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)

Thirty-two asthmatic children, mean age 9.6 years (range: 6-14 years), were studied by oral challenge with acetylsalicylic acid (Aspirin), and their PEFR was recorded at 30 min intervals for 3 hr. They had been asthmatic for a mean of 7.1 years. Other allergic symptoms (urticaria, rhinitis or atopic dermatitis), were present in 81% of the patients, and a family history of atopy in 94%; the mean blood eosinophilia was 590 cells per mm3. In three children aspirin induced a fall in PEFR values less than 8% which was non-significant. In the group as a whole there was an increase in the PEFR values of 13.9%, 150 min after aspirin challenge. These values where subjected to statistical analysis (Kolmogorov-Smirnov, Student's and Wilcoxon tests), which showed this increase to be significant at a level of P = 0.001. Possible mechanisms involving prostaglandin synthetase inhibition by aspirin are discussed as an explanation for this increase.
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PMID:Oral acetylsalicylic acid (aspirin) challenge in asthmatic children. 42 38

The following beliefs about aspirin sensitivity are widely held: (1) it usually is accompanied by nasal polyps. (2) It occurs primarily in nonallergic patients. (3) Its most common manifestation is asthma. (4) When it is combined with polyps and asthma (the so-called "aspirin triad"), the prognosis is unfavorable. (5) Polypectomy may precipitate asthma in aspirin sensitive patients. This paper, based on a study of 112 private patients, presents clinical evidence to refute these beliefs. It shows the following: (1) Aspirin allergy is accompanied by polyps in less than 5% of cases (13% of asthma patients). (2) In most cases, patients show well-defined allergy to an inhalant, food, or other drug. (3) Its most common manifestations are urticaria and angiodema, not asthma. (4) The prognosis is favorable, whether or not polyps are present. (5) Polypectomy does not precipitate asthma in aspirin-sensitive patients.
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PMID:Aspirin allergy: a clinical study. 111 72

The aim of this study was to determine the value of challenge tests with acetylsalicylic acid in the diagnosis of ASA-induced urticaria. The study was performed in 71 patients with suspected urticaria/angioedema-type sensitivity to ASA. Anamnesis confirmed sensitivity in 67 patients (94.4%) and showed that sensitive patients usually suffered from extensive urticaria (37 patients, i.e 55.5%) after ingestion of ASA. Eight patients (12%) reacted with loss of consciousness and 4 (6.0%) with edema of the larynx. Oral challenge test with acetylsalicylic acid was performed in 53 patients, in 49 (92.4%) of whom it was positive. Threshold doses of acetylsalicylic acid ranged from 40 to 300 mg. In 11 patients, the test was repeated and in 8 it was performed 3 times. It was observed that both the threshold acetylsalicylic acid doses and the time of appearance of sensitivity symptoms were variable. All ASA-sensitive patients reacted to indomethacin in a similar manner as to ASA. Paracetamol, on the other hand, was well tolerated by all 25 evaluated patients with urticaria/angioedema-type sensitivity to ASA.
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PMID:Urticaria/angioedema-type sensitivity to aspirin and other nonsteroidal anti-inflammatory drugs. Diagnostic value of anamnesis and challenge test with acetylsalicylic acid. 134

