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)

Ninety patients suffering from recurrent urticaria were orally exposed to 500 mg acetyl salicylic acid (ASA). 36.6% proved to be ASA intolerant in this group. 26 ASA-positive and 18 ASA-negative probands were selected to take part in an additional provocation test with 8 different food additives (preservative and colouring matters). Altogether 31 tests sheets were exaluated. Urticarial reactions were seen after administration of p-hydroxybenzoic acid methylester (5), p-hydroxybenzoic acid propylester (6), benzoic acid (9), sodium benzoate (6), tartrazine (6). Ponceau rouge (5) and indigo carmine (3). Detailed research was carried out on the occurrence of the tested substances. With a diet avoiding salicylates, benzoates and colouring matter 20% of these patients recovered spontaneously and became symptom-free, whilst a further 55% of cases showed marked improvement.
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PMID:[Intolerance to acetylsalicylacid and food additives in patients suffering from recurrent urticaria (author's transl)]. 54 91

Aspirin sensitivity is divided into 2 main subgroups: the bronchospastic and the urticaria/angioedema type. The bronchospastic type of aspirin sensitivity is frequently associated with nonallergic asthma and nasal polyps, producing a classical triad. Nonsteroid anti-inflammatory drugs (NSAID) crossreact with aspirin in aspirin-sensitive patients. Desensitization to aspirin is possible, but should be carried out with caution in selected patients. Desensitization to aspirin also produces desensitization to NSAID. Acetaminophen and nonacetylated salicylic acid (neither are considered NSAID) cross-react with aspirin in a small number of aspirin-sensitive individuals, usually when large doses are administered. The pathogenic mechanism may involve arachidonic acid and prostaglandin metabolism in the bronchospastic type of aspirin sensitivity.
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PMID:Aspirin sensitivity and allergy. 306 9

Anaphylaxis, the most emergent manifestation of allergy, is best described by its clinical pathologic alterations. Sites of involvement include skin (urticaria), upper respiratory tract (laryngeal edema), lower respiratory tract (bronchospasm), and the cardiovascular system (severe hypotension). Ultrastructural analysis of skin biopsies obtained from individuals experiencing exercise-induced anaphylaxis prior to and immediately after exercise revealed changes indistinguishable from those observed following immunologic challenge of pulmonary mast cells. These alterations included enlargement of the mast cell granules, solubilization (discharge) of mast cell granule contents, merger of the granule membranes with adjacent granule membranes, as well as the mast cell membrane. The successful reversal of anaphylaxis requires the prompt recognition of symptoms and early institution of therapy for anaphylaxis. Patients suffering from exercise-induced anaphylaxis should avoid any foods, drinks, or pharmaceutical agents, particularly acetyl salicylic acid for four and preferably six hours prior to exercise.
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PMID:Exercise-induced anaphylaxis. 341 89

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

Idiosyncrasy to salicylic acid and related substances is well known, the most common symptoms being asthma, rhinorrhea and urticaria. We here describe two cases whose only symptoms were hoarseness and in which inspection revealed laryngeal edema when the patients ingested any of these substances. In cases of chronic recurring hoarseness, a history should be taken with respect to such hypersensitivity and suspect cases should be challenged, since a strict diet may improve the symptoms.
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PMID:Laryngeal edema as the only symptom of hypersensitivity to salicylic acid and other substances. 671 90

Allergic reactions to food colors have been known since 1958. Reactions to tartrazine, our example, include generalized pruritus, urticaria, angioedema, paresthesias, vomiting, migraine, rhinorrhea and nasal obstruction, coughing, asthma attacks and purpura. Many patients who are allergic to antiinflammatory drugs such as acetyl-salicylic acid and indomethacin show cross-reaction to tartrazine. Doses producing these reactions range from minimal amounts up to 750 mg. Symptoms appear after periods of time ranging from minutes to 6 to 14 hours. In view of these facts (some of which represent a threat to the patient's life), additives, colouring matter, etc, do not usually appear in product labels or specifications, or in handbooks or catalogues used in practice. We drew up a list of drugs which may contain food dyes and coloring matter, yellow No. 5. A letter was written to 233 laboratories of which 159 (68%) replied. 72 (45%) in the affirmative and 87 (55%) in the negative, 74 (32%) did not reply.
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PMID:[Pharmaceutical preparations which contain tartrazine]. 725 46

We report a case of angioedema limited to the nape of the neck. The symptoms occurred every morning for fifteen days, two or three hours after taking aspirin. The patient took salicylic acid, 100mg per day, orally for two years. The angioedema occurred alone, without urticaria. When aspirin was stopped, the symptoms disappeared. A few weeks later, the patient took napoxen, with occurrence of more pronounced symptoms. The causality score was I3 for both drugs. The most common side-effects of aspirin intake are asthma and urticaria/angioedema. The mechanism of this hypersensitivity is unknown. There are numerous cross-reactions between aspirin and other NSAIDs. This case points out the importance of accurate history taking concerning self-medication for the diagnosis of angioedema.
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PMID:[Aspirin-induced angioedema of the nape of the neck with naproxen cross-reaction: a case report]. 1089 77

