Aspirin hypersensitivity

The term refers to a distinct clinical syndrome characterized by aggressive and continuous inflammatory disease of the airways with chronic eosinophilic rhinosinus-itis, asthma and often nasal polyposis [6-8]. Aspirin and other NSAIDs that inhibit COX-1 exacerbate the condition, precipitating violent asthmatics attacks. This is a hallmark of the syndrome. The prevalence of aspirin hypersensitivity in the general population ranges from 0.6 to 2.5%, but is much more frequent in adult asthmatic subjects where it reaches 10-15%, although it is often underdiagnosed. 

AIA runs a characteristic clinical course [9]. It is more frequent in women than men, and is unusual in children, beginning in adulthood, on average at the age of 30 years. Rhinorrhea and nasal congestion are usually the first symptoms, subsequently complicated by polyposis. Asthma and aspirin hypersensitivity develop 2-15 years later. Once developed, aspirin intolerance remains through life, although sporadic disappearance of intolerance has been reported. Asthma, characterized by blood and nasal eosinophilia, rims a protracted course despite avoidance of analgesics. In about half the patients, the course of asthma is severe, necessitating use of systemic corticosteroids. 

Szczeklik A, Sanak M The broken balance in aspirin hypersensitivity. Eur J Pharmacol 2006 533 145-155. 

Kim SH, Park HS. (2006) Genetic markers for differentiating aspirin-hypersensitivity. Yonsei MedJ. 47, 15-21. 

Peripheral neuritis Peripheral neuritis evidenced by paresthesias, numbness, and tingling, has been observed. Add pyridoxine to the regimen if symptoms develop. Hematologic effects Blood dyscrasias consisting of reduction in hemoglobin and red cell count, leukopenia, agranulocytosis, and purpura have been reported. If such abnormalities develop, discontinue therapy. Periodic blood counts are advised. Tartrazine sensitivity Some of these products contain tartrazine, which may cause allergic-type reactions in susceptible individuals. Tartrazine sensitivity is frequently seen in patients who also have aspirin hypersensitivity. 

Hypersensitivity to salicylates or nonsteroidal anti-inflammatory drugs (NSAIDs). Use extreme caution in patients with history of adverse reactions to salicylates. Cross-sensitivity may exist between aspirin and other NSAIDs that inhibit prostaglandin synthesis, and aspirin, and tartrazine. Aspirin cross-sensitivity does not appear to occur with sodium salicylate, salicylamide, or choline salicylate. Aspirin hypersensitivity is more prevalent in those with asthma, nasal polyposis, chronic urticaria. 

Contraindications Complete biliary obstruction, hypersensitivity to cholestyramine ortartrazine (frequently seen in aspirin hypersensitivity)... 

Tablet form conf ains f arf razine risk of allergicdype reacf ions, especially in pafienfs with aspirin hypersensitivity... 

A topical 3% gel formulation of the nonsteroidal anti-inflammatory drug diclofenac (Solaraze) has shown moderate effectiveness in the treatment of actinic keratoses. The mechanism of action is unknown. As with other NSAIDs, anaphylactoid reactions may occur with diclofenac, and it should be given with caution to patients with known aspirin hypersensitivity (see Chapter 36). 

Aspirin hypersensitivity is also a potential concern and can occur in two ways (1) a respiratory reaction, which is more profitimd in patients with rhinitis, asthma, or nasal polyps, or (2) a typical type I hypersensitivity reaction, including urticaria, wheals, angioedema, itching, rash, bronchospasm, laryngeal edema, hypotension, shock, or syncope. This latter response generally occurs within 1 hour of aspirin ingestion. Such aspirin intolerance may manifest itself in 4% to 19% of patients with asthma and may approach 40% of steroid-dependent asthmatics. 

Patients who are sensitive to aspirin shonld not be given any other NSAID becanse of possible cross-sensitivity reactions. Aspirin cross-sensitivity however, does not appear to occur with the nonacetylated salicylates such as sodium salicylate or choline salicylate. As mentioned previously, aspirin hypersensitivity is more prevalent in patients with asthma, rhinitis, or nasal polyposis. This syndrome has been termed the aspirin triad. ... 

