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)

35 individuals showing reactions to penicillin of anaphylactic shock, angioedema or urticaria were investigated. Their skin sensitivity was analysed using 16 different penicillin derivatives. In addition, the content of circulating reagins against the penicilloyl structure in the patient's sera were analysed using RAST. 17 of the patients had negative skin reactions and RAST results to all substances tested. The other 18 were skin test-positive to at least one derivative but showed markedly heterogeneous patterns of skin reactivity. 14 had positive reactions against penicilloyl structures accompanied by anti-penicilloyl reagins. Four patients showed doubtful reactions only to penicillin or penicilloate and/or penilloate. These patients also had very low levels of reagins against penicilloyl in their sera. Positive skin test results using monovalent penicillin derivatives such as penicillin, penicilloate, penilloate, penicilloyl amide, penicilloyl-formyl-lysine, penicillamine, which cannot form a multivalent antigen with penicillyol specificity, indicated formation of other derivatives of importance in penicillin allergy, e.g., penicillamine protein conjugates. Three patients showed skin reactions to ampicillin polymer and two to benzyl-penicillin polymer. The skin tests performed with the penicillin derivatives used do not seem to give more information on the sensitivity of the patients than does the RAST using penicilloyl structures.
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PMID:Antibody reactivity in penicillin-sensitive patients determinated with different penicillin derivatives. 40 32

The inhalation challenge with lysine-aspirin (L-ASA) using the dosimeter method allows the construction of a dose-response curve and the quantitative estimation of airway responsiveness to the drug. We assessed the modifications of airway responsiveness to methacholine in four groups of subjects: aspirin-sensitive asthmatics, aspirin-sensitive subjects with urticaria/angioedema, subjects with an equivocal history of aspirin intolerance and normal control subjects. The L-ASA challenge was positive in all aspirin-sensitive asthmatics. The pattern of bronchial response to the challenge was different from that observed after challenge with allergens or occupational sensitizers. The main difference was found in the recovery from induced bronchoconstriction. The recovery lasted from 3 to 6-8 hours, and a peculiar dose-response curve was obtained that we call "early prolonged reaction". In five of 18 ASA-sensitive subjects there was a significant increase in airway responsiveness. Airway responsiveness was normal in aspirin-sensitive nonasthmatic subjects and in the other two groups studied. We conclude that L-ASA inhalation challenge may increase bronchial hyperresponsiveness in some ASA-sensitive asthmatics. This presence of enhanced bronchial hyperesponsiveness seems to be a marker with which to distinguish ASA-sensitive asthmatics from ASA-sensitive subjects with urticaria/angioedema.
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PMID:Aspirin-induced asthma and bronchial hyperresponsiveness. 181 46

To determine the incidence of adverse reactions to analgesics in unselected asthmatic children, histories were obtained from 486 children, using questionnaires and interviews. Mean age was 11.4 +/- 2.3 (+/- 1 SD) years (range 6-17 years), and mean duration of disease was 7.6 +/- 3.6 (1-15) years. The majority of 21 children gave an equivocal history, and only 7 (1.4%) of all children had a reliable history of adverse reactions to various analgesics. Inhalation challenge with increasing doses of lysine acetylsalicylate (LASA) was performed in 75 randomly selected asymptomatic children. Two boys of these (2.7%) had a positive test, defined as a 25% or more decrease of FEV1 and/or a 50% or more increase of the oscillatory airway resistance, compared with base line values. Both children had a mild airway obstruction, and had no personal or family history of analgesics intolerance. Further 27 children with suspected positive personal or family histories were also challenged. One girl of these manifested a mild urticaria; her pulmonary function remained unchanged. The incidence of analgesics intolerance in unselected asthmatic children is much lower than that of 12.5% to 28% reported in severe chronic asthma. The inhalation challenge with LASA proved simple, safe, effective and time saving, and thus, it offers an alternative method to the oral challenge in suspected children.
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PMID:The incidence of analgesics intolerance in asthmatic children detected by history and inhalation challenge with lysine acetylsalicylate. 249 82

Skin testing for penicillin allergy with penicillin G (Pen G), penicilloic acid (PA), and penicilloyl poly-L-lysine (PPL) was performed on 740 subjects, and the results were assessed from epidemiologic and immunologic perspectives. Approximately 95% of these patients had histories of apparent allergic reactions to beta-lactam antibiotics, and 63% were skin-test positive. The prevalence of positive skin tests was related to the time that had elapsed between clinical reactions and skin testing. Ninety-three percent were skin-test positive 7 to 12 mo after reactions, and 22% were positive 10 yr or more after reactions. Patients under 30 yr of age had a prevalence of positive skin tests 1.7-fold higher than older patients. Testing with PPL, PA, and Pen G detected 76.3%, 55.3%, and 57.1% of the positive patients, respectively. Omission of PPL, PA, or Pen G would have led to a failure to detect 25.6%, 7.2%, and 6.2% of the positive patients, respectively. Subjects with skin tests positive to penicillin often reacted to skin tests with other beta-lactam antibiotics; 73% (41 of 56) reacted to ampicillin and 51% (38 of 74) reacted to cephalothin. No serious allergic reactions were provoked by testing. None of the 83 skin test--negative patients treated with beta-lactam antibiotics immediately after testing experienced acute allergic reactions. Two patients developed mild urticaria beginning 3 and 5 days into therapy. One skin test--negative patient experienced urticaria 3 hr after receiving oral penicillin 6 mo after skin testing. This patient's skin-test status immediately before therapy was unknown. These results support the position that testing with PPL, PA, and Pen G is a rapid, safe, and effective method for identifying patients at risk, or not at risk, for allergic reactions to penicillin.
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PMID:Skin testing to detect penicillin allergy. 626 15

