Intolerance to Aspirin

Samter, Max; Beers, Ray F.

doi:10.7326/0003-4819-68-5-975

Cited by 769 publications

(59 citation statements)

References 16 publications

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“…Angioedema may occur by itself in response to aspirin. Aspirin-induced urticaria may occur in females with nasal polyposis eosinophilia and asthma (asthma triad) (Widal’s syndrome) [28]. These patients may also react adversely to other NSAID.…”

Section: Pseudoallergic Urticaria Due To Nsaidsmentioning

confidence: 99%

Drug-Induced Urticaria and Angioedema: Pathomechanisms and Frequencies in a Developing Country and in Developed Countries

Greaves

Hussein²

2002

Int Arch Allergy Immunol

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A careful drug history should be obtained from all patients with acute or chronic urticaria/angioedema, especially in the elderly. Although strictly comparable data are lacking, drug-induced urticaria appears to be more common in developed countries than in Malaysia, at least in a Hospital setting. Culprit drugs include antibiotics, analgesics and contrast media. Pseudoallergic drug-induced urticaria mimicks true allergic urticaria, but without an evident immunological basis, and is at least as common as the allergic type. In Malaysia, and in many other countries compulsory, ingredient labelling of ‘traditional’ medicines would do much to reduce the frequency of drug-induced urticaria.

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Section: Pseudoallergic Urticaria Due To Nsaidsmentioning

confidence: 99%

Drug-Induced Urticaria and Angioedema: Pathomechanisms and Frequencies in a Developing Country and in Developed Countries

Greaves

Hussein²

2002

Int Arch Allergy Immunol

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“…This predominant production by the eosinophil of LTC4 with its capacity to impair normal airflow in human airways (7) and to elicit vasooactive changes in human skin (8) suggests that the eosinophil may contribute to the manifestations of the allergic diseases with which it is frequently associated (28). In bronchial asthma eosinophilia of respiratory tissues and secretions is common, and increases in blood eosinophilia have been correlated with symptomatic exacerbations, including those associated with idiosyncratic reactions to nonsteroidal anti-inflammatory agents (29,30). The effects of LTC4 generation by human eosinophils may contribute to the pathobiology of allergic, metazoan parasitic, and other diseases characterized by blood or tissue eosinophilia.…”

mentioning

confidence: 99%

Generation and metabolism of 5-lipoxygenase pathway leukotrienes by human eosinophils: predominant production of leukotriene C4.

Weller¹,

Lee²,

Foster³

et al. 1983

Proc. Natl. Acad. Sci. U.S.A.

