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)

Pemphigus and bullous pemphigoid are autoimmune bullous diseases of the skin. Pemphigus, an intraepidermal blistering disease, is characterized by autoantibodies reactive with antigens located in the intercellular spaces or on the surfaces of epidermal cells. These antibodies, which have recently been shown to activate complement, appear to be the cause of the basic pathologic process of pemphigus, acantholysis. The complement system and the plasminogen-plasmin system may be important mediators in the detachment of epidermal cells. Bullous pemphigoid, a subepidermal blistering disease, is characterized by autoantibodies reactive with an antigen located in the lamina lucida region of the basement membrane zone. These autoantibodies, which will avidly fix complement, appear to mediate subepidermal separation by attraction of a variety of inflammatory cells. Anaphylatoxins, released by activation of C4 and C3, or specific IgE antibodies, may activate mast cells with release of ECF-A attracting eosinophils. With activation of C5, C5a is released which could attract polymorphonuclear leukocytes. Antigen-specific lymphocytes, which can also contribute histamine releasing substances, may also be involved. The exact mechanism by which the epidermis separates from the dermis in bullous pemphigoid, however, remains unresolved.
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PMID:Immunopathologic mechanisms in pemphigus and bullous pemphigoid. 389 83

Stimulation of normal rat splenic T cells with pertussigen (lymphocytosis-promoting factor, LPF, from Bordetella pertussis) resulted in the release of a soluble factor that enhanced the glycosylation of IgE-binding factors during their biosynthesis. The soluble factor was detected by the ability of a culture filtrate of LPF-stimulated spleen cells to switch a T cell hybridoma, 23A4, from the formation of unglycosylated IgE-binding factor to the formation of glycosylated IgE-binding factor. The glycosylation-enhancing factor (GEF) had affinity for D-galactose, and the binding of the factor to hybridoma cells via a cell surface galactose was essential for modulation of IgE-binding factors. The GEF was inactivated by irreversible inhibitors of serine proteases such as phenylmethylsulfonyl fluoride, diisopropylfluorophosphate, and p-nitrophenyl ethylpentylphosphonate but was not affected by nonphosphorylating analogues of the organophosphorus compounds. Benzamidine, a competitive and reversible inhibitor of trypsin, also inhibited the glycosylation of IgE-binding factors by GEF. The factor could be purified by absorption to p-aminobenzamidine agarose followed by elution with benzamidine. The capacity of GEF to enhance the glycosylation of IgE-binding factors was inhibited by synthetic substrates of trypsin but not by substrates of chymotrypsin, indicating that GEF is a trypsin-like enzyme. Indeed, trypsin, plasmin, and kallikrein enhanced the glycosylation of IgE-binding factors during their biosynthesis. An inhibitor of trypsin-like enzyme(s), N-alpha-p-tosyl-L-lysine chloromethylketone (TLCK), inhibited trypsin and plasmin but not kallikrein, and TLCK failed to inhibit the GEF-mediated enhancement of glycosylation. It was also found that bradykinin, the biologically active product of cleavage of kininogen by kallikrein, enhanced the glycosylation of IgE-binding factors. The results indicate that GEF is a kallikrein-like enzyme.
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PMID:Modulation of the biologic activities of IgE-binding factor. IV. Identification of glycosylation-enhancing factor as a kallikrein-like enzyme. 655 15

In an attempt to access the possible role of protease-antiprotease mechanisms of non-immune defence in pollinosis, only low levels of trypsin-, kallikrein- or plasmin-like proteinases could be detected in aqueous pollen extracts. In contrast, several pollen species displayed appreciable trypsin inhibitory activity, e.g. Parietaria, Olea, Ambrosia, Rumex, Chenopodium, Holcus and Poa spp. These proteins of the serpin family of anti-proteinases were found to bind specific IgE-antibodies from the serum of hay fever patients. As examples, the IgE-binding trypsin inhibitors from the pollen of Parietaria judaica and Ambrosia elatior were purified and characterized as acidic proteins with pI 4.2 and a molecular weight of 20-24 kDa.
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PMID:IgE-binding trypsin inhibitors in plant pollen extracts. 755 77