Results of a study carried out in 21 patients with acetylsalicylic acid (Aspirin), hypersensitivity, 17 females and 4 males, aged 16 to 69 years (mean 45.7) are presented. Some patients suffered from several types of allergic symptoms - 11 from Asthma, 3 Rhinitis, 3 Quinke edema, 5 Urticaria and 2 Anaphylactic Shock. Concomitant drug allergies, route of administration and composition of the ingested drug, familiar complaints of drug allergy, nasopharyngeal examination and lung function by spirometry and Acetylcholine tests were evaluated. Blood, sputum and nasal mucous eosinophil count, as well as secretory IgA and its secretory piece identification in saliva and nasal mucous, serotonin and histaminopexic power of serum and immunoelectrophoresis of serum proteins were performed in all patients. Human basophil degranulation test to Aspirin were evaluated in 12 patients. Skin prick tests with one standard range of 21 common allergens were done in all patients and intradermal skin tests with 1 lysine acetyl-salicylate (1/100 and 1/1000) were performed in all patients as well as in a selected control group of 12 healthy subjects.
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PMID:Our experience with acetylsalicylic acid hypersensitivity. 647 95

We report the first human trial of immunotherapy employing the nonimmunogenic carrier, D-glutamic acid:D-lysine linked to short ragweed (SRW) fraction A (fraction A:D-GL). Twelve SRW-sensitive patients with no immunotherapy during the previous 19 yr received a 2-mo (7/79 to 9/79) course of fraction A:D-GL (average dose 49.5 mg, range 21 to 78 mg). We compared their symptom scores and serologic changes with two control groups of SRW-sensitive patients. Patients receiving fraction A:D-GL demonstrated at least a tenfold decrease in skin-test sensitivity to SRW and had statistically lower mean seasonal symptom scores (p less than 0.02) than untreated controls. Mean seasonal symptom scored did not differ statistically from those of control patients on year 4 of immunotherapy. In contrast to the expected suppression of IgE, we found that fraction A:D-GL stimulated both IgE and IgG responses to SRW and SRW-antigen E. These increases in IgE and IgG antibodies were significantly greater than in the control groups and appeared to be due largely to injection of fraction A:D-GL. Though fraction A:D-GL was generally well tolerated, we noted mild generalized urticaria in three patients, and large local reactions in five others. The difference between our results and the earlier results in mice may reside in the particular characteristics of this preparation of fraction A:D-GL.
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PMID:Immunotherapy with short ragweed fraction A:D-glutamic acid:D-lysine polymer in ragweed hay fever. 697 Jul 63

A large group of patients with suspected allergic reactions to beta-lactam antibiotics was evaluated. A detailed clinical history, together with skin tests, RAST (radioallergosorbent test), and controlled challenge tests, was used to establish whether patients allergic to beta-lactam antibiotics had selective immediate allergic responses to amoxicillin (AX) or were cross-reacting with other penicillin derivatives. Skin tests were performed with benzylpenicilloyl-poly-L-lysine (BPO-PLL), benzylpenicilloate, benzylpenicillin (PG), ampicillin (AMP), and AX. RAST for BPO-PLL and AX-PLL was done. When both skin test and RAST for BPO were negative, single-blind, placebo-controlled challenge tests were done to ensure tolerance of PG or sensitivity to AX. A total of 177 patients were diagnosed as allergic to beta-lactam antibiotics. We selected the 54 (30.5%) cases of immediate AX allergy with good tolerance of PG. Anaphylaxis was seen in 37 patients (69%), the other 17 (31%) having urticaria and/or angioedema. All the patients were skin test negative to BPO; 49 of 51 (96%) were also negative to MDM, and 44 of 46 (96%) to PG. Skin tests with AX were positive in 34 (63%) patients. RAST was positive for AX in 22 patients (41%) and to BPO in just 5 (9%). None of the sera with negative RAST for AX were positive to BPO. Challenge tests with AX were performed in 23 subjects (43%) to establish the diagnosis of immediate allergic reaction to AX, and in 15 cases (28%) both skin test and RAST for AX were negative. PG was well tolerated by all 54 patients. We describe the largest group of AX-allergic patients who have tolerated PG reported so far. Diagnosis of these patients can be achieved only if specific AX-related reagents are employed. Further studies are necessary to determine the exact extent of this problem and to improve the efficacy of diagnostic methods.
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PMID:Immediate allergic reactions to amoxicillin. 809 27

