Subject aspirin sensitivity

Aspirin-sensitive subjects may have attacks induced by other NSAIDs (82). 

Settipane RA, Stevenson DD. Cross sensitivity with acetaminophen in aspirin-sensitive subjects with asthma. J Allergy Clin Immunol 1989 84(l) 26-33. 

From the first study in patients with local IgE against SEs [10] it appeared that the highest IgE concentrations were obtained from samples of aspirin-sensitive subjects. We therefore extended our observations in a nonallergic, but severely inflamed subgroup of patients, who also suffered from asthma. Subjects with nasal polyposis from Poland were classified as aspirin-sensitive (ASNP) or aspirin-tolerant (ATNP) asthmatics, based on a bronchial aspirin challenge test [47], Homogenates prepared from NP tissue were analyzed for concentrations of eosinophilic markers, total IgE and IgE antibodies to enterotoxins (SEA, SEC, TSST-1) [22], and compared to inferior nasal turbinates from healthy subjects. 

Our findings have recently been confirmed by Suh et al. [48], who also studied IgE antibodies to SEs and eosinophilic markers in Korean aspirin-sensitive and aspirin-tolerant asthmatics with NPs. These authors also found an increase in ECP, but not IL-5, between these groups, and significantly increased levels of IgE to SEs in aspirin-sensitive subjects. The authors confirmed the impact of SEs on NP disease in Korea, expanding on our European observations, and discussed a direct impact of SEs on the manifestation of aspirin sensitivity. 

Chiu, J. T., 1983, Improvement in aspirin-sensitive asthmatic subjects after rapid aspirin desensitization and aspirin maintainance (ADAM) treatment, J. Allergy Clin. Immunol. 71 560. 

Proceeding from the observation that aspirin specifically triggers the release of 15-hydroxyeicosatetraenoic acid (15-HETE) (Fig. 9.3 Sect. 3.2.5.2 and Fig. 3.8) from epithelial cells of nasal polyps and peripheral blood leukocytes from patients with aspirin-induced asthma/rhinosinusitis, 15-HETE generation was utilized as a test for the identification of aspirin-sensitive patients. Stimulation in vitro of peripheral blood leukocytes with 200 pM of aspirin resulted in a mean increase of over 400 % in 15-HETE generation but only small to insignificant responses were seen in aspirin-tolerant asthmatic and control subjects. Sensitivity of the test was 83 % and specificity 82 % positive and negative predictive values were 0.79 and 0.86, respectively. The NSAID COX-1 inhibitor naproxen also triggered 15-HETE release but COX-2-selective NSAIDs did not. 

In sensitive subjects, aspirin (and other NS AIDs) is associated with the so-called aspirin triad or aspirin-induced asthma (AIA also called aspirin-exacerbated respiratory disease). Classic AIA consists of chronic asthma and rhinosinus-itis together with nasal polyps. The incidence of AIA in adult asthmatics is about 3-5 %. 

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). 

---