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)

Chronic rhinosinusitis with nasal polyposis may be a symptom of aspirin-intolerance. If the other symptoms of aspirin intolerance -- above all urticaria and asthma -- are absent, the rhinologist and not the pulmologist or dermatologist has to do the etiological diagnosis. In doubtful cases rhinorheomanometry is to use.
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PMID:[Rhinosinusitis polyposa as the only symptom of aspirin intolerance -- a rhinorheomanometric diagnosis (author's transl)]. 13 15

In 131 patients with chronic urticaria, including physical urticarias, oral provocation tests were done with aspirin. A total of thirty-one patients showed a reaction on aspirin challenge. Reactions were seen in 35% of patients with idiopathic urticaria, 52% of patients with cholinergic urticaria, and 43% of those with pressure urticaria. The patients with reactions to aspirin were also tested with tartrazine, sodium benzoate, 4-hydroxybenzoic acid, sodium- and phenyl salicylate and the analgesics indomethacin, paracetamol and mefanamic acid. In nineteen of twenty three aspirin sensitive patients, positive reactions to one or more of these substances were observed. Indomethacin and tartrazine had the highest scores. There was no statistically significant correlation between aspirin reactions and the presence of nasal polyposis, sinusitis, asthma or atopy.
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PMID:Reactions to aspirin and food additives in patients with chronic urticaria, including the physical urticarias. 110 92

Evidence has been presented supporting the hypothesis that at least 2 different types of mechanisms may be involved in aspirin intolerance, one resulting in bronchospasm and the other producing urticaria/angioedema. Bronchospasm is the predominant symptom of aspirin intolerance in patients who have asthma. In contrast, the predominant symptom of aspirin intolerance in patients who have rhinitis is urticaria/angioedema. In the bronchospastic type of aspirin intolerance, there is a significant correlation with an increased frequency of nasal polyposis, and with a similar ageonset of asthma and aspirin intolerance. These correlations were not present in the urticari/angioedema type. Additional evidence for familial occurrence of aspirin intolerance is presented, and its relationship with subtypes of aaspirin intolerance is discussed. In a double-blind, crossover study with normal control subjects matched by age and sex 15% (6/40) of aspirin-intolerant individuals had significant adverse reactions to tartrazine challenge and not to the placebo. None of the 40 normal control subjects had any adverse reactions.
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PMID:Aspirin intolerance. III. Subtypes, familial occurence, and cross-reactivity with tartarazine. 115 Oct 14

A case of a ten year old adopted girl is presented, who had gastrointestinal disturbances, anal pruritus and relapses of urticaria from her fourth year of age. By means of radiological and endoscopis analysis, multiple gastrointestinal polyposis was established. Pathohistological examination of the polyp indicated that tubular adenomas were in question, therefore in the case of this girl it can be stated that she has diffuse tubular gastrointestinal adenomatous polyposis, which is a characteristic of Gardner's syndrome. At the moment of the setting of the diagnosis, the girl had no skin changes nor did she have any radiological changes on the bones of her skull. The first skin changes appeared one year after the diagnosis was set, and they were in the form of maculopapular nodules, comedos of the closed and open type on the forehead and chin.
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PMID:[Multiple gastrointestinal polyps]. 180 74

Nonsteroidal anti-inflammatory drugs and certain food or drug additives are known to induce acute bronchospasms, angioneurotic edema, and urticaria in susceptible patients. Thirty-four patients (17 with asthma and 17 with urticaria), whose case history suggested such intolerance, were challenged orally with increasing doses of seven compounds: acetylsalicylic acid, glafenine, sodium benzoate, sulfur dioxide, potassium sorbate, sodium glutamate, and tartrazine. Among 162 oral provocation tests, 38 were positive (20% decrease in peak flow rate or appearance of acute urticaria/angioneurotic edema). Twenty-four of the 34 patients (nine with asthma and 15 with urticaria) were intolerant to at least one compound. However, no serious reaction was observed. In 20 of these 24 patients (six with asthma and 14 with urticaria), a diet free of additives and nonsteroidal anti-inflammatory drugs resulted, within 5 days, in a marked improvement of symptoms, which persisted 8 to 14 mo after starting the diet. Age, prevalence of IgE-mediated allergy, and nasal polyposis were similar in patients with or without reactions of intolerance. Under the conditions used, oral provocation tests proved to be feasible, safe, and useful in many patients not helped by existing methods.
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PMID:Value of oral provocation tests to aspirin and food additives in the routine investigation of asthma and chronic urticaria. 286 Dec 22

The historic triad of bronchial asthma, nasal polyposis, and intolerance to aspirin and related chemicals, recently designated as Samter's syndrome, is an inflammatory condition of unknown etiology and pathogenesis. The condition is probably acquired, perhaps secondary to a viral infection, but a hereditary factor may be important in some patients. Most patients with this syndrome are adults, with an occasional case being identified in a teenager or older child. Although not every patient will have the fully developed syndrome, the typical patient will have all three of the classic features. Many patients with Samter's syndrome also have a marked eosinophilia of both bronchial and nasal secretions as well as the circulating blood. Approximately 10 per cent of the patients have urticaria and/or angioedema, alone or in combination with respiratory inflammation. The diagnosis usually can be established easily on the basis of the history and physical examination, and only rarely in clinical practice is it necessary to perform a confirmatory aspirin challenge test. As with all allergic diseases, the cornerstone of treatment is environmental control with avoidance of respiratory irritants, aspirin, and aspirin-like medications. Management of upper airway disease requires careful prescription of medication supplemented by judicious selection of surgery. A variety of medications, including bronchodilators and corticosteroids, can be used to treat the bronchial symptoms. The results of current research are expected to lead to better understanding followed by further improvements in treatment for patients with Samter's syndrome.
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PMID:Bronchial asthma, nasal polyps, and aspirin sensitivity: Samter's syndrome. 306 89

