Aspirin and Asthma

K. Suresh Babu, MD, DNB; and Sundeep S. Salvi, MD, DNB, PhD, From the Department of Respiratory Cell and Molecular Biology, University of Southampton, Southampton General Hospital, Southampton, UK.

Disclosures

CHEST. 2000;118(5) 

In This Article

Management and Prevention

In most cases, the clear history should enable the physician to make a diagnosis. Most patients have moderate or severe persistent asthma. In doubtful cases, carefully controlled challenge testing with aspirin or other NSAIDs is justified, however, these tests should be performed in hospitals with full facilities for resuscitation. Lysine aspirin by inhalation could be used for challenge testing, although it is of value in the diagnosis of analgesic sensitivity rather than in assessing sensitivity to specific NSAIDs. Nasal provocation tests with lysine aspirin have been found to be safe, simple, and specific in the diagnosis of AIA. [30] There are a few practical aspects regarding aspirin sensitivity. If asthmatic patients have healthy sinuses on radiographs and/or CT scans, then the likelihood of having AIA is low. Patients with clear evidence of IgE-mediated upper and lower airway diseases have a low incidence of AIA. This could serve as predictive information in the probable risk of AIA. The general rules concerning the treatment of AIA do not differ from the published guidelines of asthma management.

In the long term, patients should be advised to avoid aspirin and products containing aspirin. NSAIDs that cross-react with aspirin also should be avoided ( Table 1 ). Patients can usually take acetaminophen for mild analgesia, but occasional cross-reactions have been observed. [31] Patients with AIA can also safely take sodium salicylate, salicylamide, choline magnesium trisalicylate, benzydamine, chloroquine, azapropazone, and dextropropoxiphene. These drugs are either devoid of anti-COX activity or are weak COX-2 inhibitors. Nimesulide and meloxicam, which are predominantly COX-2 inhibitors, induced mild bronchial obstruction but only at high doses.[32,33]

It has been observed that patients with AIA sporadically cross-react with hydrocortisone hemisuccinate, thereby provoking bronchoconstriction. [34] This cross-reactivity has been attributed to the succinate molecule rather than to cross-sensitivity by the fact that hydrocortisone succinate continued to induce respiratory symptoms in ASA-desensitized patients. [35]

Anti-LT drugs are being used currently in the treatment of patients with AIA. [36] There are two classes of anti-LT drugs, the 5-LO inhibitors (ie, zileuton) and the specific cysteinyl LT receptor antagonists (ie, zafirlukast, montelukast, and pranlukast). LT-modifying drugs have been found to attenuate the aspirin-induced bronchial reactions in AIA patients.6,37 However, a recent study has reported that a higher therapeutic dose of aspirin overcame the protection from pretreatment with zileuton. [38] Anti-LTs also induce bronchodilation in patients with AIA. A Swedish-Polish study [39] found that zileuton provided short-term and long-term improvement in pulmonary function measurements compared to baseline in patients with AIA. Monte-lukast also has been found to be effective in patients with AIA. [40] A few instances of Churg-Strauss syndrome (CSS) have been reported in patients on anti-LT drug. [41] The exact mechanism of the development of CSS in patients receiving anti-LTs remains unclear. One possibility involves the unmasking of previously unrecognized CSS with the tapering of steroids used for the treatment of moderate to moderately severe asthma. [41] The other possibility that the drug reaction is a hypersensitivity reaction to anti-LTs, with individuals having an unusual eosinophil-based response to LT receptor blockade, should also be considered. [42]

Salmeterol, a long-acting b 2-agonist also has been found to be effective in the management of AIA and also has attenuated the bronchial hyperresponsiveness to lysine-ASA. [43]

There is now good evidence to implicate the LT pathway in the pathogenesis of AIA. The inhibition of COX-1 and COX-2 by aspirin results in the diversion of the arachidonic acid products toward the LO pathway, thereby paving the way for the role of LT-modifying drugs in the management of AIA. It remains to be seen whether selective COX-2 inhibitors, which theoretically should not cross-react with aspirin because of the preservation of PGE2, will provide an alternative in patients with AIA.

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