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)

The aim of this prospective study was to evaluate the incidence of allergic reactions to drugs compared to other kinds of medical emergencies admitted to the main Hospital in Milan during a 6 months period. At the same time we drew a list of drugs most frequently involved in allergic reactions, and a list of the most frequent symptoms. Using special forms, the medical staff collected patients' data: age, history of atopy, identification of the drug causing the reaction, and any previous reactions. Among 11,407 cases of medical emergencies, we found 163 (1.43%) patients showing drug reactions: the mean age was 27.3; 58.90% were female; atopy was present in 16.56%. The drugs most frequently involved were: pyrazon group (22%); ASA (20.86%); penicillin and derivatives (9.20%); sulfa drugs (6.14%); group B vitamins (4.30%); tetanus toxoid (4.30%); hyposensitizing extracts (3.68%); propionic acid derivatives (2.46%); paracetamol (1.84%); indomethacin (1.23%); rifampicin (1.23%); erythromycin (1.23%); glafenine (1.23%); others (17.80%). Urticaria and/or angioedema were the most frequent symptoms (86.51%), then anaphylactic shock (9.81%) and asthma (3.68%) with regard to anaphylactic shock only 6.20% of the patients had had a previous reaction to the same drug. From these data we can see that the incidence of drug reactions is very low compared to other medical emergencies; penicillin evidenced fewer reactions than expected, while the pyrazon group and ASA confirmed the data from literature.
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PMID:[Occurrence of drug reactions]. 287 4

43 children who presented with angio-oedema and/or urticaria and who responded to an additive-free diet were challenged with artificial food additives in a double-blind study. 24 children reacted to 1 or more of the additives. 18 children did not react to any additives and remained well when a normal diet was re-introduced. Aspirin sensitivity was found in only 1 of the 24 children who could not tolerate additives. Atopy was less common in these patients than in the general population. The mechanism of additive intolerance is unknown and double-blind challenge is the only reliable means of diagnosis.
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PMID:Artificial food additive intolerance in patients with angio-oedema and urticaria. 287 37

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

The study was performed on 22 patients with sensitivity to aspirin which manifested as urticaria and angioedema. Sensitivity to aspirin was established based on the anamnesis of urticaria and angioedema occurring after ingestion of aspirin and oral challenge tests with acetylsalicylic acid. At first, the threshold dose of aspirin in all patients and additionally of indomethacin in 12 patients was established. Aspirin "desensitization" was induced by administering increasing doses of acetylsalicylic acid every 24 hr until a good tolerance of 600 mg was obtained. The following day after the ingestion of 600 mg acetylsalicylic acid, 12 patients received 50 mg indomethacin. A good tolerance of 600 mg aspirin was achieved in all examined patients and 50 mg of indomethacin was also well tolerated. The authors assume that mechanism of urticaria and angioedema type of sensitivity to aspirin has the same pathogenic background as aspirin-induced bronchoconstriction.
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PMID:Aspirin "desensitization" in patients with aspirin-induced urticaria and angioedema. 322 50

From the report of Hirschberg, only 3 years after aspirin synthesis, there have been numerous works dedicated to showing the different types of adverse reactions found following aspirin administration. However, there are few publications on the process of urticaria and/or acute angioedema induced by ASA and few reported cases were found in children. Thus, we present 6 atopic children with urticaria and/or angioedema related with ASA. A carefully detailed history, oral provocation with ASA, oral provocation with other NSAI and HBDT with ASA were done to all of them. The oral provocation with ASA was positive in 5 of the 6 cases. The provocations with the rest of the NSAI and tartrazine and sodium benzoate were negative in all of the patients. The HBDT was positive in 5 of the cases. In conclusion, we insist that aspirin intolerance is not infrequent in infancy and it is not rare to see urticaria and or angioedema, in spite of the fact that asthmatics, atopics or non atopics, usually present as bronchospasm. We also believe that the HBDT can be a method of diagnosis used in these cases.
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PMID:Acetyl salicylic acid induced-urticaria and/or angioedema in atopic children. 338 13