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

In population studies, the provocative dose (PD) of bronchoconstrictor causing a significant decrement in lung function cannot be calculated for most subjects. Dose-response curves for carbachol were examined to determine whether this relationship can be summarized by means of a continuous index likely to be calculable for all subjects, namely the two-point dose response slope (DRS) of mean resistance (Rm) and resistance at 10 Hz (R10) measured by the forced oscillation technique (FOT). Five doses of carbachol (320 microg each) were inhaled by 71 patients referred for investigation of asthma (n=16), chronic cough (n=15), nasal polyposis (n=8), chronic rhinitis (n=8), dyspnoea (n=8), urticaria (n=5), post-anaphylactic shock (n=4) and miscellaneous conditions (n=7). FOT resistance and forced expiratory volume in one second (FEV1) were measured in close succession. The PD of carbachol leading to a fall in FEV1 > or = 20% (PD20) or a rise in Rm or R10 > or = 47% (PD47,Rm and PD47,R10) were calculated by interpolation. DRS for FEV1 (DRSFEV1), Rm (DRSRm) and R10 (DRSR10) were obtained as the percentage change at last dose divided by the total dose of carbachol. The sensitivity (Se) and specificity (Sp) of DRSRm, DRS10 delta%Rm and delta%R10 in detecting spirometric bronchial hyperresponsiveness (BHR, fall in FEV1 > or = 20%) were assessed by receiver operating characteristic (ROC) curves. There were 23 (32%) "spirometric" reactors. PD20 correlated strongly with DRSFEV1 (r=-0.962; p=0.0001); PD47,Rm correlated significantly with DRSRm (r=-0.648; p=0.0001) and PD47,R10 with DRSR10 (r=-0.552; p=0.0001). DRSFEV1 correlated significantly with both DRSRm (r=0.700; p=0.0001) and DRSR10 (r=0.784; p=0.0001). The Se and Sp of the various FOT indices to correctly detect spirometric BHR were as follows: DRSRm: Se=91.3%, Sp=81.2%; DRSR10: Se=91.3%, Sp=95.8%; delta%Rm: Se=86.9%, Sp=52.1%; and delta%R10: Se=91.3%, Sp=58.3%. Dose-response slopes of indices of forced oscillation technique resistance, especially the dose-response slope of resistance at 10Hz are proposed as simple quantitative indices of bronchial responsiveness which can be calculated for all subjects and that may be useful in occupational epidemiology.
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PMID:Dose-response slope of forced oscillation and forced expiratory parameters in bronchial challenge testing. 1006 71

Hypersensitivity to aspirin usually takes the form of a clinical syndrome combining chronic rhinitis, nasal polyposis and asthma attacks that are exacerbated by aspirin or other non steroidal anti-inflammatory drugs (NSAIDs). This syndrome, first described by Widal in 1922, is very frequent: it affects nearly 15% of asthmatic patients and is usually associated with severe and sometimes fatal asthma. In other instances, hypersensitivity to NSAIDs manifests in the form of skin lesions, such as urticaria and angioedema. Until recently, the pathophysiological mechanism of NSAID hypersensitivity was somewhat mysterious. The fact that the main mediators involved are sulfidoleukotrienes (LTC4, LTD4, LTE4) and that the drugs responsible all inhibit cyclooxygenase-1 (COX-1), pointed to a pharmacogenetic abnormality of arachidonic acid metabolism. An immunopharmacological study of basophil activation (detected by flow cytometry), sulfidoleukotriene production in the presence of NSAIDs in vitro, and other related studies reviewed here have revealed that: a) basophils from patients with the Widal syndrome are hyperactivated in a non specific manner, probably related to chronic inflammation in the skin or airways; b) these hyperactive basophils produce increased amounts of sulfidoleukotrienes but decreased amounts of PGE2 when exposed to NSAIDs in vitro. These observations led to the development of an in vitro diagnostic test which, in many cases, can replace challenge tests. The pathogenic mechanism of the Widal syndrome now appears to involve the combined effects of chronic inflammation (causing non specific cellular hyper-reactivity, particularly of mast cells, basophils and eosinophils) and a pharmacogenetic abnormality of arachidonic acid metabolism in response to NSAIDs. This leads to sulfidoleukotriene overproduction and to a decrease in the anti-inflammatory prostaglandin PGE2. This concept is compatible with the onset and outcome of most cases of the Widal syndrome, and provides a therapeutic rationale.
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PMID:[New pathophysiological concepts on aspirin hypersensitivity (Widal syndrome); diagnostic and therapeutic consequences]. 1643 44

Omalizumab is a recombinant humanized monoclonal antibody. Use of omalizumab is reported to benefit significantly patients with inadequately controlled moderate-to-severe persistent allergic asthma that is not controlled with high-dose inhaled corticosteroids. However, recent studies suggest that omalizumab might play an important role in the treatment of other potentially IgE mediated disease processes including: urticaria and angioedema, atopic dermatitis, allergic rhinitis, nasal polyposis and severe ocular allergies. Furthermore, addition of omalizumab to immunotherapy protocols is reported to be highly advantageous. Although omalizumab is generally well tolerated, reports on potential anaphylactic reactions as well as an association with Churg-Strauss syndrome necessitate close monitoring. The data reviewed are discussed with the aim of underlining unmet needs and making recommendations for future studies on omalizumab use. This might better guide future clinical practice regarding omalizumab treatment. This review article also discussed some patent related to the field.
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PMID:Omalizumab: not only for asthma. 1907 9


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