandwich RIA-assays. Twenty eight seasonal allergic patients (16 with active allergy and 12 with extraseasonal allergy) and 11 patients with chronic sinusitis were studied. Twenty one normal healthy donors served as controls. We could not detect increased levels of tryptase and ECP in the serum of all patients and healthy donors. In contrast, patients with active allergy showed very higher levels of ECP than patients of the three other groups. Similarly, nasal ECP was higher in patients with nasal pathology than in healthy subjects. The highest levels were found in the patients with active allergic rhinitis. Our results show that both native nasal fluid tryptase and ECP can be used as markers of local inflammation and that the assessment of their levels can be useful in the diagnosis and follow up of mucosal inflammation in the nose.
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PMID:[Diagnosis of allergic rhinitis by determining of tryptase and eosinophil cationic protein in nasal secretions]. 787 34

A quantitative determination of the inflammatory mediators was performed and correlated with complaints and the measurement of the inflammatory cells in nasal secretions of 18 seasonal allergic rhinitis patients (group 1) outside the pollen season and 40 symptomatic patients (group 2) with seasonal allergic rhinitis during the pollen season. Ten nonallergic subjects (group 3) were also studied as a normal control group. In group 1, 17 (94%) out of 18 patients had an immediate response of nasal symptoms accompanied by a significant increase of histamine, leukotriene C4 (LTC4), and tryptase 5 min after nasal allergen challenge (NAC). One hour later, a simultaneous increase was seen both in the percentage of the eosinophils and in the eosinophil cationic protein (ECP) concentration. The eosinophil count reached a peak 2 h after NAC with a duration of 8 h, while the highest ECP level was reached only after 24 h with no clear-cut plateau. In group 2, a high percentage of eosinophils was observed. Mostly one observed significantly (p < 0.01) higher concentrations of ECP, LTC4 and histamine but not of tryptase than the baseline values of group 1. The authors concluded that during the pollen season allergic rhinitis reflects mainly a chronic state of allergic inflammation of the nasal mucosa involving various inflammatory components induced by one or more episodes of early-phase type allergic reaction. Infiltration of eosinophils and consequently release of the various late-phase inflammatory mediators into the nasal secretions are certainly believed to be the predominant pathophysiologic condition in the patients.
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PMID:Correlations between complaints, inflammatory cells and mediator concentrations in nasal secretions after nasal allergen challenge and during natural allergen exposure. 788 90

Serum levels of eosinophil cationic protein (ECP), myeloperoxidase (MPO), tryptase, total IgE and differential blood cell counts were studied in atopic children with: 1) moderate to severe asthma using inhaled steroids and symptom-free for the last 3 weeks (n = 13), 2) mild asthma with sporadic symptoms, using only inhaled beta 2-agonists < 3 times/week (n = 15), 3) acute asthmatic attacks admitted to hospital (n = 12), 4) mild to moderate atopic dermatitis (n = 14). Fifteen children without any history of atopy served as controls. ECP, MPO, tryptase and IgE were measured in serum by radioimmunoassays (RIA). The symptom-free children with inhaled steroids had similar median ECP and MPO values as the controls, 8.0 and 360 micrograms/l, vs. 9.0 and 310 micrograms/l, while both ECP and MPO were significantly (p < 0.001) increased in the symptom-free children without anti-inflammatory treatment, 32 and 887 micrograms/l and in those with acute asthma, 28 and 860 micrograms/l. The children with atopic dermatitis had increased ECP but normal MPO levels, 16.0 and 455 micrograms/l. Tryptase in serum was not measurable in any patient. All groups except the control group had significantly elevated total IgE levels. The results indicate that in atopic children serum ECP is a good marker of ongoing asthma or atopic dermatitis. The normal levels of ECP and MPO in the children with asthma using inhaled steroids seem to reflect successful anti-inflammatory treatment. The increased levels of ECP and MPO in the children with mild asthma and no anti-inflammatory treatment may indirectly reflect airway inflammation.
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PMID:Eosinophil cationic protein, myeloperoxidase and tryptase in children with asthma and atopic dermatitis. 789 29

It had been postulated from earlier studies that platelets of aspirin-sensitive asthmatics reacted to aspirin and other cyclo-oxygenase inhibitors. Similarly, a generalized abnormality had been suggested in the regulation of arachidonic acid oxidative pathways in blood leukocytes of patients with aspirin-induced asthma. Studies of activation in vitro as well as in vivo assessment of polymorphonuclear leukocytes have not been conclusive of metabolic pathways inducing bronchospasm in aspirin-sensitive asthmatic patients. Serum levels of tryptase, a specific marker of mast cell activation, appear to increase during bronchoconstriction following ingestion of oral aspirin. Eosinophil cationic protein (ECP) levels in serum are concomitantly elevated. Leukotriene antagonists may partially protect individuals with allergen-provoked or aspirin-provoked bronchoconstriction.
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PMID:Mediator assays in aspirin-induced asthma. 792 12

