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)

All patients with aspirin exacerbated respiratory disease (AERD) can be desensitized to ASA. After achieving this state, patients can then take ASA daily without adverse effect. ASA desensitization can be maintained indefinitely as long as the patient takes ASA each day. Crossdesensitization with older NSAIDs also occurs. After ASA desensitization, patients can take daily ASA in order to treat their underlying respiratory disease. In AERD patients treated with ASA 650 BID for at least a year, 115/172 (67%) improved in their clinical courses while decreasing systemic and topical corticosteroids. Sixteen failed to improve, 24 stopped ASA because of intractable side effects (gastritis or hives) and 17 patients discontinued ASA treatment in the first year of study for unrelated reasons. Therefore, treatment with daily ASA is a significant therapeutic option for patients afflicted with AERD. It should be used for AERD patients who do not respond to topical corticosteroids and leukotriene modifier drugs. Those who respond to systemic steroids or have intractable or recurrent nasal polyps are particularly well-suited for this therapeutic intervention.
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PMID:Aspirin desensitization in patients with AERD. 1266 96

The underlying respiratory disease is activated by unknown mechanism and results in an intense infiltration of mast cells and eosinophils into the entire respiratory mucosa. These cells synthesize leukotrienes (LTs) at a very high rate and mast cells also release histamine and tryptase and synthesize PGD(2) a vasodilator and bronchoconstrictor. Furthermore, AERD patients under synthesize from arachidonic acid (AA) a peculiar product called lipoxins, which opposes inflammation generated by leukotrienes. Finally, cysLT1 receptors are over expressed and highly responsive to LTE(4), further augmenting the underlying inflammatory disease. This inflammatory condition is partly inhibited by synthesis of PGE(2) through COX-1. PGE(2) partially inhibits 5-lipogygenase conversion of AA to LTA(4) and blocks release of histamine and tryptase from mast cells. When COX-l is inhibited by ASA or NSAIDs, PGE(2) synthesis stops and an enormous release of histamine and synthesis of LTs occurs. The upper respiratory reaction is mediated by both histamine and LTs but the bronchospastic reaction is mediated by LTs. The systemic effects of flush, gastric pain and hives are mediated by histamine. Aspirin desensitization can not be explained by disappearance of LT synthesis since urine LTE(4) levels are still elevated at acute ASA desensitization. However, mast cell products such as histamine, tryptase and PGD(2) are no longer released or synthesized at acute desensitization. It is more likely that a diminution in number or function of cysLT receptors accounts for the diminished inflammatory response found in ASA desensitization.
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PMID:Pathogenesis of aspirin-exacerbated respiratory disease. 1266 97

Aspirin and all nonsteroidal anti-inflammatory drugs (NSAIDs) are a chemically heterogeneous group of compounds that share the ability to inhibit the enzyme cyclooxygenase (COX). This inhibitory effect, especially of COX-1, is suggested as the mechanism underlying NSAID-induced hypersensitivity reactions. In this study, we evaluated the safety and convenience of a single full-dose challenge with nabumetone, a selective COX-2 inhibitor, in patients with hypersensitivity to nonselective NSAIDs (ns-NSAIDs). Twenty-four subjects with a history of hypersensitivity reactions to at least two different ns-NSAIDs on two different occasions were enrolled in the study. The patients were otherwise healthy and did not suffer from NSAID- or aspirin-induced asthma or urticaria. All subjects were orally challenged by a single full dose (1000 mg) of nabumetone, monitored closely in the hospital for the next 4 hours and contacted by telephone the next morning and 3-12 months afterward. Twenty-two patients tolerated nabumetone without any reaction during and after the challenge. One patient had a single urticarial lesion and one patient reported mild pruritus without objective signs, both of which resolved spontaneously. Thirteen patients, including the patient who responded with pruritus to the challenge, used nabumetone on several occasions during the follow-up period without any adverse reaction. Our study shows that in patients with a history of aspirin- and ns-NSAID-induced hypersensitivity reaction, a rapid one-step challenge with nabumetone was well tolerated. These initial data support the possibility that a single full dose of nabumetone can be tried as a safe alternative in most patients with a hypersensitivity reaction to ns-NSAIDs.
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PMID:Safe full-dose one-step nabumetone challenge in patients with nonsteroidal anti-inflammatory drug hypersensitivity. 1297 96

