Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.7 (plasmin)
 9,023 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Objective improvement in the diagnosis of immuno-allergology can only be obtained by application of reliable and reproducible immuno-biological methods, but until now, only measurements of total and specific IgE can be used and this has certain limitations. Presence of specific serum IgE, correlated with skin tests, favours a sensitization and implies nothing about the responsibility of the allergens. This is why we must consider if a definite improvement of diagnostic methods can be obtained by measurement of mediators. From an observation of food allergy to pork meat, we now show that it is possible to use sequential measurements of the mediators plasma histamine and urinary methylhistamine, ECP and serum tryptase to refine the diagnosis and provide proof of the responsibility of the food allergen. We report here a didactic observation which is characterised by reproducibility and specificity of the measurements. It illustrates the progress in diagnostic methods in allergy: we give a statistical diagnosis by measurement of antibodies and a dynamic diagnosis by measurement of mediators.
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PMID:[Dynamic diagnosis of allergy by the sequential measurement of mediators: apropos of a case of food allergy]. 816 38

The inflammatory mediators of allergy were investigated in symptomatic patients suffering from upper respiratory tract allergy. The serum tryptase level as an indicator of mast cell activation and serum eosinophil cationic protein level as an indicator of eosinophil activation were measured. They did not find any alteration in the serum level of tryptase. The level of eosinophil cationic protein significantly increased in symptomatic patients comparing to normal healthy controls. There was not any correlation to the severity of symptoms and to the absolute eosinophil count in the peripheral blood. The different activation possibilities of the eosinophil granulocytes are discussed, highlighting the role of Th2-helper lymphocytes.
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PMID:[Allergic inflammatory markers in upper respiratory allergies]. 846 28

In this study the routine use of different parameters for evaluation of the overall therapeutic outcome in atopic dermatitis was investigated. The disease activity of 117 randomly selected hospitalized patients suffering from atopic dermatitis was routinely assessed using the Severity Scoring of Atopic Dermatitis (SCORAD) index on admission and at discharge. Serum levels of eosinophil cationic protein and mast cell tryptase were determined in parallel both on admission and at discharge. After a mean treatment period of 24+/-12 days a decrease in the SCORAD index from 47.6+/-19.5 to 7.7+/-8.2 was achieved (p<0.001). Serum levels of eosinophil cationic protein decreased from 22.8+/-19.7 microg/l to 15.4+/-17.5 microg/l, whereas serum tryptase levels did not change. However, there was no significant correlation between the changes in SCORAD, eosinophil cationic protein and tryptase in our cohort. Thus, routine determination of serum eosinophil cationic protein or tryptase levels, in addition to evaluation of disease activity using the SCORAD index, is not recommended in unselected patients with atopic dermatitis.
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PMID:Comparison of severity scoring of atopic dermatitis values and serum levels of eosinophil cationic protein and mast cell tryptase for routine evaluation of atopic dermatitis. 1102 63

Recent studies suggest that many fatal heroin overdoses are caused by anaphylactoid reaction. In the present study we measured tryptase and eosinophil cationic protein in post-mortem blood of 48 deaths after heroin injection. We also investigated the presence and pulmonary distribution of mast-cells using specific immunohistochemical antibody for tryptase and morphometric evaluation in those cases of heroin-related deaths. The data were compared with 44 subjects who died following head trauma and to 32 cases of fatal anaphylactic shock. In the heroin-related death cases, the measurements of serum tryptase levels and eosinophil cationic protein dosages resulted in particularly elevated concentrations compared with the trauma cases. Nevertheless, the data that our study supplies by immunohistochemical techniques indicate that when mast-cells count in the lung was determined, no definite pattern was obtained between fatal heroin overdose cases and the control groups. Furthermore, the wide range of morphine concentrations found in post-mortem blood samples suggest that the term 'overdose' is relative and does not sufficiently characterize death associated with heroin addiction. Our study confirms that elevated concentrations of serum tryptase are associated with many heroin-related deaths. At this moment to attribute the cause of these deaths to 'heroin overdose' ignores the likely causal contribution of other possible systemic reactions to the mechanism of death.
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PMID:Immunohistochemical quantification of pulmonary mast-cells and post-mortem blood dosages of tryptase and eosinophil cationic protein in 48 heroin-related deaths. 1147 1

Tryptase is a specific marker of mast-cell activation and plays a part in the pathophysiology of various allergic diseases including asthma, but little is known of the spillover of this enzyme into the systemic circulation. Therefore, we measured serum levels of mast-cell-derived tryptase in 21 patients with mild to moderate asthma and 20 healthy, subjects, using a B12 monoclonal antibody-based immunofluoroassay that detects both monomers and tetramers of alpha- and beta-tryptases. There was a good correlation between serum and sputum tryptase levels, and, compared with healthy subjects (1.68 +/- 0.31 ng/ml), asthma patients had higher concentrations of serum tryptase (atopic asthma, 4.18 +/- 0.95 ng/ml, p = 0.022; nonatopic asthma, 3.93 +/- 0.82 ng/ml, p = 0.031). Although serum tryptase levels did not correlate with asthma symptom scores, peak expiratory flow, or forced expiratory volume in 1 s, they positively correlated with mast-cell and eosinophil counts (p = 0.041 and p = 0.025, respectively) and eosinophil cationic protein contents (p = 0.029) in induced sputum. These results suggest that serum tryptase detected with B12 antibody is a marker of allergic airway inflammation in asthma.
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PMID:Serum B12 tryptase level as a marker of allergic airway inflammation in asthma. 1209 81

