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)

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

The pathogenic mechanism of acetyl salicylic acid (ASA)-induced urticaria (AIU) is not fully understood. We compared the levels of neutrophil activation and related cytokines in patients with ASA-intolerant acute urticaria (AIAU) and ASA-intolerant chronic urticaria (AICU). A total of 51 patients with AIAU, 88 patients with AICU, and 102 normal controls (NC) were enrolled in this study. The serum levels of myeloperoxidase (MPO), interleukin-8 (IL-8), and IL-18 were compared among the three groups. The serum levels of MPO were highest in the AIAU group, followed by the AICU and NC groups, and the serum levels of IL-18 were significantly higher in the AIAU and AICU groups than in NC group. Within the AIU groups, significant correlations were noted between the levels of MPO and IL-8, and IL-8 and IL-18. In conclusion, neutrophil activation, which was associated with the levels of IL-8 and IL-18 in the AIAU group, may be involved in the pathogenic mechanism of AIU. A role for IL-18 in the pathogenesis of AIU is also suggested.
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PMID:Neutrophil activation in patients with ASA-induced urticaria. 1820 66

The management of patients who have developed a contact dermatitis due to topical drugs requires to stop the suspected drug application, to treat the patient with corticosteroid ointments, to perform dermatoallergological investigations e.g. drug patch tests in case of contact eczema and diluted prick tests in case of contact urticaria in order to determine whether the adverse drug reaction was due to excipients or to the drug itself. Patients with chronic leg ulcers have a high risk of contact dermatitis to topical drugs and to antiseptics. It is necessary to advise the patient concerning the avoidance of topical but also systemic readministration of the responsible molecule. An excipient responsible in inducing a contact sensitization to a topical drug can also be found in cosmetics, the name of the responsible excipient has to be given to the patient under the common name but also under the INCI name. In most of the cases there is no risk in systemically administering iodine, sulfites or vehicles in a sensitized patient who had developed a contact dermatitis to topical medications. When the drug itself is responsible in inducing a contact allergy it is necessary to determine if cross reactions with other drugs can occur and if the responsible molecule can induce systemic cutaneous adverse drug reactions if the drug is systemically readministered. Among NSAID there is no cross reactions between bufexamac and diclofenac, between salicylamide, glycol salicylate, salicylic acid and acetylsalicylic acid. In case of photosensitization 1) to ketoprofen or 2) piroxicam the topical and/or systemic administration of the following molecules are contraindicated with respectively 1) ketoprofen, tiaprofenic acid, fenofibrate, oxybenzone or 2) piroxicam, thimerosal. A patient sensitized to corticosteroid ointment has to be tested in order to determine which corticosteroid classes are sensitizing. The topical and systemic administrations of molecules belonging to the sensitizing classes (A, B, C, D1 or D2) have to be forbidden.
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PMID:Contact dermatitis due to topical drugs. 1983 31

Analgesic intolerance brings on cutaneous, respiratory and/or gastrointestinal reactions. This review provides an overview of sensitivity to nonsteroidal anti-inflammatory-drugs (NSAR) and its management. The full clinical picture of analgetic intolerance--the association of bronchial asthma (with severe acute attacks), sensitivity to NSAR and nasal polyps--is commonly summarized as the "Samter triad". The symptoms include chronic rhinosinusitis with nasal polyps, asthma bronchiale, gastrointestinal ulcers, angioedema, and urticaria. The prevalence of analgetic intolerance in the general population ranges from 0.6 to 2.5%. Clinical reactions after ingestion of NSAR are often obvious in the further progress of disease. In order to initiate early therapy the diagnosis of analgesic intolerance should occur before the complete picture of analgesic intolerance is obvious. Carefully controlled challenge tests with acetyl salicylic acid or other NSAR are performed as the diagnostic but not potential undamaged tool of choice. Adaptive desensitization (Aspirin desensitization therapy) is currently the single causal therapy. Severe asthma and reactions after ingestion of NSAR are avoided. Frequency of endonasal revision surgery is reduced after desensitization.
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PMID:[Analgesic intolerance: pathogenesis, diagnosis and treatment]. 2008 46

Acetyl salicylic acid (ASA) is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6), cytochrome P4502C9 (CYP2C9), and N-acetyl transferase 2 (NAT2). Variations in the activities of these enzymes may modulate adverse ASA-related symptoms such as urticaria. We examined whether polymorphisms in the UGT1A6, CYP2C9, and NAT2 genes are related to ASA-intolerant urticaria (AIU). The genotypes of 148 subjects with AIU (AIU group) and 260 normal healthy control subjects (NC group) were analyzed with respect to the following single nucleotide polymorphisms: CYP2C9 -1188T>C and CYP2C9(*)3A1075C; UGT1A6 T181A A>G and UGT1A6 R184S A>C; and NAT2 9796A>T, NAT2 197G>A, NAT2 286G>A, NAT2 9601A>G, and NAT2 9306A>G. There were significant differences in the allele frequencies for the CYP2C9 polymorphisms between the two groups. The frequency of the minor allele CYP2C9 -1188T>C was significantly higher in the AIU group than in the NC group (P=0.005). The frequency of the variant genotype CC was higher in the AIU group compared with the controls in both the co-dominant (P=0.007) and recessive models (P=0.012). The frequency of haplotype 2 [CA] was also significantly higher in the AIU group in both the co-dominant (P=0.006) and dominant models (P=0.012). There was no significant difference in genotype frequencies for any of the UGT1A6 or NAT2 polymorphisms between the two groups. Clinical parameters did not differ according to genotype. These results suggest that the C allele of CYP2C9 -1188T>C may be associated with AIU.
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PMID:Polymorphisms of Aspirin-Metabolizing Enzymes CYP2C9, NAT2 and UGT1A6 in Aspirin-Intolerant Urticaria. 2196 8