We measured serial serum tryptase levels in a case of intraoperative anaphylaxis caused by allergy to latex. The serum tryptase level was elevated 7 hours after the hypotensive episode and returned to normal after recovery 4 months later. Both skin tests to latex and serum IgE to latex confirmed latex allergy in this patient. To our knowledge, this is the first report of an elevated serum tryptase level in intraoperative anaphylaxis caused by latex allergy. This observation confirms the role of mast cell degranulation in anaphylaxis caused by allergy to latex.
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PMID:Elevated serum tryptase level in a case of intraoperative anaphylaxis caused by latex allergy. 794 46

Changes in transfusion behaviour induce a widespread use of colloid plasma substitutes, the range of which has recently been enlarged by the marketing of starch derivatives. The product chosen depends, at least in part, on its adverse effects, anaphylactoid reactions being a part of these. This study aimed to discover the frequency and severity of these reactions according to the type of substitute available in France, to look for possible risk factors, and determine the mechanisms involved. A prospective inquiry was carried out in 49 public and private hospitals spread throughout France. It lasted for 15 months, between June 1991 and October 1992. A data sheet was filled in for each patient who was given a plasma substitute, whether or not there was an incident. When a reaction did occur, an assessment was carried out in two stages: straightaway, with the measurement of the concentrations of serum tryptase, antigelatin antibodies, urinary methylhistamine; and four to six weeks later, with skin tests. A series of 19.593 patients was thus collected: 48.1% were given gelatins, 26.7% starches, 15.7% albumin, and 9.5% dextrans. 43 anaphylactoid reactions were recorded, giving an overall frequency of 0.219%, or 1 reaction for 456 patients. The frequency differed according to the substitute considered: 0.345% for gelatins, 0.273% for dextrans, 0.099% for albumin, and 0.058% for starches. These reactions (grades III and IV) were serious in 20% of cases. Multivariate analysis revealed four independent risk factors: giving gelatins (odds ratio: 4.81), giving dextrans (odds ratio: 3.83), a history of drug allergy (odds ratio: 3.16), and being male (odds ratio: 1.98). The relative risks of anaphylactoid reactions due to one type of substitute with respect to another were estimated to be 6 times less for starches with respect to gelatins, and 4.7 times less than with dextrans. The relative risk of albumin is 3.4 times less than that of gelatins, and almost identical to that of the starches. An immuno-allergological assessment was only carried out in 15 patients who had been given a gelatin (Plasmion). IgE-dependent anaphylaxis was proven in 7 of these. To conclude, it was shown that gelatins and dextrans should be avoided in patients with a known history of drug allergy. When a reaction does occur, an allergological assessment must be carried out, as this may be due to specific antibodies. Should this prove to be the case, that particular substitute would be contraindicated for the rest of the patient's life.
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PMID:[Anaphylactoid reactions to colloid plasma substitutes: incidence, risk factors, mechanisms. A French multicenter prospective study]. 767 80

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

Although allergenic cross-reactivity of neuromuscular blocking drugs (NMBDs) is recognised clinically and has been firmly established at the serological and immunochemical levels, interpretation of in vitro inhibition findings for clinical purposes is not always straightforward. Points to be taken into account when considering serum IgE direct binding and inhibition results and when determining which NMBDs a patient may be sensitive to, include the relationship between in vitro potencies and clinical findings and the nature of the drug solid phase used for testing. It should also be remembered that the stimulating antigenic source for the patients' NMBD-reactive IgE antibodies is almost always unknown. A comparison of skin and IgE radioimmunoassay (RIA) tests for NMBDs in 29 patients is presented and difficulties involved in interpreting the results of both tests are discussed. Methods for increasing the detection of NMBD-reactive IgE antibodies are outlined. In screening sera of patients for IgE antibodies to thiopentone and morphine as well as NMBDs, multiple drug reactivities have been detected in a few subjects. Attention is drawn to defects in the existing thiopentone RIA although it is clear that the test is specific in patients who react to the drug. Addition of the serum tryptase assay to skin tests and IgE RIAs for NMBDs, thiopentone and morphine provides a powerful combination of diagnostic tests for the investigation of anaphylactoid reactions to anaesthetic drugs.
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PMID:Diagnosis of IgE-dependent anaphylaxis to neuromuscular blocking drugs, thiopentone and opioids. 836 86

