Aspirin desensitization: Difference between revisions
No edit summary |
|||
| Line 16: | Line 16: | ||
==Mechanism of Aspirin Desensitization== | ==Mechanism of Aspirin Desensitization== | ||
The pathophysiology aspirin hypersensitivity involves both excess [[leukotriene]] producation as well as the development of antibodies directed toward aspirin. The goal of a desensitization protocol is to deplete the leukotrienes (as well as other mediators) and to down-regulate the leukotriene receptors. | The pathophysiology aspirin hypersensitivity involves both excess [[leukotriene]] producation as well as the development of IgE antibodies directed toward aspirin. The goal of a desensitization protocol is to deplete the leukotrienes (as well as other mediators) and to down-regulate the leukotriene receptors. | ||
== Protocol for Aspirin Desensitization: == | == Protocol for Aspirin Desensitization: == | ||
Revision as of 16:39, 1 July 2010
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Keri Shafer, M.D.
Please Join in Editing This Page and Apply to be an Editor-In-Chief for this topic: There can be one or more than one Editor-In-Chief. You may also apply to be an Associate Editor-In-Chief of one of the subtopics below. Please mail us [2] to indicate your interest in serving either as an Editor-In-Chief of the entire topic or as an Associate Editor-In-Chief for a subtopic. Please be sure to attach your CV and or biographical sketch.
Overview
Approximately 10% of patients will develop a hypersensitivity reaction to aspirin. Dual antiplatelet therapy with both aspirin and clopidogrel has been associated with improved clinical outcomes in the management of patients with acute coronary syndromes. Although there is a lack of supporting data, patients with aspirin hypersensitivity are sometimes managed with clopidogrel monotherapy. Aspirin desensitization is required when continued aspirin administration is essential (e.g. management of an acute coronary syndrome with stent placement). A rapid protocol can be used as described below. [1]. While this protocol can be implemented over the course of several hours, it may not applicable to those patients who must proceed to the cardiac catheterization laboratory such as the patient with ST segment elevation myocardial infarction where "time is muscle".
Diagnosis
Signs and Symptoms
The signs and symptoms of hypersensitivity include rhinorrhea, exacerbation of asthma, urticaria, angioedema, and anaphylaxis. The majority of patients develop asthma, asthma exacerbation or rhinitis. [2]
History
While aspirin is often the culprit, the reaction can also be induced by cross reaction with cycloxygenase 1 inhibitors (COX 1) such as ibuprofin (Motrin) and naproxen [2].
Mechanism of Aspirin Desensitization
The pathophysiology aspirin hypersensitivity involves both excess leukotriene producation as well as the development of IgE antibodies directed toward aspirin. The goal of a desensitization protocol is to deplete the leukotrienes (as well as other mediators) and to down-regulate the leukotriene receptors.
Protocol for Aspirin Desensitization:
The dose of aspirin is increased every 15 minutes until the maximum dose of aspirin is administered:
Dose
0 minutes: 0.1 mg
15 minutes: 0.3 mg
30 minutes: 1 mg
45 minutes: 3 mg
60 minutes: 10 mg
75 minutes: 20 mg
90 minutes: 40 mg
105 minutes: 81 mg
120 minutes: 162 mg
135 minutes: 325 mg
References
- ↑ Page NA, Schroeder WS (2007). "Rapid desensitization protocols for patients with cardiovascular disease and aspirin hypersensitivity in an era of dual antiplatelet therapy". The Annals of Pharmacotherapy. 41 (1): 61–7. doi:10.1345/aph.1H437. PMID 17200429. Retrieved 2010-07-01. Unknown parameter
|month=ignored (help) - ↑ 2.0 2.1 Gollapudi RR, Teirstein PS, Stevenson DD, Simon RA (2004). "Aspirin sensitivity: implications for patients with coronary artery disease". JAMA : the Journal of the American Medical Association. 292 (24): 3017–23. doi:10.1001/jama.292.24.3017. PMID 15613671. Retrieved 2010-07-01. Unknown parameter
|month=ignored (help)