Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The different clinical presentations of analgesics-intolerance are presented in four asthmatic children. Analgesics-intolerance is rare in children and both sexes are equally affected. The affected children have either a severe mixed asthma and often a chronic sinusitis and nasal polyps, or a chronic urticaria. Often, the first manifestation occurs several years after onset of asthma and is triggered by respiratory infections. Ingestion of most analgesics may cause severe bronchial obstruction, urticaria, angioedema, collaps and rhinitis. The diagnosis can be established by an unequivocal history, or, in uncertain cases, by an inhalation challenge with lysin-acetylsalicylate. The best prophylaxis and therapy is to avoid all responsible drugs. The inhibitory effect of most analgesics on the cyclooxygenase initiates impairments in the metabolism of prostaglandins and leukotrienes, which are suspected to cause the bronchial obstruction in intolerant patients.
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PMID:[Analgesic intolerance in asthmatic children]. 296 30

After a short historical review, the clinical symptomatology of the pseudoallergic reactions (PAR) after intake of acetylsalicylic acid (ASS) is examined. An intolerance to ASS mostly becomes manifest as bronchial asthma--sometimes up to a status asthmaticus: it is frequently combined with vasomotoric rhinopathia and nasal polyps (so-called "aspirin triad") or as urticaria and angio-edema, seldom as a shock reaction. These symptoms can - in contrast to an allergy--appear at the first intake of the drug. Changes in the arachidonic acid metabolism are of pathogenetic importance, as all substances that inhibit the cyclooxygenase pathway [e.g., most of the nonsteroidal anti-inflammatory drugs (NSAIDs)] are not tolerated by ASS-sensitive patients. Generally, a typical clinical history is sufficient for the diagnosis. Due to the fact that the ASS and NSAID pseudoallergy so far cannot be proved by in vitro methods, oral or inhalative provocation tests are needed when the tolerance situation to the drugs is unknown. However, these tests present high risks. A research group working with Capron (Lille) has recently been able to prove that washed platelets from patients with an analgetic asthma syndrome show an abnormal in vitro response to ASS or NSAID - like indomethacin and fluriprufen - which is characterized by liberation of cytocydal supernatants against parasites, as well as of free O2 radicals, which can be detected by chemiluminescence. Therefore, a platelet anomaly of arachidonic acid metabolism seems to be pathognomonic for ASS asthma. It is not yet known whether or not this is also related to ASS urticaria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acetylsalicylic acid pseudoallergy: an anomaly of thrombocyte function?]. 314 93

Nonsteroidal anti-inflammatory drugs (NSAID) are among the most frequent causes of adverse drug reactions. The clinical symptoms often resemble allergy and consist of anaphylactic shock, bronchospasm, urticaria, angioedema, and various skin eruptions. Patients with asthma or urticaria are particularly prone to these reactions. In about 10% of adult asthmatics, aspirin and several other NSAID precipitate open asthmatic attacks, most likely through inhibition of cyclooxygenase. This distinct clinical syndrome has a characteristic sequence of symptoms and clinical course. In 20% to 40% of patients with active urticaria, aspirin increases wheals and swelling. Pyrazolones might provoke two different types of clinical reactions, acting as allergens or interfering pharmacologically with cyclooxygenation of arachidonic acid. Other mechanisms might operate in some of the remaining adverse reactions to NSAID. Emerging clinical syndromes help to guide the clinicians through the maze of symptoms and often provide a unique insight into the mechanism of basic disease.
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PMID:Adverse reactions to aspirin and nonsteroidal anti-inflammatory drugs. 331 75

Intolerance to analgesics is common in patients with bronchial asthma, nasal polyps and urticaria. Symptoms of intolerance resemble those of allergy, but the events precipitating them can rarely be traced to reactions between the drug and a specific antibody or sensitised T-lymphocytes. In 8 to 20% of adult asthmatics, aspirin and several other analgesics provoke asthmatic attacks, probably through inhibition of cyclo-oxygenase. This is a distinct and important clinical syndrome with a specific history, course and clinical presentation and a number of unique peculiarities which still require elucidation at the biochemical level. Up to 40% of patients with chronic urticaria develop an obvious increase in weals and swelling after taking aspirin. These reactions occur only when urticaria is active, and though the reason for them is not known, it appears that different mechanisms may be responsible in different patients. Skin reactions other than exacerbation of chronic urticaria are less common, but may create serious clinical problems. The clinical background of a patient often determines the type of adverse response to an analgesic. Thus, in certain individuals, analgesics can produce anaphylactic reactions and/or urticaria, probably through an immunological mechanism, while in some asthmatics they precipitate bronchoconstriction, probably through inhibition of bronchial cyclooxygenase. Study of untoward reactions to analgesics not only leads to safer pharmacotherapy, but it also offers a fascinating model for better understanding of some diseases.
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PMID:Analgesics, allergy and asthma. 355 81