A protocol has been produced for the study of anaphylactic accidents that occur post-operatively that allows definition of the anaphylactic origin, and so reactions that are mediated by IgE in post-operative accidents. This protocol occurs in two stages, the first is done in the minutes and hours that follow the anaphylactic accident, and the second a month or 6 weeks afterwards. At first, we evaluate the sequential study of the liberation of the mediators of anaphylaxis, plasma histamine, serum tryptase, urinary methylhistamine and, more recently, leucotriene E4. The second study is devoted to reactions that are mediated by IgE, essentially, specific serum IgE, tests of activation of basophils by flow cytometry, measurement of leucotriene C4 and skin tests. A study on 16 subjects has evaluated and validated the protocol and shown a significant level of correspondence of results between the sequential measurement of mediators on one hand and on the other the search for IgE-mediated reactions every time that there was an anaphylactic reaction.
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PMID:[Allergic immunobiology and anesthesiology]. 968 38

Adverse reactions to antibacterial agents are not uncommon in children. They are classified as 'immediate' or 'nonimmediate' according to the time interval between drug administration and onset. Immediate reactions occur within 1 hour and are manifested by urticaria and/or angioedema, bronchospasm and anaphylactic shock; immunological reactions are mediated by IgE antibodies. The main nonimmediate reactions (occuring after more than 1 hour) are maculopapular rash, urticaria and serum sickness; T lymphocytes may participate in maculopapular rash. Clinical assessment of such reactions is complex. The patient's history is fundamental; the allergological examination includes in vivo and in vitro tests selected on the basis of the clinical features and the phase of reaction. In the late phase, prick and intradermal tests are sensitive in evaluating beta-lactam allergy. Together with delayed-reading intradermal testing, patch testing seems to be useful in diagnosing maculopapular reactions to systemically administered aminopenicillins. Determination of specific IgE levels is the most common in vitro method for diagnosing immediate reactions. In the acute phase, serum tryptase and urinary N-methylhistamine assays are reliable in diagnosing type I pathogenic mechanisms in immediate reactions. Unfortunately, there are few in vitro tests for evaluating other reactions, and most are not fully validated. In selected cases, provocation tests should be performed.
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PMID:Recognising antibacterial hypersensitivity in children. 1093 62

Food anaphylaxis is now the leading single cause of anaphylactic reactions treated in emergency departments in Westernized countries. In the US, it is estimated that there are 29,000 anaphylactic reactions to foods treated in emergency departments and 125-150 deaths each year. Peanuts, tree nuts, fish and shellfish account for the vast majority of severe food anaphylactic reactions. Immunopathogenic mechanisms responsible for food anaphylaxis may differ somewhat from other forms of anaphylaxis, since elevation of serum tryptase is rarely seen following food anaphylactic reactions. Education regarding the strict avoidance of food allergens, the early recognition of anaphylactic symptoms, and the early use of self-injectable epinephrine remain the mainstays of therapy. However, clinical trials are now underway for the treatment of patients with peanut anaphylaxis utilizing anti-IgE antibody therapy and novel immunomodulatory therapies utilizing 'engineered' recombinant proteins, overlapping peptides, and immunostimulatory deoxyoligonucleotide sequences are being tested in animal models of anaphylaxis.
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PMID:Food anaphylaxis. 1135 29


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