The factors underlying analgesic intolerance (AI), particularly the role of ethnic characteristics, are readily not clear. In this trial, we aimed to assess the predictive features of AI in Turkish subjects. One hundred and ninety patients with AI were enrolled into the study conducted in our tertiary care clinic. The types of drug causing adverse reaction(s) and types of reaction(s) were recorded. The presence of atopy was assessed by skin prick tests. According to the results, the most frequently intolerated analgesic was acetyl salicylic acid (72.1%), followed by nonsteroidal anti-inflammatory drugs (68.4%) and paracetamol (15.8%). Urticaria/angioedema (52.6%) and asthmatic response (40.5%) were the most common reactions to analgesics. Compared with the general adult population of Turkey, the rate of atopy was found be higher in patients with AI and asthma (25% vs. 45%, p = 0.004) but comparable in patients with AI but no atopic disorder (25% vs. 29.2%, p> 0.05). In conclusion, subjects exhibiting intolerance to analgesics have particular features in our population; the presence of atopy in these subjects seems to be associated with the coexistent asthma rather than the drug allergy itself.
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PMID:Clinical features and atopy profile in Turkish subjects with analgesic intolerance. 1199 Feb 26

Autologous serum skin test (ASST) reactivity is positive in up to 60% of patients with chronic idiopathic urticaria (CIU). About 21 to 30% of patients with CIU have intolerance to acetyl salicylic acid (ASA) and/or other chemically unrelated non-steroidal anti-inflammatory drugs (NSAIDs). To investigate the relationship between ASA/NSAID intolerance and ASST reactivity, a case-control study was performed in 110 patients with CIU and 60 healthy controls. A positive ASST was defined as an erythematous wheal with a diameter of > 5 mm more than the saline-induced response. Patients were assessed at 10-minute intervals for a minimum of three hours. ASA/NSAID intolerance was ascertained by a placebo controlled-provocation test with offending drug (s). Forty-two patients with CIU (38.2%) had autoreactivity whereas only two of the controls (3.3%) displayed early and weak skin responses (P<.0001). ASA/NSAID intolerance was demonstrated in 30 (27.3%) patients with CIU. The prevalences of autoreactivity were 93.3% (28/30) and 17.5% (14/80) in patients with and without ASA/NSAID intolerance, respectively (P<.001). Thirteen of the 25 ASST-positive patients (52%) who had single (n: 7) or multiple (n: 6) NSAID intolerance showed early (before or at 30 min) and mild autoreactivity of short duration, whereas 15 of the remaining 17 ASST-positive patients (88.2%) who all had multiple NSAID intolerance showed delayed (later than 30 min) and prolonged autoreactivity (P<.05). These findings suggest that a common mechanism may be responsible for the pathogeneses of both delayed autoreactivity and multiple NSAID intolerance in CIU. It might be further speculated that delayed, prolonged, and pronounced autoreactivity may be a possible predictor for multiple NSAID sensitivity in CIU.
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PMID:Multiple NSAID intolerance in chronic idiopathic urticaria is correlated with delayed, pronounced and prolonged autoreactivity. 1518 4

Intolerance reactions to acetyl salicylic acid (ASA) and nonsteroidal anti-inflammatory drugs (NSAIDs) are common and caused by inhibition of COX-1 enzyme. Therefore, drugs that selectively inhibit COX-2 enzyme may be safe in these subjects. In this study, we evaluated the tolerability of celecoxib, a selective COX-2 inhibitor, in patients with analgesic intolerance. The eligible study population consisted of patients with a history of urticaria/angioedema, naso-ocular symptoms, bronchospasm, and/or anaphylactoid reaction induced by ASA and/or NSAIDs. A single-blind, placebo-controlled oral challenge test was performed in the hospital setting. On 2 separate days, 1/4 and 3/4 divided doses of placebo and celecoxib (Celebrex 200 mg, Pfizer, Turkey) were given with 2-hour intervals. Seventy-five subjects (mean age: 38.2 +/- 1.4 years; F:M: 55:20) were included in the study. Twenty-one subjects had asthma. No reaction was observed with placebo or celecoxib provocation. Although celecoxib seems to be a safe alternative drug in our study group, considering its serious adverse events reported in the literature, the drug should be recommended for patients with analgesic intolerance only after being tested by an experienced allergist.
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PMID:Tolerability of selective cyclooxygenase inhibitor, celecoxib, in patients with analgesic intolerance. 1587 45


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