Oranges are suspected of inducing adverse skin reactions in patients with atopic eczema. We studied 21 adult patients with atopic eczema and a history of adverse reactions to oranges and 10 patients without. A dietary history, skin tests, serum IgE and oral provocation tests with oranges were obtained. Severity of eczema was monitored by SCORAD, and serum tryptase, eosinophil cationic protein and urinary methylhistamine were measured. No allergic reactions were found to orange in skin prick or patch tests. However, 23 patients (74%) had specific serum IgE to orange. Oral provocation testing resulted in pruritic eczematous or maculopapular skin lesions predominantly at the predilection sites in 16 patients (52%). The SCORAD increased significantly in patients positive to the oral provocation test (p <0.05). Specific IgE to orange did not correlate with the clinical outcome of the oral provocation test. No significant changes were found in serum mast cell tryptase, eosinophil cationic protein or in urinary methylhistamine excretion. The negative results in the skin tests and a lack of correlation between specific IgE and oral provocation tests indicate that non-IgE-mediated mechanisms are involved in cutaneous adverse reactions to oranges in patients with atopic eczema.
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PMID:Orange-induced skin lesions in patients with atopic eczema: evidence for a non-IgE-mediated mechanism. 1263 22

Numerous biological tests point to the diagnosis of food sensitization: detection of specific IgEs by Rast techniques, multi-detection assays, immunoblotting, screening of basophil activation (BAT or FAST), assays for leukotriene LTC4 release (CAST), measurement of plasma histamine, serum tryptase, serum ECP, urinary EDN, completed by mannitol-lactulose test evaluating intestinal permeability, assay of fecal IgEs, Rast for specific IgG4. Primary screening for anti-food IgEs by multi-detection assays seeks justification from insufficient clinical data and false positive tests are common in patients sensitized to pollens or latex, on account of in vitro cross reactivities (CR). Multiple CR explain positive Rast to vegetal food allergens in such patients. Biological tests should not be performed as the first line of diagnosis. In vivo sensitisation is assessed by positive prick-tests, demonstrating the bivalence of allergens, as well as the affinity of specific IgEs, two conditions necessary to bridge membrane bound specific IgEs, leading to the release of mediators. Prick-tests are closer to clinical symptoms than biological tests. However, the diagnosis of food allergy is based on standardised oral challenges. Exceptions are high levels of specific IgEs to egg (> 6 kUl/l), peanut (> 15 kUl/l), fish (> 20 kUl/l) and milk (> 32 kUl/l), reaching a 95% predictive positive value. Rast inhibition tests are useful to identify masked allergens in foods. Research developments will have impact on the development of new diagnostic tools: allergen mixes reinforcing a food extract by associated recombinant major allergens, multiple combination of recombinant allergens (chips) or tests with synthetic epitopes aimed a the prediction of recovery. Laboratory tests take place in the decision free for the diagnosis for the food allergy and the follow-up of the levels specific IgEs is a tool to assess outcome and contributes to predict recovery or persistent allergy. Up to now the significance of positive laboratory tests showing the implication of IgEs is at the crossroads of the allergist's and biologist's expertise.
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PMID:Laboratory tests for diagnosis of food allergy: advantages, disadvantages and future perspectives. 1279 13

Based on generally accepted criteria and the WHO-classification, a subset of patients with systemic mastocytosis (SM) have (or develop) an associated clonal hematologic non-mast cell lineage disease (SM-AHNMD). We describe a case of SM with coexisting chronic eosinophilic leukemia (SM-CEL). The patient, a 51-year-old male, was first seen in 1992 with small-sized infiltrates of spindle-shaped mast cells in his marrow, and marked eosinophilia. Retrospectively, a CHIC2 deletion and the FIP1L1/PDGFRalpha fusion gene-product were demonstrable by FISH analysis and RT-PCR, respectively. SM-associated organopathy or mediator-related symptoms were not recorded. However, the patient developed cardiomyopathy. Therapy with interferon-alpha, hydroxyurea, and corticosteroids were without effects. By contrast, therapy with imatinib was followed by a fast and sustained response with complete and stable regression of eosinophilia, drop in eosinophil cationic protein, and decrease of serum tryptase to normal levels. This case provides further evidence for the potential of co-existence of SM with a primary eosinophilic disorder (CEL) defined by the FIP1L1/PDGFRalpha fusion gene. Because of the availability of a superior targeted drug (imatinib), it is of importance to screen for FIP1L1/PDGFRalpha in suspected CEL with or without co-existing SM.
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PMID:Systemic mastocytosis (SM) associated with chronic eosinophilic leukemia (SM-CEL): detection of FIP1L1/PDGFRalpha, classification by WHO criteria, and response to therapy with imatinib. 1640 18