Recent studies of idiosyncratic reactions to analgesics have revealed several clinical patterns with different pathogeneses. In the common type of asthma precipitated by aspirin, inhibition of cyclooxygenase leads to disturbances in the metabolism of arachidonic acid. Drugs that precipitate possibly life-threatening bronchoconstriction and are absolutely contraindicated in patients with aspirin-induced asthma include indomethacin, mefenamic acid, flufenamic and meclofenamic acids, ibuprofen, fenoprofen, ketoprofen, naproxen, diclofenac, amidopyrine, noramidopyrine, phenylbutazone, flumizole, and ditazol. If necessary, patients with aspirin-induced asthma can safely take, even on a long-term basis, salicylamide, dextropropoxyphene, benzydamine, guaiacolic ester of salicylic acid, and chloroquine. In some patients with urticaria/angioedema, symptoms are due to inhibition of cyclooxygenase by analgesics; in others, the cause may be impurities in commercial preparations of aspirin; and in still others, the mechanisms remain unknown.
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PMID:Antipyretic analgesics and the allergic patient. 660 63

1 Recent studies of idiosyncratic reactions to analgesics have revealed several clinical patterns with a different pathogenesis. 2 In the pathogenesis of a common type of asthma precipitated by aspirin, inhibition of cyclooxygenase leading to disturbances in metabolism of arachidonic acid is of fundamental importance. 3 In some patients with urticaria/angioedema, symptoms are due to inhibition of cyclo-oxygenase by analgesics; in others the cause might be impurities in commercial preparations of aspirin; and in others the mechanisms are still unknown. 4 There is a distinct group of patients who develop anaphylactic shock or urticaria following administration of pyrazolone drugs, but who tolerate aspirin and other cyclo-oxygenase inhibitors. This type of hypersensitivity seems to have an immunological background.
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PMID:Analgesics, allergy and asthma. 700 92

Studies carried out in 68 patients with idiosyncratic reactions to noramidopyrine and/or aminophenazone led to distinction of two different groups. In the first group: 1) noramidopyrine, aminophenazone, phenylbutazone and sulfinpyrazone as well as several other inhibitors of cyclooxygenase, including aspirin, precipitated bronchoconstriction; 2) skin tests with pyrazolone drugs were virtually negative; 3) all patients had chronic asthma. In the second group: 1) noramidopyrine and aminophenazone induced anaphylactic shock and/or urticaria; 2) skin tests with these drugs were highly positive; 3) phenylbutazone, sulfinpyrazone and several other cyclooxygenase inhibitors, including aspirin, could be taken with impunity; 4) chronic bronchial asthma was present in only one-fourth of the patients. We suggest that the pathogenic mechanisms responsible for the idiosyncratic reactions involve inhibition of cyclooxygenase in the first group, and allergic reactions in the second group. Distinction of these two groups is of clinical importance since in individual patients it gives insight into the safe administration of pyrazolone and aspirin-like drugs.
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PMID:Idiosyncrasy to pyrazolone drugs. 731 7

Intolerance to acetylsalicylic acid (ASA) in asthmatics has been widely studied in the adult population, and to a lesser extent in children. In the present study, we present 16 asthmatics between the ages of 2 and 14 suffering from asthma induced by ASA ingestion, and the clinical characteristics are compared with a population of asthmatic children with a negative challenge test. The following results were obtained: 1) in contrast to in adults, females are not predisposed to ASA intolerance in childhood, the male:female ratio being the usual 2:1 in infantile asthma; 2) ASA intolerance can appear at a very early age (in our series the youngest was 1 year old); 3) extrinsic asthmatics are the most commonly affected, and also children with exercise-induced asthma; 4) in extrinsic asthmatics with asthma attacks precipitated by ASA, sinusitis is more frequent than in extrinsic asthmatics with ASA tolerance; 5) polyposis is exceptional; 6) the presence of associated urticaria is frequent, and much greater than in adult ASA-intolerant asthmatics; and 7) the results of the challenge with NSAIDs are similar to those obtained in adult patients, which would indicate a common pathophysiological mechanism related to the capacity of these drugs to inhibit cyclooxygenase activity.
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PMID:Asthma in children and ASA intolerance. 801 49