History of bronchial asthma, nasal polyps, or aspirin hypersensitivity... 

Hypersensitivity reactions, such as urticaria and angio-edema, are relatively common in subjects with aspirin hypersensitivity. Purpura, hemorrhagic vasculitis, erythema multiforme, Stevens-Johnson syndrome, and Lyell s syndrome have also been reported, but much less often. Fixed drug eruptions, probably hypersensitive in origin, are periodically described. In some patients they do not recur on rechallenge, that is the sensitivity disappears (74). 

Of adult asthmatics 2-20% have aspirin hypersensitivity (9). The mechanism is related to a deficiency in bronch-odilator prostaglandins prostaglandin inhibition may make arachidonic acid produce more leukotrienes with bronchoconstrictor activity. Oral challenge in asthmatic patients is an effective but potentially dangerous method for establishing the presence of aspirin hypersensitivity (63). 

Aspirin hypersensitivity is relatively common in adults (about 20%). Estimates of the prevalence of aspirin-induced asthma vary from 3.3 to 44% in different reports (SEDA-5,169), although it is often only demonstrable by challenge tests with spirometry, and only 4% have problems in practice. Patients with existing asthma and nasal polyps or chronic urticaria have a greater frequency of hypersensitivity (76), and women appear to be more susceptible than men, perhaps particularly during the childbearing period of life (77). Acute intolerance to aspirin can develop even in patients who have taken the drug for some years without problems. 

Henoch-Schbnlein purpura has been reported (81). Life-threatening respiratory distress, facial edema, and lethargy occurred in a woman with a history of severe asthma and aspirin hypersensitivity (SEDA-22,118). 

Patients with known triad symptoms (aspirin hypersensitivity, rhinitis/nasal polyps, and asthma) are at high risk for bronchospasm. NSAlDs may mask the signs and symptoms of acute infection, fever, myalgia, and erythema. 

Although less common in children, this syndrome may occur in 10-25% of patients with asthma, nasal polyps, or chronic urticaria, and in 1 % of apparently healthy individuals. It is provoked by even low doses (<80 mg) of aspirin and apparently involves COX inhibition. Aspirin hypersensitivity is associated with an increase in biosynthesis of LTs, perhaps reflecting diversion ofAA to lipoxygenase metabolism. 

Acetaminophen is a suitable substitute for aspirin for analgesic or antipyretic uses it is particularly valuable for patients in whom aspirin is contraindicated (e.g., those with peptic ulcer, aspirin hypersensitivity, children with afebrile illness). The conventional oral dose of acetaminophen is 325-1000 mg (650 mg rectally) total daily doses should not exceed 4000 mg (2000 mg/day for... 

A 17-year-old patient complains that he gets severe shortness of breath whenever he takes aspirin for headache. Increased levels of which of the following may be responsible, in part, for some cases of aspirin hypersensitivity ... 

It is thought that the leukotrienes may be produced in increased amounts when cyclooxygenase is blocked in patients with aspirin hypersensitivity, this might precipitate the bronchoconstric-tion often observed in this condition. The answer is (D). 

Bavbek S, Dursun AB, Dursun E, Eryilmaz A, MisirUgil Z. Safety of meloxicam in aspirin-hypersensitive patients with asdraia and/or nasal polyps. IntArch Allergy Immunol (2007) 142, 64-9. 

Juhlin L, Michaelsson G, Zetterstrom O (1972) Urticaria and asthma induced by food - and drug - additives in patients with aspirin hypersensitivity. J Allergy Clin Immunol 50 92-98... 

Gwin E, Kerby GR, Ruth WE (1977) Cromolyn sodium in the treatment of asthma associated with aspirin hypersensitivity and nasal polyps. Chest 72 148-154 Harnett JC, Spector SL, Farr RS (1978) Aspirin idiosyncrasy. In Middleton E Jr, Reed CE, Ellis EF (eds) Allergy. Principles and practice. Mosby, St. Louis, pp 1002-1022 Hennemann HH, Schief A (1975) Rezidive von Agranulozytose. Dtsch Med Wochenschr 100 519-522... 

---