Nasal provocation tests with lysine acetylsalicylic acid (ASA) have been used in the diagnosis of ASA-induced asthma and rhinitis. To establish its possible role in identifying aspirin sensitivity manifested by urticaria or angioedema, 18 patients suffering from chronic or acute recurring urticaria/angioedema (10 ASA-sensitive and 8 ASA-nonsensitive) were submitted to nasal provocation tests with freshly prepared solutions of lysine ASA. Clinical response and variation of nasal expiratory peak-flow were evaluated, classified according to previously defined scores, and compared. The results showed a significant difference between ASA-sensitive and ASA-nonsensitive patients, suggesting that this test can be an important diagnostic tool for ASA-induced urticaria/angioedema.
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PMID:Nasal provocation tests in the diagnosis of urticaria induced by acetylsalicylic acid. 933 27

Haptens causing type I allergy have been shown to predominantly form lysine adducts in the carrier protein, while many haptens giving rise to type IV allergy preferentially form adducts with cysteine residues. Hexahydrophthalic anhydride derivatives are strong sensitizers capable of inducing allergic rhinitis, asthma and urticaria (type I allergy) and allergic contact dermatitis (type IV allergy). The ability of hexahydrophthalic anhydride (HHPA) to form adducts with nucleophilic amino acids and a model peptide in vitro is presented. Adduct formation was monitored by high-performance liquid chromatography with ultraviolet light/vis detection (LC-UV/vis) and high-performance liquid chromatography with mass spectrometric detection (LC/MS). The characterization was obtained by nuclear magnetic resonance spectroscopy (NMR) and mass spectrometry (MS and MS/MS). It was found that HHPA formed adducts with N(alpha)-acetylated lysine and cysteine and the non-acetylated alpha-amino group of proline and, to some extent, also with other nucleophilic amino acids. The adducts with lysine and proline were chemically stable. Addition of one HHPA to a model carrier peptide with all important nucleophilic amino acid residues showed N-terminal proline to be the major site of reaction. The addition of a second hapten gave a lysine adduct, but a minor cysteine adduct was also found. The cysteine-HHPA adducts were shown to be chemically unstable and participated in further reactions with lysine forming lysine-HHPA adducts. The results will be useful for understanding the formation of HHPA-protein adducts with the capability of being markers of exposure, and also to a deeper understanding of the chemical structures causing types I and IV allergy.
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PMID:Adducts between nucleophilic amino acids and hexahydrophthalic anhydride, a structure inducing both types I and IV allergy. 1624 18

Beta-lactam intolerance, most of which is not IgE or even immunologically mediated even though it is commonly called an "allergy," can be safely managed using the following seven steps: 1. Avoid testing, re-challenging, or desensitizing individuals with histories of beta-lactam associated toxic epidermal necrolysis, Stevens-Johnson syndrome, drug reaction with eosinophilia and systemic symptoms syndrome, severe hepatitis, interstitial nephritis, or hemolytic anemia. 2. Avoid unnecessary antibiotic use, especially in the setting of viral infections. 3. Expect new intolerances to be reported after 0.5 to 4% of all antibiotic utilizations, dependent on gender and the specific antibiotic used. 4. Expect a higher incidence of new intolerances in individuals with three or more medication intolerances already noted in their medical records. 5. For individuals with an appropriate penicillin class antibiotic intolerance based on a history of anaphylaxis, urticaria, macular papular rashes, unknown symptoms, or symptoms not excluded in step one, proceed with penicillin skin testing. Skin test with penicilloyl-poly-lysine and native penicillin. If skin test is negative, proceed with an oral amoxicillin challenge. If skin test and oral challenge are negative, penicillin class antibiotics may be used. If skin test or oral challenge is positive, avoid penicillin class antibiotics. If skin test or oral challenge is positive, non-penicillin-beta-lactams may be used, unless there is a history of intolerance to a specific non-penicillin-beta-lactam, then avoid that specific non-penicillin-beta-lactam. If there is life-threatening infection that can only be treated with a penicillin class antibiotic, proceed with oral penicillin desensitization prior to any oral or parenteral penicillin use. 6. For individuals with an appropriate non-penicillin-beta-lactam intolerance, avoid re-exposure to the beta-lactam implicated. An alternative beta-lactam may be used, ideally with different side chains. Penicillin allergy testing is not useful in the management of non-penicillin-beta-lactam intolerance. Non-penicillin-beta-lactam skin testing is not clinically useful and should not be done outside of a research setting. If the non-penicillin-beta-lactam implicated is needed to treat a life-threatening infection, proceed with desensitization. 7. Be ready to treat anaphylaxis with all parenteral beta-lactam use.
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PMID:Recommendations for the management of beta-lactam intolerance. 2354 54


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