Aspirin Sensitivity
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The experience in the United States with aspirin sensitivity associated with rhinosinusitis and asthma is generally in agreement with the European perspective offered by Drs. Most aspirin-sensitive patients no not have a family history of aspirin sensitivity. Aspirin sensitivity is found in one third of patients having nasal polyps, rhinosinusitis, and asthma, the remaining two thirds of these patients having no adverse response to aspirin ingestion. In 85% of asthmatics who give a history of aspirin-induced bronchospasm, oral aspirin challenges are positive. Thus, a small group of patients have inappropriately assigned aspirin-sensitive asthmatic (ASA) as the cause of a prior asthmatic attack that in reality had been induced by an independent provoking factor. 1
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. 2
Aspirin sensitivity is a condition in which people have strong reactions to aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs). These reactions include asthma attacks, symptoms that mimic those of an allergic reaction, and gastrointestinal problems. 3
Aspirin and other NSAIDs are used to reduce inflammation and relieve pain and fever. They do so by inhibiting an enzyme called cyclooxygenase-1 (COX-1). This enzyme is a prime factor in the production of prostaglandins, chemicals that trigger inflammation and pain within the body. 4
Only about five out of 100 persons with asthma are sensitive to aspirin in this way. Ninety five out of 100 persons with asthma will be able to take aspirin and related medications without any effect on their asthma. Children with asthma rarely have aspirin sensitivity, and it does not tend to run in families. Many people with asthma and aspirin sensitivity will also have nasal congestion and polyps in their nose. 5
Aspirin sensitivity is most likely to affect those who suffer from both moderate to severe asthma and chronic rhinosinusitis. It is more often found in females and becomes more likely as people age or as their asthma progresses. 6
All patients had been initially treated with medical therapy, which included intranasal steroid sprays, mucolytics, normal saline nasal washes, and antibiotics when indicated. Patients with nasal polyps were also treated with oral steroid tapers as needed, based on disease severity. Patients with objectively documented (by computed tomography and nasal endoscopy) chronic rhinosinusitis were offered FESS if medical management failed to control their symptoms. 7
The answer is not a simple “allergy” to aspirin, because persons sensitive to aspirin in this way will also be sensitive to the related medications called “non-steroidal antiinflammatory drugs” or NSAIDs. Common NSAIDs available without a prescription include ibuprofen (Advil� and Motrin�) and naproxen (Aleve�). A more complete list of aspirin-containing medications and NSAIDs is provided in the accompanying table. What all of these medicines have in common is their chemical effect: they inhibit the action of one of the proteins in the body, called cyclooxygenase. Persons with asthma and aspirin sensitivity have an unexplained sensitivity to the inhibitors of cyclooxygenase. It is as of yet uncertain how the new class of cyclooxygenase inhibitors used to treat arthritis (Vioxx� and Celebrex�) will affect persons with aspirin-sensitive asthma. 8
There is no simple test to determine if you have aspirin sensitivity, other than your own past experience with having taken aspirin or any of the NSAIDs. If as an adult you have never taken aspirin or a NSAID, perhaps because your doctor told you to avoid it because of your asthma, then you have two options. One is to continue to avoid aspirin and related medications on the possibility that your asthma involves aspirin sensitivity (a chance of about one in 20) or to take a small test dose of aspirin in a safe place, preferably your doctor’s office, and have your breathing closely observed for three hours thereafter. 9
The prevalence of Samter’s triad was much higher among adults (9 of 152 [5.9%]) than children (1 of 56 [1.8%]). The mean age of patients with Samter’s triad was slightly higher than the mean age of the study population as a whole (37.6 vs. 33.3 years;p = 0.47); while this difference was not statistically significant, it is consistent with the observation that aspirin sensitivity most commonly manifests when patients are in their 30s and 40s2 Patients with Samter’s triad were disproportionately female (70% of all cases) and black (50%), but again, neither finding was statistically significant. 10
To study whether an initial ischaemia could influence the results of current application due to possible prolonged post-ischaemic release of vasoactive mediators, transient ischaemia was applied before current application. The ischaemia was attained through suprasystolic inflation of an arm pressure cuff for 2min. Next, 7min were allowed for the return to stable baseline values. Thereafter, the 0.10-mA current was applied for 5min followed by 20min of recovery and then 24min of local warming to 44�C, as in the previous protocols. 11
Aspirin sensitivity is not an allergic reaction, because neither IgE nor mast cells are involved. What causes this problem is a metabolic abnormality � a malfunction in one aspect of the body�s chemistry. The details of this are very complicated: you may want to skip the next three paragraphs and simply read about how to cope with the problem. 12
The exact nature of aspirin sensitivity is still far from clear, but it seems to involve a relatively poor production of prostaglandins, combined with a plentiful production of leukotrienes. Both these substances are messenger chemicals which, broadly speaking, promote inflammation. But the details of their pro-inflammatory activities differ. It seems that, ideally, the body should have a harmonious balance between the two, and an imbalance produces problems. 13
References
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