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)

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

In the present study we examined the effects of chlorpheniramine and ranitidine, indomethacin, BW755C (an inhibitor of cyclo-oxygenase and lipo-oxygenase enzymes of arachidonic acid metabolism), dexamethasone, and capsaicin on nonimmunologic contact urticaria (NICU) induced in the guinea pig ear by benzoic, acid cinnamic acid, cinnamic aldehyde, methyl nicotinate, diethyl fumarate, or dimethyl sulfoxide. The intensity of edema in the urticarial reaction was quantified by measuring the ear thickness. Antihistamines inhibited reactions to intradermal histamine but not to agents causing NICU. Indomethacin and dexamethasone inhibited reactions to cinnamic acid and cinnamic aldehyde but not to other NICU agents. BW755C and capsaicin had no effect on reactions to any of the NICU agents. Mast cell degranulation during the reaction was not seen in histologic sections. Histamine and capsaicin-sensitive nerves did not seem to be essential for the development of NICU in the guinea pig ear. The details of the inhibitory effects of indomethacin and dexamethasone are not clear, but it seems probable that more than one mechanism is involved in NICU due to different agents.
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PMID:Pharmacological studies on nonimmunologic contact urticaria in guinea pigs. 310 19

Several therapeutic regimes for solar urticaria were evaluated. A short course of PUVA therapy produced a marked increase in the minimal dose of radiation required to produce urticaria in the six patients treated. This objective evidence of improvement was supported by the patients' reports of greatly increased tolerance to sun-exposure. Chlorpheniramine, an antihistamine, produced a slight increase in the minimal dose of radiation necessary to produce urticaria but its effectiveness was limited by side-effects. Indomethacin, an inhibitor of prostaglandin synthetase, produced no beneficial effect.
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PMID:Solar urticaria: treatment with PUVA and mediator inhibitors. 707 82

Ten patients with urticarial vasculitis, characterized clinically by persistent painful urticarial lesions, angioedema, recurrent arthralgia, abdominal pain, and low-grade fever, were selected for study. All patients had histologic evidence of leukocytoclastic vasculitis in the urticarial lesions. Results of direct immunofluorescence microscopy of urticarial lesions were positive in all nine of the patients tested. Treatment with indomethacin in dosages from 25 mg three times daily to 50 mg four times daily resulted in complete clearing of all disease manifestations in six of ten patients within 17 days and partial improvement in three. In eight of the ten patients, disease activity recurred within 48 hours after discontinuation of the use of indomethacin. Gastrointestinal irritation was the only side effect noted. Indomethacin is proposed as an effective mode of therapy in a disorder unresponsive to treatment with conventional medications for urticaria, including high-dose corticosteroids.
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PMID:The therapeutic response of urticarial vasculitis to indomethacin. 743 Apr 55

Aspirin is the oldest non-steroidal anti-inflammatory drug (NSAID), and it sometimes causes asthma-like symptoms known as aspirin-exacerbated respiratory disease (AERD), which can be serious. Unwanted effects of aspirin (aspirin intolerance) are also observed in patients with food-dependent exercise-induced anaphylaxis, a type I allergy disease, and aspirin-induced urticaria (AIU). However the target and the mechanism of the aspirin intolerance are still unknown. There is no animal or cellular model of AERD, because its pathophysiological mechanism is still unknown, but it is thought that inhibition of cyclooxygenase by causative agents leads to an increase of free arachidonic acid, which is metabolized into cysteinyl leukotrienes (cysLTs) that provoke airway smooth muscle constriction and asthma symptoms. As the bed-tobench approach, to confirm the clinical discussion in experimental cellular models, we have tried to develop a cellular model of AERD using activated RBL-2H3 cells, a rat mast cell like cell line. Indomethacin (another NSAID and also causes AERD), enhances in vitro cysLTs production by RBL-2H3 cells, while there is no induction of cysLTs production in the absence of inflammatory activation. Since this suggests that all inflammatory cells with activation of prostaglandin and cysLT metabolism should respond to NSAIDs, and then I have concluded that aspirin intolerance should be separated from subsequent bronchoconstriction. Evidence about the cellular mechanisms of NSAIDs may be employed for development of in vitro AERD models as the approach from bench-to-bed.
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PMID:Aspirin Intolerance: Experimental Models for Bed-to-Bench. 2771 58