Previous work from this laboratory established that caffeic acid esters, present in the propolis of honey bee hives, are potent inhibitors of human colon tumor cell growth, suggesting that these compounds may possess antitumor activity against colon carcinogenesis. The present study was designed to investigate (a) the inhibitory effects of methyl caffeate (MC) and phenylethyl caffeate (PEC) on azoxymethane (AOM)-induced ornithine decarboxylase (ODC), tyrosine protein kinase (TPK), and arachidonic acid metabolism in liver and colonic mucosa of male F344 rats, (b) the effects of caffeic acid, MC, PEC, phenylethyl-3-methylcaffeate (PEMC), and phenylethyl dimethylcaffeate (PEDMC) on in vitro arachidonic acid metabolism in liver and colonic mucosa, and (c) the effects of PEC, PEMC, and PEDMC on AOM-induced aberrant crypt foci (ACF) formation in the colon of F344 rats. At 5 weeks of age, groups of animals were fed diets containing 600 ppm MC or PEC (biochemical study) or 500 ppm PEC, PEMC, or PEDMC (ACF study). Two weeks later, all animals except the vehicle-treated groups were given s.c. injections of AOM, once weekly for 2 weeks. The animals intended for the biochemical study were sacrificed 5 days later and colonic mucosa and liver were analyzed for ODC, TPK, lipoxygenase, and cyclooxygenase metabolites. The animals intended for the ACF study were sacrificed 9 weeks later and analyzed for ACF in the colon. The results indicate that the PEC diet significantly inhibited AOM-induced ODC (P < 0.05) and TPK (P < 0.001) activities in liver and colon. The PEC diet significantly (P < 0.001) suppressed the AOM-induced lipoxygenase metabolites 8(S)- and 12(S)-hydroxyeicosatetraenoic acid (HETE). The animals fed the MC diet exhibited a moderate inhibitory effect on ODC and 5(S)-, 8(S)-, 12(S)-, and 15(S)-HETEs and a significant (P < 0.001) effect on colonic TPK activity. However, the MC and PEC diets showed no significant inhibitory effects on cyclooxygenase metabolism. In an in vitro study, caffeic acid and MC showed inhibitory effects on HETE formation only at a 100 microM concentration, whereas PEC, PEMC, and PEDMC suppressed in vitro HETE formation in a dose-dependent manner. AOM-induced colonic ACF were significantly inhibited in the animals fed PEC (55%), PEMC (82%), or PEDMC (81%). The results of the present study indicate that PEC, PEMC, and PEDMC, present in honey, inhibit AOM-induced colonic preneoplastic lesions, ODC, TPK, and lipoxygenase activity, which are relevant to colon carcinogenesis.
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PMID:Inhibitory effect of caffeic acid esters on azoxymethane-induced biochemical changes and aberrant crypt foci formation in rat colon. 836 13

Prostaglandins likewise leukotriens are proinflammatory mediators resulting from metabolic degradation of the arachidonic acid originating from membrane phospholipids. The most important products of enzyme cyclooxygenation of arachidonic acid are prostaglandins D2, E2, F2a, tromboxane A2 and prostacyclin. Prostaglandins express their tissue effects via the five basic receptor types. Within the allergic inflammation activated mast cell synthesizes prostaglandin D2 (first lipid mediator) which has bronchoconstrictive and vasodilating effects and attracts neutrophilic leukocytes. Moreover, it also participates in the late phase reactions, six hours subsequent to the exposure to the allergen. This mediator is also important in pathogenesis of urticaria, allergic rhinitis and allergic bronchial asthma. In addition to prostaglandin D2, prostaglandin F2a and tromboxane A2 also have bronchoconstrictive actions, while prostacyclin and prostaglandin E have bronchodilating effects. Inhalation of prostaglandin E prevents asthmatic attacks caused by allergens, strain, metabisulfite and ameliorates attacks of aspirin asthma, which confirms the hypothesis that aspirin asthma is based on cyclooxigenase inhibition and increased leukotriene production. In patients with atopic dermatitis, prostaglandin E has suppressive effects on Interferon gamma production by Th1 helper cells and increases production of Interleukin 4 by the Th2 cells. Tromboxane A2 plays a certain role in the development of bronchial hyperreactivity and late asthmatic response. Prostaglandins are also important mediators in the pathogenesis of allergic conjunctivitis. Most of nonsteroidal antiinflammatory drugs inhibit the enzyme cyclooxygenase and thus also prostaglandin biosynthesis and release.
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PMID:[The role of prostaglandins in allergic inflammation]. 986 13


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