Sulfasalazine is an important therapeutic agent in the management of chronic inflammatory bowel disease (CIBD). Unfortunately, adverse reactions to this drug have been reported in 5-55% of treated patients. These include dose-related side effects like nausea, malaise, and headache or hypersensitivity reactions such as rash, fever, hives, arthralgia, hepatitis, etc. Studies in adults with successful reintroduction of sulfasalazine after a desensitization program have been reported; however, with regard to children, no such data are available. Fourteen children and adolescents (5-16 yr old) diagnosed to have CIBD manifested hypersensitivity to sulfasalazine within 2 months of onset of treatment. All had pancolitis--secondary to Crohn's disease (CD) in four and to ulcerative colitis (UC) in 10. All of them were on steroids. Sulfasalazine was discontinued in all after symptoms of hypersensitivity developed. Three patients with severe reaction were diagnosed prior to desensitization experience. Desensitization, beginning with 5-50 mg of sulfasalazine/day, was attempted in the other 11 children. The dose was gradually increased by 5-50 mg increments every 3 days. Desensitization was successful in only five children, who were ultimately able to tolerate 1.5-3.0 g of sulfasalazine daily again. In the rest (six of 11 patients), oral 5-ASA (Asacol) was administered, and three could not tolerate it. One of these three with intolerance to Asacol required colectomy. One did not tolerate Asacol or Dipentum. Our findings suggest that sulfasalazine desensitization should be attempted in all patients developing hypersensitivity reactions before trying alternative therapy.
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PMID:Sulfasalazine desensitization in children and adolescents with chronic inflammatory bowel disease. 809 41

We studied 251 outpatients affected by chronic and acute urticaria-angioedema syndrome, triggered or exacerbated by drugs, to evaluate the prevalence of adverse reactions to each pharmacological group. Among these patients, 134 (53.4%) presented one or more adverse reactions to a single drug: 100 (74.7%) reacted to NSAIDs, 33 (24.7%) to antibiotics and 1 to B vitamin complex. The remaining 117 patients (46.6%) presented adverse reactions to more than one drug. Considering the patients all together, 123 (49%) had adverse reactions to ASA, 116 (46.2%) to pyrazones, 65 (25.9%) to antibiotics, 26 (10.3%) to NSAIDs different from ASA and pyrazones. In our experience, according to other reports, there is a greater frequency of drug reactions to NSAIDs vs other drugs. ASA is the more frequently involved drug.
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PMID:[Prevalence of reactions to drugs in 251 patients with urticaria-angioedema syndrome]. 178 91

The inhalation challenge with lysine-aspirin (L-ASA) using the dosimeter method allows the construction of a dose-response curve and the quantitative estimation of airway responsiveness to the drug. We assessed the modifications of airway responsiveness to methacholine in four groups of subjects: aspirin-sensitive asthmatics, aspirin-sensitive subjects with urticaria/angioedema, subjects with an equivocal history of aspirin intolerance and normal control subjects. The L-ASA challenge was positive in all aspirin-sensitive asthmatics. The pattern of bronchial response to the challenge was different from that observed after challenge with allergens or occupational sensitizers. The main difference was found in the recovery from induced bronchoconstriction. The recovery lasted from 3 to 6-8 hours, and a peculiar dose-response curve was obtained that we call "early prolonged reaction". In five of 18 ASA-sensitive subjects there was a significant increase in airway responsiveness. Airway responsiveness was normal in aspirin-sensitive nonasthmatic subjects and in the other two groups studied. We conclude that L-ASA inhalation challenge may increase bronchial hyperresponsiveness in some ASA-sensitive asthmatics. This presence of enhanced bronchial hyperesponsiveness seems to be a marker with which to distinguish ASA-sensitive asthmatics from ASA-sensitive subjects with urticaria/angioedema.
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PMID:Aspirin-induced asthma and bronchial hyperresponsiveness. 181 46

Aspirin intolerance has become increasingly important in clinical dermatology during the past decade, especially as a diagnostic aid in chronic urticaria. It is recommended, to distinguish clinically between the intolerance syndrome and an intolerance provocation (of preexistent asthma or urticaria). Pathogenetically, various antibody-independent mechanisms are discussed of which most authors favour a defective regulation of arachidonic acid metabolism.
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PMID:[Clinical and pathogenetic aspects of aspirin intolerance]. 242 78