To determine whether the measurement of specific markers of inflammatory cells in peripheral blood might be used to detect the inflammatory activity in the airways in asthma induced by toluene diisocyanate (TDI), we measured the levels of eosinophil cationic protein (ECP), histamine and tryptase in peripheral blood before and during inhalation challenge with TDI or methacholine in two groups of subjects who exhibited or did not exhibit an asthmatic reaction after exposure to toluene diisocyanate in the laboratory. When the subjects developed a late asthmatic reaction after exposure to TDI, they showed an increase in their ECP serum levels. By contrast, there were no significant changes in serum ECP levels after exposure to TDI in the control group or after methacholine challenge in either group. Tryptase levels in serum were not detectable before or during inhalation challenge with TDI or methacholine. There was no significant increase in plasma histamine levels during inhalation challenge with TDI or methacholine. These results suggest that eosinophils are 'activated' in subjects who develop a late asthmatic reaction after exposure to TDI and that the measurement of ECP levels in peripheral blood may be a useful marker to monitor airway inflammation.
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PMID:Eosinophil cationic protein (ECP), histamine and tryptase in peripheral blood before and during inhalation challenge with toluene diisocyanate (TDI) in sensitized subjects. 798 22

To determine whether analysis of the constituents of induced sputum permits detection of changes provoked by aerosolized antigen challenge, we performed sputum induction (20-minute inhalation of aerosolized 3% saline solution) before and after aerosolized allergen challenge in eight subjects with asthma. Total cell counts and cell differentials of nonsquamous cells in induced sputum samples were determined after the samples were homogenized in dithiothreitol. Centrifugation of the entire homogenized sputum sample yielded supernatant that could be analyzed for biochemical constituents. We found that the median percentage of eosinophils and neutrophils in induced sputum samples was significantly higher 4 hours after allergen challenge neutrophils in induced sputum samples was significantly higher 4 hours after allergen challenge than at baseline (12% vs 0.5%, p < 0.05; 30.5% vs 7.5%, p < 0.05) and remained high 24 hours after challenge. Median levels of eosinophil cationic protein and histamine in induced sputum supernatants were significantly higher 4 hours after challenge than at baseline (151.3 vs 39.8 ng/ml, p < 0.05; 19.4 vs 8.8 micrograms, p < 0.05) and remained significantly higher 24 hours after challenge. Tryptase was detectable in sputum from seven of the subjects, and in these subjects, we found a trend toward an increase in median tryptase levels 4 hours after allergen challenge (4.4 vs 2.2 U/L, p = 0.09). We conclude that analysis of induced sputum after aerosolized allergen challenge reveals changes in inflammatory cells and markers similar to those reported in bronchoalveolar lavage fluid and that sputum induction is a useful noninvasive method for studying allergic airway inflammation in asthma.
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PMID:Analysis of cellular and biochemical constituents of induced sputum after allergen challenge: a method for studying allergic airway inflammation. 800 8

A study was performed in 43 workers exposed to methyltetrahydrophthalic anhydride (MTHPA) used as a hardener in an epoxy resin system. Ten workers sensitized to MTHPA (group SS; presence of serum IgE antibodies against a conjugate of MTHPA and human serum albumin (HSA) detected by RAST) had significantly higher levels of tryptase in nasal lavage fluid than 19 nonsensitized workers with work-related nasal symptoms (group NS) and 14 nonsensitized workers without nasal symptoms (group NN). This suggests an ongoing mast-cell-mediated reaction in the sensitized group. No statistically significant differences were found in the three groups concerning eosinophil cationic protein (ECP) and TAME-activity in lavage fluid. However, there was a significant increase in serum ECP in the SS group, as compared with a group of unexposed controls. Nasal challenge with MTHPA-HSA, performed in a subsequent study in seven workers from the SS group, six from the NS group, and seven from the NN, caused a larger increase of symptom score and a more pronounced decrease in nasal inspiratory peak flow in the SS group than in the other two groups. No significant rise was recorded for tryptase and ECP in lavage fluid in any of the three groups after challenge. The combined results of the two studies indicate that specific IgE antibodies play a pathogenetic role in at least some of the cases of work-related nasal symptoms associated with MTHPA exposure.
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PMID:Symptoms and immunologic markers induced by exposure to methyltetrahydrophthalic anhydride. 803 60


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