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)

Aspirin (ASA) and nonsteroidal anti-inflammatory drugs (NSAIDs) share common pharmacologic effects in the prevention of inflammation, at least in part through inhibition of prostaglandin formation. ASA and NSAIDs have predictable side effects such as gastric pain, ecchymosis, and tinnitus. They also cause anaphylactoid shock, urticaria/angioedema, nephropathy, and hepatitis in individuals who appear to be normal and in whom prediction of such reactions cannot be made. Two selected populations of patients are likely to experience hypersensitivity reactions to both ASA and NSAIDs. Patients with asthma have an 8% to 20% chance of experiencing asthmatic attacks after ingesting ASA and NSAID. If such patients have associated rhinosinusitis (polyps), prevalence increases to 30% to 40%. Patients with chronic urticaria/angioedema have a 21% to 30% chance of experiencing an urticarial flare after ingesting ASA and NSAIDs.
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PMID:Diagnosis, prevention, and treatment of adverse reactions to aspirin and nonsteroidal anti-inflammatory drugs. 643 54

Of a total of 131 patients suffering from chronic urticaria, 15 were cautiously re-exposed to ASA after an initial provocative exposure during an urticaria test programme 2-11 years before. Only 1 of these patients, who had undergone the initial provocative test 7 years earlier, reacted at the same intensity; 1 other patient reacted with much less intense symptoms 4 years after the original test. Among 3 other patients, who merely reacted to ASA intake with urticarial eruptions and did not suffer from chronic urticaria, only 1 presented 4 years after the initial exposure with oedema of the skin and itching. The tolerance threshold was markedly higher. These results suggest that the sensitivity to intolerance-inducing agents is reduced relatively quickly and may subside completely in most cases.
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PMID:[Catamnestic studies of patients with chronic urticaria and aspirin intolerance ]. 815 Jun 10

From 1974 to 1989, 37,392 patients were admitted to the divisions of general internal medicine of the CHDM hospitals. 19,082 of them were treated with a minor analgesic or an NSAID. In 95 of the exposed patients, an allergic or a pseudoallergic reaction to one or two of these drugs was observed. From 1981 to 1990, general practitioners, hospitals and the pharmaceutical industry reported to SANZ 158 individual cases with comparable reactions to 175 exposures of the same kind. Of the 15 different syndromes and symptoms registered in both institutions, most were reactions of the skin, mainly the usual maculopapular exanthemas (rash), urticaria and angioedema. In the CHDM, allergic or pseudoallergic reactions were observed in 0.23% of patients exposed to minor analgesics (including ASA preparations on a daily dose up to 1.0 g and pyrazolones, mainly metamizole, propyphenazone) and in 0.81% of patients exposed to NSAIDs (including the pyrazolone oxyphenbutazone). In the experience of the Comprehensive Hospital Drug Monitoring in Berne and St. Gallen (CHDM) and the Spontaneous Adverse Drug Reactions Center of Switzerland (SANZ).
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PMID:[Incidence of drug side effects by symptoms and syndromes. From the experiences of the Comprehensive Hospital Drug Monitoring and the Swiss Drug Side Effect Center. As an example: allergic and pseudo-allergic reactions with mild analgesics and NSAID]. 837 61

The increase in neutrophil chemotactic activity (NCA) is related to degranulation of mast cells. The study included 10 patients in whom aspirin-induced urticaria was related to NCA increase. Tolerance state to ASA was achieved by administering this drug in incremental doses. In none of the examined patients after 600 mg of ASA given during induced tolerance state, the increase of NCA was observed. The authors conclude that in patients with ASA-urticaria, after ASA desensitization, mast cells degranulation does not occur.
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PMID:[Chemotactic activity of serum granulocytes after aspirin in patients with aspirin-sensitive urticaria who find themselves in a state of tolerance for this drug]. 840 40

The aim of the paper was to estimate the value of challenge tests with acetylsalicylic acid in diagnosis of ASA-induced urticaria. The study was performed in 71 persons with suspected urticaria/angioedema type of sensitivity to ASA. The anamnesis confirmed sensitivity in 67 examined patients (94.4%) and showed that the sensitive patients usually suffered from extensive urticaria (37 persons, i.e. 55.5%) after ingestion of ASA. Eight persons (12%) reacted with loss of consciousness and 4 (6.0%) with oedema of the larynx. Oral challenge test with acetylsalicylic acid was performed in 53 examined persons, in 49 (92.4%) of which it was positive. Threshold doses of acetylsalicylic acid ranged from 40 to 300 mg. In 11 persons the test was repeated and in 8 performed three times. It was observed that both the threshold acetylsalicylic acid doses and the time of appearance of the sensitivity symptoms were changeable. All ASA-sensitive reacted to indomethacin in the similar way as to ASA. Paracetamol, on the other hand, was well tolerated by all 25 tested patients with urticaria/angioedema type of sensitivity to ASA.
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PMID:[Urticaria-angioedema type of sensitivity to aspirin and other nonsteroidal anti-inflammatory drugs; diagnostic value of anamnesis and challenge tests with acetylsalicylic acid in detecting this sensitivity]. 849 80