Aspirin desensitization can be carried out in all aspirin sensitive patients in whom the reaction is confined to the respiratory tract. Because only a few patients with urticarial reactions to ASA have been studied and the results are inconsistent, desensitization of urticaria patients cannot be recommended at this time. In asthmatic patients with aspirin sensitivity, who undergo ASA desensitization, continuous treatment with ASA or NSAIDs is realistic. Such treatment maintains the desensitized state indefinitely while allowing the beneficial anti-inflammatory effects of these drugs to participate in the treatment of various diseases, including arthritis, thromboembolic diseases, and probably inflammation in the respiratory tract.
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PMID:Aspirin desensitization. 347 38

Progressively increasing doses of aspirin (acetylsalicylic acid--ASA) were tolerated by 14 out of 15 patients with confirmed aspirin-sensitive urticaria and in 7 out of 9 patients with aspirin-sensitive asthma. Blood levels of histamine and prostaglandin (PG) F2 alpha were significantly raised in these patients before ASA administration. PGF2 alpha levels fell to within the normal range after challenge doses of ASA which were sufficient to cause symptoms. Skin prick testing with histamine and codeine phosphate did not show evidence of abnormal tissue reactivity or mast cell reactivity. A wider spectrum of mediators will need to be considered if the mechanism of symptom production is to be understood.
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PMID:Clinical and biochemical aspects of "aspirin-sensitivity". 347 39

Acetylsalicylic acid (ASA) and other nonsteroidal anti-inflammatory drugs (NSAID) cause a variety of symptoms in patients sensitive to these drugs. These include wheezing, rhinorrhea, flushing, pruritus, urticaria, hypotension and loss of consciousness. Conversely, improvement of asthma with the use of these drugs in patients who do not have idiosyncratic reactions to ASA (ASA-nonsensitive) has also been observed both with respect to clinical symptoms and pulmonary function tests.
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PMID:Asthma improved by acetylsalicylic acid and other nonsteroidal anti-inflammatory agents. 347 42

We have evaluated the usefulness of HBDT as an in vitro method for the diagnosis of drug allergy. Two hundred and thirty six patients with suspected drug sensitization to penicillin, streptomycin, sulfamides, pyrazolones and A.S.A. were analyzed. Seventy-nine of them were allergic; in 43 cases it was confirmed by in vivo methods. Other patients were diagnosed by clinical history only if they had more than two reactions to the same drug. In order to be included in this group patients with reactions to pyrazolones and A.S.A. had to have tolerated other NSAI, therefore these patients were allergic to one compound only. All patients were considered non-allergic were determined by a negative provocation test. In the group of allergic patients we obtained 63 (79%) positive degranulations and 16 (21%) negative. One hundred and thirty two (84%) negative degranulations and 25 (16%) positive were obtained in the group of non-allergic patients. Once having analyzed 10 statistical parameters with each drug, the HBOT appears to be a useful method for these drugs except for streptomycin. In 16 (80%) out of 20 aspirin sensitive asthmatic patients we found that their basophils were degranulated. In 7 patients with urticaria and/or angioedema by A.S.A. and other NSAI the degranulation was negative, confirming the absence of the involvement of basophils in this reactions.
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PMID:Human basophil degranulation test in drug allergy. 373 76

Aspirin intolerance is particularly common in asthmatic patients who additionally have chronic rhinitis and/or nasal polyps. These individuals differ in several respects from patients who experience urticaria and/or angioedema after aspirin administration, and differing mechanisms may be involved. Data regarding the latter are indirect and incomplete, but suggest that ASA-sensitive asthma is most likely to be related in some manner to the capacity of ASA to inhibit cyclooxygenases, enhanced lipoxygenase metabolism perhaps playing a crucial role. Current research employing ASA "desensitization" may help to elucidate these enigmas.
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PMID:Aspirin-sensitive asthma. 391 38


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