Aspirin or acetylsalicylic acid (ASA) is still one of the most widely sold drugs in the world and its side effects are well known. Among these, hypersensitivity reactions represent one of the most frequently described since the first report of urticaria and angio-oedema by Hirshberg in 1902.1 The hypersensitivity reactions to aspirin may be divided into two major categories2: type A characterised by respiratory symptoms (bronchial asthma, rhinitis) which account for about 15% of cases, and type B with urticaria and angio-oedema which occur in more than 75% of cases.3 A third category (type C) which includes any other peculiar clinical presentation (such as multiform erythema, fixed exanthema, Stevens-Johnson's syndrome, Lyell's syndrome) occurs in a small number of cases. Females are more affected than males, except in childhood in which the asthmatic type A reactions are rare. A familial (and sometimes a personal) history of allergic disease is reported in about one third of cases.3 An extra-immunological (“pseudo-allergic”) mechanism is involved in the pathogenesis of nearly all aspirin hypersensitivity reactions. The most accepted pathogenetic theory4 5 postulates that the cyclo-oxygenase (COX) block (COX-1 and COX-2) induced by aspirin leads to an increase in arachidonic acid metabolism by an alternative pathway represented by lipoxygenase. This in turn increases the synthesis of leukotrienes C4, D4, and E4 which are able to exert a powerful bronchospastic action.6 7 An increasing number of reports concerning the existence of a relationship between bronchial asthma and the presence of nasal polyposis in the clinical picture of hypersensitivity reactions to aspirin has been accumulating in the literature since the late 1920s. The association of bronchial asthma and nasal polyposis in aspirin intolerant patients was first described by Widal in 19228and confirmed by several …