Sensitivity to aspirin and other nonsteroidal anti-inflammatory drugs

Klinika Gruźlicy, Chorób i Nowotworów Płuc Uniwersytetu Medycznego w Łodzi.
Kierownik Kliniki: prof. dr hab. n. med. Iwona Grzelewska-Rzymowska
Correspondence to: Klinika Gruźlicy, Chorób i Nowotworów Płuc Uniwersytetu Medycznego, ul. Okólna 181, 91-520 Łódź,
tel./faks: 042 617 72 95, e-mail:
Source of financing: Department own sources

Pediatr Med rodz Vol 5 Numer 3, p. 186-193

Clinically, two types of the sensitivity to aspirin (ASA) are distinguished: bronchospastic and urticaria/ angioedema. Bronchospastic type of ASA sensitivity occurs in patients with asthma and it is called ASA- asthma. In these patients the symptoms of ASA- sensitivity are: dyspnoea and extrabronchial symptoms i.e. watery rhinorrhoea, conjunctivitis and lacrimation, flushing of the face, neck and chest. Dramatic oedema of the larynx, fall in blood pressure and even death have been described as well. ASA- induced urticaria/ angioedema is called ASA- urticaria and this type sensitivity concerns mainly patients with chronic or recurrent urticaria and angioedema. ASA- asthma and ASA- urticaria occur in patients of any age, but it especially concerns women between 30 and 50 years of age (70% of examined patients). In some patients with ASA- sensitivity atopy is stated. The typical feature of ASA- asthma are nasal and paranasal polyps, which are recurrent and persistent. They are presented in 80% asthmatics sensitive to ASA. Nasal mucosa of ASA- asthmatics is inflamed with T- lymphocytes, eosinophils, mast cells and macrophages. The majority of proinflammatory cells elicit expression mRNA for IL- 5. Bronchial mucosa is also inflamed with eosinophils, which are the rich source of leukotriene C4, which probably takes part in the pathomechanism of sensitivity to ASA. The clinical course of ASAasthma is usually severe, but using inhaled corticosteroids and long- acting β2-agonist control asthma may be achieved. It was reported, that majority of nonsteroidal anti- inflammatory drugs (NSAID’s) elicited dyspnoea in patients with ASA- asthma and skin eruption in ASA- urticaria patients. The above mentioned symptoms are produced by indomethacin, mefenamic acid, flufenamic acid, ibuprofen, phenylbutazone, naproxen, diflunisal and zomepirac. On the other hand, paracetamol, chloroquine, benzydamine, salicylic acid and dextropropoxyphene are well- tolerated by patients with ASA- asthma. Detection of sensitivity to ASA and other NSAID’s is based mainly on the anamnesis and oral challenge with administration of increasing ASA doses at 24 hours intervals. Sometimes, nasal and inhaling tests with ASA lysine are performed. These test are more safely, but less sensitive. In provocative test only ASA is recommended. In patients with ASA- asthma and ASA- urticaria, ASA desensitization may be induced by administering increasing doses of ASA every 24 hours until a good tolerance of 600 mg is obtained. There is hypothesis, that pathomechanism of the ASA- asthma and ASA- urticaria is related cyclooxygenase inhibition – an enzyme, which is involved in prostaglandins, prostacycline and thromboxane synthesis.

Keywords: mild asthma, inhaled corticosteroids, airway inflammation, remodeling