413

154

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5-Lipoxygenase pathway-derived products of arachidonic acid released by human eosinophils activated in vitro have been measured by using radioimmunoassays specific for leukotriene B4 (LTB4) and for sulfidopeptide leukotrienes including leukotriene C4 (LTC4). Eosinophil-enriched leukocytes (mean, 85% eosinophils) from five hypereosinophilic donors activated with 5.0 pAM ionophore A23187 for 15 min at 37C in the presence of 50 mM L-serine released 69 ± 28 and 1.5 + 0.8 (mean ± SEM) ng of LTC4 and LTB4, respectively, per 106 cells; ratios of LTC4 to LTB4 ranged from 16 to 149. Eosinophils stimulated with ionophore (2.5 ,M) or phorbol myristate acetate (1 ,ug per ml) metabolized exogenously added LTC4 to products that coeluted on reverse-phase high-performance liquid chromatography with synthetic S-diastereoisomeric LTC4 sulfoxides and 6-trans-LTB4 diastereoisomers, and this metabolic inactivation was inhibited by Lserine or catalase. Ionophore-activated eosinophils purified from three normal donors also preferentially generated LTC4 (38 ± 3 ngper 106cells) relative to LTB4 (6.0 ± 3.1 ng per 106cells), whereas neutrophils from the same donors released LTB4 (48 ± 21 ng per 106 cells) in a >7-fold excess to LTC4. The predominant production by human eosinophils of LTC4 with its potent smooth muscle spasmogenic and vasoactive properties may contribute to the pathobiology of allergic and other diseases associated with eosinophilia.Human polymorphonuclear leukocytes, activated with diverse stimuli, oxidatively metabolize arachidonic acid by the 5-lipoxygenase-dependent pathway to 5,6-trans-oxido-7,9-trans-11, 14-cis-icosatetraenoic acid (leukotriene A4, LTA4) (1), which in turn is converted enzymatically to (5S,6R)-5,6-dihydroxy-6,14-cis-8, 10-trans-icosatetraenoic acid (leukotriene B4, LTB4) or to (5S,6R)-5-hydroxy-6-S-glutathionyl-7,9-trans-11, 14-cis-icosatetraenoic acid (leukotriene C4, LTC4) (2-4). LTB4 is a potent chemoattractant and aggregating stimulus for both neutrophilic and eosinophilic polymorphonuclear leukocytes (5, 6), and LTC4 is exquisitely active as a spasmogenic and vasoactive substance when administered locally to human airways and skin, respectively (7,8).Human polymorphonuclear leukocytes, predominantly neutrophils, when stimulated with the calcium ionophore A23187 produce LTB4 in marked preference to the sulfidopeptide leukotrienes, LTC4 and its peptide cleavage products (5S,6R)-5-hydroxy-6-S-cysteinylglycyl-7,9-trans -11, 14 -cis-icosatetraenoic acid (leukotriene D4, LTD4) and (5S,6R)-5-hydroxy-6-Scysteinyl-7,9-trans-11,14-cis-icosatetraenoic acid (leukotriene E4, LTE4) (2,4,9,10 diastereoisomers, and the S-diastereoisomeric sulfoxides of LTC4 were prepared as described (11)(12)(13)(14).Cell Purification. Human neutrophils were prepared from citrate-anticoagulated blood of normal volunteer donors by dextran sedimentation of erythrocytes, centrifugation on cushions of Ficoll/Hypaque, and hypotonic lysis of erythrocytes (15). Human eosinophils were obtained from the citrate-anticoagulated b...

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“…At least 10% of patients with a history of asthma will have NSAID hypersensitivity 10 . The triad of ASA sensitivity, asthma, and nasal polyposis has been called Samter's triad since the seminal paper in 1968 11 . The more modern term of aspirin exacerbated respiratory disease (AERD) is used today to refer to the asthma, although worsened by ASA, is generally a progressive process over life.…”

Section: Casementioning

confidence: 99%

Aspirin Allergy Desensitization in Cerebrovascular Disease

et al. 2014

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Aspirin (ASA) is the mainstay of treatment in cerebrovascular and systemic vascular disease. ASA hypersensitivity can pose a challenge to achieving optimum medical management prior to and after neurointerventional treatment. Desensitization to ASA is well described in the allergy and cardiovascular literature, but there are no similar discussions specific to neurointervention. The purpose of our study was to describe our experience with ASA hypersensitivity management and review the relevant literature. Two cases of patients with symptomatic cerebrovascular disease requiring neurointervention who were successfully desensitized to their ASA hypersensitivity prior to treatment are described. The subsequent literature is reviewed. Several ASA desensitization protocols exist and have been proven to successfully treat ASA hypersensitivity and allow for ASA therapy to be safely initiated. We describe several previously published protocols. ASA desensitization is a safe and simple way to manage ASA hypersensitivity. We provide comprehensive management guidelines for the neurointerventionalist engaging in ASA desensitization.

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Intolerance to Aspirin

Cited by 769 publications

References 16 publications

Drug-Induced Urticaria and Angioedema: Pathomechanisms and Frequencies in a Developing Country and in Developed Countries

Drug-Induced Urticaria and Angioedema: Pathomechanisms and Frequencies in a Developing Country and in Developed Countries

Generation and metabolism of 5-lipoxygenase pathway leukotrienes by human eosinophils: predominant production of leukotriene C4.

Aspirin Allergy Desensitization in Cerebrovascular Disease

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