Aspirin and food additives are known to induce bronchoconstriction, angioedema or urticaria in susceptible patients. To evaluate the incidence of hypersensitivity to aspirin and food additives, 36 subjects with bronchial asthma, 33 of whom were non-allergic asthmatics and 3 were allergic asthmatics who had a history of aspirin sensitivity, were challenged orally with six compounds: acetylsalicylic acid (ASA), sodium bisulfite, tartrazine, sodium benzoate, 4-hydroxy benzoic acid, and monosodium L-glutamate. Significant bronchoconstrictions were found in 15 (41.7%) of the 36 subjects tested. Eight of the 15 subjects showed positive asthmatic responses to the aspirin, two showed asthmatic responses to the food additives, and five responded to both aspirin and the food additives. It is suggested that ASA and food additives could be causes of clinically significant bronchoconstriction in moderately severe non-allergic asthmatic patients.
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PMID:Oral provocation tests with aspirin and food additives in asthmatic patients. 262 38

Aspirin and other non-steroidal antiinflammatory drugs (NSAIDS) are known to cause urticaria and aggravate symptoms of bronchial asthma. This report describes a patient with allergic rhinitis whose symptoms were improved after ingestion of aspirin and the NSAIDS. The beneficial effect was confirmed by oral double-blind challenges.
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PMID:Allergic rhinitis relieved by aspirin and other nonsteroidal antinflammatory drugs. 283 19

Arachidonic acid undergoes two metabolic pathways in leukocytes. The first, catalysis by prostaglandin cyclo-oxygenase, yields the prostaglandin endoperoxides G2 and H2 and thromboxane A2, which induce rapid irreversible aggregation of human platelets and are potent inductors of smooth muscle contraction. The second pathway, catalysis by lipoxygenase, yields various hydroperoxy acids. In platelets, 12-hydroperoxyeicosatetraenoic acid is the predominant product; in polymorphonuclear leukocytes, 5-hydroperoxyeicosatetraenoic acid is formed. These are primarily reduced to 12-hydroxyeicosatetraenoic acid and 5-hydroxyeicosatetraenoic acid. 5-Hydroperoxyeicosatetraenoic acid may also be dehydrated to leukotriene A4. Enzymatic hydrolysis of leukotriene A4 yield leukotriene B4, a potent mediator of leukocyte function. Prostaglandins, thromboxanes, and some hydroxyeicosatetraenoic acids exert chemotactic effects on polymorphonuclear leukocytes. In this respect, leukotriene B4 is the most active compound derived from arachidonic acid. In vivo, adherence of leukocytes to the endothelium of microvessels near inflammatory areas and the sticking phenomenon of these cells are the initial hallmarks of an inflammatory response. In vitro, these responses seem to correspond with leukocyte aggregation and adherence. Leukotriene A4 may also react to form leukotriene C4 (a natural component of slow-reacting substance of anaphylaxis), leukotriene D4, leukotriene E4, and the 11-trans-isomers. All three leukotrienes are virtually unable to induce chemotaxis, enzyme release, or leukocyte aggregation, but they possess biologic properties previously attributed to slow-reacting substances, such as a potent effect on smooth muscle in the peripheral airway and an ability to markedly increase macromolecular permeability in venules. In addition to prolonging bleeding time and causing gastric ulcers, aspirin and other nonsteroidal anti-inflammatory drugs can trigger or aggravate an asthmatic attack. Aspirin can also trigger or aggravate urticaria, probably as a direct effect of thioether leukotrienes rather than from antibody mediation. Many nonsteroidal anti-inflammatory drugs increase formation of slow-reacting substance-A after challenge with allergen, perhaps by inhibiting cyclo-oxygenase, thereby releasing more arachidonic acid for metabolism by lipoxygenase. Alternatively, certain prostaglandins inhibit liberation of arachidonic acid from phospholipids; inhibiting their formation causes release of more arachidonic acid, which must be metabolized by different lipoxygenase pathways, since the cyclo-oxygenase pathway is closed.
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PMID:Prostaglandins, thromboxanes, and leukotrienes in inflammation. 287 54


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