In subjects with non-steroidal anti-inflammatory drugs (NSAIDs)- exacerbated respiratory disease (NERD) symptoms are triggered by acetyl salicylic acid (ASA) and other strong COX-1 inhibitors, and in some cases by weak COX-1 or by selective COX-2 inhibitors. The mechanism involved is related to prostaglandin pathway inhibition and leukotriene release. Subjects who react to a single NSAID and tolerate others are considered selective responders, and often present urticaria and/or angioedema and anaphylaxis (SNIUAA). An immunological mechanism is implicated in these reactions. However, anecdotal evidence suggests that selective responders who present respiratory airway symptoms may also exist. Our objective was to determine if subjects might develop selective responses to NSAIDs/paracetamol that manifest as upper/lower airways respiratory symptoms. For this purpose, we studied patients reporting asthma and/or rhinitis induced by paracetamol or a single NSAID that tolerated ASA. An allergological evaluation plus controlled challenge with ASA was carried out. If ASA tolerance was found, we proceeded with an oral challenge with the culprit drug. The appearance of symptoms was monitored by a clinical questionnaire and by measuring FEV1 and/or nasal airways volume changes pre and post challenge. From a total of 21 initial cases, we confirmed the appearance of nasal and/or bronchial manifestations in ten, characterized by a significant decrease in FEV1% and/or a decrease in nasal volume cavity after drug administration. All cases tolerated ASA. This shows that ASA tolerant subjects with asthma and/or rhinitis induced by paracetamol or a single NSAID without skin/systemic manifestations exist. Whether these patients represent a new clinical phenotype to be included within the current classification of hypersensitivity reactions to NSAIDs requires further investigation.
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PMID:Asthma and Rhinitis Induced by Selective Immediate Reactions to Paracetamol and Non-steroidal Anti-inflammatory Drugs in Aspirin Tolerant Subjects. 2748 45

Bioactive food chemicals are substances present in food that are capable of interacting with living cells causing changes in physiological functions. Salicylic acid (SA), a plant hormone involved in plant immune response, is one such bioactive food chemical. Aspirin, a commercially available SA, might play beneficial roles in cardiovascular health and colon cancer. It may also cause urticaria, angioedema, asthma, and gastrointestinal symptoms in SA-sensitive individuals. Dietary SA might exert similar beneficial effects and/or may induce similar symptoms in hypersensitive individuals. Food-related SA sensitivity in relation to gastrointestinal symptoms is not well documented besides a few self-reported questionnaires and the knowledge that low doses of aspirin (equivalent of high dietary intake) can cause gastrointestinal injury. The only direct evidence that suggests benefits of reducing dietary SA was reported in asthmatic individuals. Although SA sensitivity in relation to gut symptoms in susceptible individuals is accepted by clinicians, the detection of this disease remains a challenge because of the complicated nature of dietary challenges and the risk of oral aspirin provocation tests in patients with severe hypersensitivity reactions. Given the non-IgE mediated nature of the disease, in vitro assays like basophil activation may have failed to produce reliable results. However, given the simplicity of this assay, further studies need to be formulated to firmly establish its reliability. Formulation of proper dietary strategies for symptom control is also impossible given the controversial and scant nature of the data on SA content of food. This issue needs to be resolved to formulate proper dietary strategies for effective symptom control.
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PMID:Bioactive food chemicals and gastrointestinal symptoms: a focus of salicylates. 2824 60

Nonsteroidal anti-inflammatory drugs (NSAIDs) are the leading cause of hypersensitivity drug reactions. The different chemical structures, cyclooxygenase 1 (COX-1) and/or COX-2 inhibitors, are taken at all ages and some can be easily obtained over the counter. Vasoactive inflammatory mediators like histamine and leukotriene metabolites can produce local/systemic effects. Responders can be selective (SR), IgE or T-cell mediated, or cross-intolerant (CI). Inhibition of the COX pathway is the common mechanism in CI, with the skin being the most frequent organ involved, followed by the lung and/or the nose. An important number of cases have skin and respiratory involvement, with systemic manifestations ranging from mild to severe anaphylaxis. Among SR, this is the most frequent entity, often being severe. Recent years have seen an increase in reactions involving the skin, with many cases having urticaria and/or angioedema in the absence of chronic urticaria. Aspirin, the classical drug involved, has now been replaced by other NSAIDs, with ibuprofen being the universal culprit. For CI, no in vivo/in vitro diagnostic methods exist and controlled administration is the only option unless the cases evaluated report repetitive and consistent episodes with different NSAIDs. In SR, skin testing (patch and intradermal) with 24-48 reading can be useful, mainly for delayed T-cell responses. Acetyl salicylic acid (ASA) is the test drug to establish the diagnosis and confirm/exclude CI by controlled administration. Desensitization to ASA has been extensively used in respiratory cases though it can also be applied in those cases where it is required.
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PMID:NSAID-induced reactions: classification, prevalence, impact, and management strategies. 3149 52


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