Effect of aspirin in "aspirin sensitive" patients.

Asad, S. I.; Kemeny, D.M.; Youlten, L. J. F.; Frankland, A. W.; Lessof, M. H.

doi:10.1136/bmj.288.6419.745

Cited by 48 publications

(11 citation statements)

References 13 publications

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“…[13][14][15] For example, the Scripps Clinic protocol involves small incremental oral doses of aspirin administered over the course of 2 to 3 days, until a dose of 400 to 650 mg is tolerated. 16 Although a long interval between doses can safeguard against undesired reactions, as symptoms can be detected at each given dose, a desensitization procedure requiring several days to be completed is not practical in patients with ACS or those who undergo stent implantation who require immediate administration of ASA.…”

Section: Discussionmentioning

confidence: 99%

Aspirin Desensitization in Patients With Coronary Artery Disease

Rossini

Iorio

Pozzi

et al. 2017

Circ: Cardiovascular Interventions

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A spirin (ASA) is the cornerstone of antithrombotic therapy in patients with coronary artery disease (CAD), both in the acute and the chronic phase of treatment.1-3 However, ≈2% of patients have hypersensitivity to ASA. 4 Although See Editorial by Tantry and Gurbelclopidogrel is recommended in practice guidelines as the antiplatelet agent of choice for patients who are unable toBackground-There are limited data on aspirin (ASA) desensitization for patients with coronary artery disease. The aim of the present study was to assess the safety and efficacy of a standard rapid desensitization protocol in patients with ASA sensitivity undergoing coronary angiography. Methods and Results-This is a prospective, multicenter, observational study including 7 Italian centers including patients with a history of ASA sensitivity undergoing coronary angiography with intent to undergo percutaneous coronary intervention. A total of 330 patients with history of ASA sensitivity with known/suspected stable coronary artery disease or presenting with an acute coronary syndrome, including ST-segment-elevation myocardial infarction were enrolled. Adverse effects to aspirin included urticaria (n=177, 53.6%), angioedema (n=69, 20.9%), asthma (n=65, 19.7%), and anaphylactic reaction (n=19, 5.8%). Among patients with urticaria/angioedema, 13 patients (3.9%) had a history of idiopathic chronic urticaria. All patients underwent a rapid ASA (5.5 hours) desensitization procedure. The desensitization procedure was performed before cardiac catheterization in all patients, except for those (n=78, 23.6%) presenting with ST-segment-elevation myocardial infarction who underwent the desensitization after primary percutaneous coronary intervention. Percutaneous coronary intervention was performed in 235 patients (71%) of the overall study population. The desensitization procedure was successful in 315 patients (95.4%) and in all patients with a history of anaphylactic reaction. Among the 15 patients (4.6%) who did not successfully respond to the desensitization protocol, adverse reactions were minor and responded to treatment with corticosteroids and antihistamines. Among patients with successful in-hospital ASA desensitization, 253 patients (80.3%) continued ASA for at least 12 months. Discontinuation of ASA in the 62 patients (19.7%) who had responded to the desensitization protocol was because of medical decision and not because of hypersensitivity reactions. Conclusions-A standard rapid desensitization protocol is safe and effective across a broad spectrum of patients, irrespective of the type of aspirin sensitivity manifestation, with indications to undergo coronary angiography with intent to perform percutaneous coronary intervention. Rossini et al Antiplatelet Desensitization Registrytake aspirin because of hypersensitivity or intolerance, ASA desensitization also represents an alternative approach. 5 This is particularly relevant for patients requiring dual antiplatelet therapy, including ASA and a P2Y 12 receptor, such as in patients experien...

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Section: Discussionmentioning

confidence: 99%

Aspirin Desensitization in Patients With Coronary Artery Disease

Rossini

Iorio

Pozzi

et al. 2017

Circ: Cardiovascular Interventions

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“…The response was not affected by ASA desensitization and there was no difference between four ASA-sensitive urticaria and four control subjects. 5 …”

Section: Blood Collection and Assay Methodsmentioning

confidence: 97%

Clinical and Biochemical Aspects of "Aspirin-Sensitivity"

Asad¹,

Youlten²,

Holgate³

et al. 1986

allergy asthma proc

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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 ofhistamine and prostaglandin (PG) F2a were significantly raised in these patients before ASA administration. PGF2a 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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“…This oc curred independently of histamine release and was probably due to a nonimmunological response. A large number of factors are known to cause degranu lation of mast cells and basophils, including aspirin, various components of complement, lectins [19][20][21], and in certain situations, physical stimuli such as cold [22], and spontaneous release has ben reported from cultured human colonic mucosa [23]. The D. pteronyssinus preparation used may also have contained some agent capable of promoting a small amount of nonIgE mediated release of GAG from basophils of non atopic individuals.…”

Section: Discussionmentioning

confidence: 99%

Release of Highly-Sulphated Glycosaminoglycans and Histamine from Human Basophils

Reilly

Dawes

Yap

et al. 1988

Int Arch Allergy Immunol

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A new assay for highly-sulphated glycosaminoglycans (GAGs) has been applied to the study of allergen (Dermatophagoides pteronyssinus)-induced release of GAG from human basophils. Highly-sulphated GAG, which was not heparin, was found only in basophil-containing cellular fractions of whole blood. Its release, like that of histamine, was Ca⁺⁺-dependent. However, allergen-induced release of GAG from the basophils of atopic individuals exhibited a different time-course and dose-response from that of histamine, and may occur at least in part by a different mechanism.

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Effect of aspirin in "aspirin sensitive" patients.

Cited by 48 publications

References 13 publications

Aspirin Desensitization in Patients With Coronary Artery Disease

Aspirin Desensitization in Patients With Coronary Artery Disease

Clinical and Biochemical Aspects of "Aspirin-Sensitivity"

Release of Highly-Sulphated Glycosaminoglycans and Histamine from Human Basophils

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