ASA and NSAIDs are responsible for a large number of adverse reactions. The association of adverse reactions to acetaminophen and to ASA is uncommon, especially in children, and raises the problem of finding alternative treatments. We present a case report of a 7-year-old boy with combined adverse reaction to acetaminophen and ASA/NSAIDs. The child, who had no history of atopy, first displayed the condition at age 6, when he suffered two episodes of urticaria and angioedema, 2 hours after administration of 500 mg of acetaminophen, following two earlier doses of 500 mg (total 1500 mg). At age 7 he suffered a third episode 3 hours after administration of 180 mg of ASA. The patient submitted to oral challenges with acetaminophen (positive at a cumulative dose of 2,040 mg), ASA (positive at a cumulative dose of 204 mg) and nimesulide (negative at a cumulative dose of 119 mg). In conclusion, nimesulide (an NSAID not available in the United States) may be regarded as an alternative treatment in such patients, but more research is needed in pediatric age groups.
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PMID:Adverse reactions to acetaminophen, ASA, and NSAIDs in children: what alternatives? 933 26

Urticaria is characterized by strongly pruritic wheals and in some cases, angioedema. On the basis of a careful case history, the type of urticaria presenting can usually be determined. In the case of the acute form, no complicated diagnostic work-up is necessary. Treatment is symptomatic: the use of ASA should be avoided, while an acute infection requires treatment. When there is recurrent angioedema, chronic urticaria and physical forms, a multitude of triggering factors must be considered. In many cases, symptoms may persist for years. Symptomatic treatment with antihistaminics is often inadequate, but long-term treatment with glucocorticoids should be avoided on account of their side effects. For this reason, further diagnostic work-up is usually necessary and, where indicated, treatment should be initiated by a dermatologist with specialist training in allergology.
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PMID:[Acute, chronic or physical urticaria. What causes the hives?]. 1192 59

Cis-atracurium is a stereoisomer of atracurium, about five times more potent than the racemate. Whereas cis-atracurium is routinely used in adults, its effects on children are still poorly defined. We compared equipotent doses of atracurium and cis-atracurium in children aged between 2 and 12 years regarding the quality of neuromuscular blockade, the intubation conditions and the occurrence of side-effects. After approval by the ethics committee and with informed parental consent, 84 children (ASA I or ASA II) were randomly allocated to receive either 0.5 mg/kg atracurium (group A, n = 42) or 0.1 mg/kg cis-atracurium (group C, n = 42). In both groups anaesthesia was induced with 15 micrograms/kg alfentanil and 5-7 mg/kg thiopentone. We assessed the intubation conditions according to the Krieg Scale. Anaesthesia was maintained with a nitrous oxide/oxygen mixture of 2:1 and isoflurane in an endexpiratory concentration of approximately 0.6 Vol.%. Neuromuscular blockade was controlled acceleromyographically in response to supramaximal stimulation of the ulnar nerve. We measured the onset time (T1 = 5%), duration of effect (T1 = 25%), recovery index (T1 = 25%-75%) and the recovery time at a train-of-four-ratio (T4/T1) of 0.7. These parameters did not show any significant differences between group A and group C: onset time: 3.1 +/- 1.5 min (group A) versus 3.4 +/- 1.1 min (group C), duration of effect: 34.1 +/- 5.5 min (group A) versus 34.1 +/- 6.5 min (group C), recovery index: 9.3 +/- 3.3 min (group A) versus 9.6 +/- 2.5 min (group C), recovery time at a TOF-ratio of 0.7:49.3 +/- 8.4 min (group A) versus 52.3 +/- 6.6 min (group C). In group A, the intubation conditions were "excellent" or "good" in 98% of the patients, whereas in group C the figure was only 69%. Regarding side-effects, we found significantly more frequent urticaria in group A (6 of the 42 patients) (p < or = 0.05) than in group C, in which no patient showed urticaria. Flush and tachycardia occurred much less frequently and there were no significant differences in the two groups: two patients in group A and only one in group C. The authors conclude that atracurium and cis-atracurium lead to comparable neuromuscular effects in children aged between 2 and 12 years. Only the intubation conditions were better after atracurium, but atracurium was followed by urticaria more often than cis-atracurium.
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PMID:[Cis-atracurium--an equivalent substitution for atracurium in pediatric anesthesia?]. 1223 66

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


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