Aspirin and the older nonsteroidal anti-inflammatory drugs (NSAIDs) that block cyclo-oxygenase-1 (COX-1) induce asthma attacks in patients with aspirin-exacerbated respiratory disease and urticaria in patients with chronic idiopathic urticaria. Weak inhibitors of COX-1, such as acetaminophen and salsalate, crossreact also but only with high doses of the drugs. Partial inhibitors of both COX-1 and COX-2, such as nimesulide and meloxicam, also cross-react but only at high drug doses. COX-2 inhibitors do not cross-react; however, all NSAIDs, including the selective COX-2 inhibitors, can sensitize patients and induce urticaria or anaphylaxis on next exposure to the drug.
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PMID:Aspirin and NSAID sensitivity. 1524 23

The pathogenic mechanism of ASA-induced urticaria/angioedema (AIU) is still poorly understood, but it has been known that histamine releasing by cutaneous mast cell activation is considered to be an important role. Considering the importance of histamine in AIU, we speculated that a genetic abnormality of histamine-related genes such as a high-affinity IgE receptor, a metabolic enzyme of histamines and histamine receptors, may be involved in the development of AIU. Enrolled in the study were 110 patients with AIU, 53 patients without ASA hypersensitivity who had various drug allergies presenting as exanthematous skin symptoms, and 99 normal healthy controls (NC). Eleven single nucleotide polymorphisms (SNPs) of the beta chain of the high-affinity IgE receptor (FCER1B) and three histamine-related genes-histamine N-methyltransferase (HNMT), histamine H1 receptor (HRH1), histamine H2 receptor (HRH2)-were screened using the SNP-IT assay based on a single base extension method. No significant differences were observed in allele and genotype frequencies, and haplotype frequencies of all the SNPs of FCER1B, HNMT, HRH1, and HRH2 among the three groups (p>0.05, respectively). These results suggest that the polymorphisms of FCER1B and the three histamine-related genes may not contribute to the development of AIU phenotype in the Korean population.
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PMID:Polymorphisms of high-affinity IgE receptor and histamine-related genes in patients with ASA-induced urticaria/angioedema. 1595 54

In some patients with chronic idiopathic urticaria (CIU), aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) that inhibit cyclooxygenase 1 (COX-1) precipitate wheals and swelling. There is no in vitro diagnostic, and diagnosis can be established only by provocation challenges with aspirin or other NSAIDs. Skin reactions triggered by aspirin are associated with the inhibition of cyclooxygenase, specifically COX-1, but not COX-2, and are characterized by overproduction of cysteinyl leukotrienes (cys-LTs). Aspirin and other NSAIDs should be avoided, but highly specific COX-2 inhibitors, known as coxibs, are well tolerated and can probably be safely used. Evidence has been accumulated that these reactions are due to the interference of aspirin-like drugs with arachidonic-acid metabolism. In this article, we discuss the mechanism of these reactions, and the characteristic course of aspirin-induced urticaria and its management.
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PMID:Mechanism of chronic urticaria exacerbation by aspirin. 1596 68

Acetylsalicylic acid, commonly known as aspirin, can induce some hypersensitive reactions with clinical symptoms such as urticaria, angioedema, acute bronchospasm, and rarely anaphylactic shock. At present, detection of aspirin allergy is still rather difficult and requires an adequate clinical history and sensitive in vivo and in vitro tests. The aim of the study was to evaluate the diagnostic utility of cellular antigen stimulation test (CAST) in the detection of allergic reaction mediated by aspirin. Fifty patients (39 women and 11 men) with a history of hypersensitivity reaction to aspirin were included in the study. Positive scratch test to aspirin was found in 72% (36/50) and positive CAST in 58% (29/50) of patients. Both skin scratch test and CAST positive results were recorded in 48% (24/50%) and negative results in 20% (9/45) of patients. The level of agreement between skin scratch test and CAST was fair with Cohen's kappa of 0.269 (0.95% CI 0.004-0.533). The observed between-test agreement was 66%. It is concluded that CAST-ELISA might be of value as an additional test for the detection of aspirin nonallergic hypersensitivity in suspected individuals.
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PMID:Clinical usefulness of cellular antigen stimulation test in detection of aspirin allergy. 1632 21

The pathogenesis of aspirin (acetylsalicylic acid, ASA)-intolerant urticaria (AIU) is still poorly understood but it has recently been suggested that it is associated with the overproduction of leukotriene (LT). This is supported by evidence that cyclooxygenase 2 inhibitor is given safely to patients with AIU. The present study was designed to investigate the role of genetic polymorphism of LT related genes in the pathogenesis of AIU via a case-control study. We screened single nucleotide polymorphisms (SNPs) in genes encoding enzymes involved in leukotriene synthesis in the Korean population with AIU (n = 101), ASA-intolerant asthma (AIA, n = 95) and normal healthy controls (n = 123). Genotype was determined by primer extension reactions using the SNapShot ddNTP primer extension kit. Among 8 SNPs of four LT related genes, the polymorphism of ALOX5 at positions of -1708 G > A showed significant difference in genotype frequency between AIU and AIA (p = 0.01). Furthermore, there were significant differences observed in the frequencies of two ALOX5 haplotypes between the AIU group and AIA group (p < 0.05). However, there were no differences in allele, genotype, or haplotype frequencies of ALOX5 between the AIU group and the normal control group. These results suggested that ALOX5 has a differing contribution in two major clinical pathogenesis related to ASA-sensitivity.
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PMID:Leukotriene-related gene polymorphisms in patients with aspirin-intolerant urticaria and aspirin-intolerant asthma: differing contributions of ALOX5 polymorphism in Korean population. 1636 98

Foods are usually the first suspect as the cause of urticaria. However, a causal relationship is found only in special subtypes of urticaria. IgE-mediated food allergy should be clearly separated from non-allergic hypersensitivity (pseudoallergic reactions). The former may play a role in acute urticaria, particularly in patients with atopic dermatitis. The responsible food proteins vary with age. IgE-mediated sensitization can apply to food-dependent exercise-induced urticaria/anaphylaxis but more often the combination of food intake (irrespective of which type) plus exercise results in symptoms. In chronic urticaria, IgE-mediated sensitization to food is normally irrelevant while pseudoallergic reactions to food additives and perhaps also to biogenic amines may be involved. Another urticaria subtype that may be caused by food is contact urticaria which is mostly found in the context of occupational food handling. Very rarely anisakiasis and nickel may cause food-induced urticaria. Aspirin is able not only to exacerbate and aggravate urticaria but can also enhance food-dependent urticaria.
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PMID:[Current position of the role of allergic and non-allergic food hypersensitivity in urticaria]. 1639 42

Mesalazine is a derivative of 5-aminosalicylic acid (5-ASA), which is useful in the treatment of intestinal inflammatory disease. Sulfasalazine is formed by two parts, sulfapyridine and 5-ASA, the latter being the active part of the molecule. The new preparatives derived from 5-ASA were developed in an attempt to avoid the traditionally associated side effects to sulfapyridine, although they are still observed and new effects appear. We present two cases. The first is a man diagnosed of inflammatory intestinal disease, with background of two previous reactions of urticaria and angioedema after acetyl salicylic acid, who presented urticaria after taking mesalazine. The second one had generalized urticaria after three months of initiating treatment with mesalazine. Given the need for treatment in both cases, a desensitization protocol to mesalazine was made. It was developed in 17 days in our service. Tolerance to that drug to therapeutic doses is reached. When faced with patients with hypersensitivity to different drugs, that are necessary to treat their disease, "desensitization" regimes, that assure good tolerance, can be made.
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PMID:[Induction of tolerance in hypersensitivity to mesalazine (5-ASA)]. 1645 98


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