Cutaneous Reactions to Aspirin and Nonsteroidal Antiinflammatory Drugs

Abstract

Soon after the introduction of aspirin for the treatment of pain, fever, and inflammation more than a century ago, clinicians were challenged by the frequent observation of ASAtriggered allergic and pseudoallergic reactions occurring in the skin. This problem was further enhanced by the development of a number of other analgesic and antiinflammatory drugs that, having different chemical structures, cross-reacted with acetilsalycilic acid in many patients. This paper reviews the information presently available for the management of individuals who develop urticaria and angioedema when exposed to drugs that inhibit cyclooxygenase isoenzymes. The immune and nonimmunologic mechanisms leading to the pathogenesis of such reactions, their prevalence in selected groups of the population, clinical picture, and useful diagnostic approaches are described, and current guidelines used in our institutions for the clinical orientation of the patients, taking advantage of the recent introduction of various new and more selective NSAIDS that inhibit preferentially the COX-2 enzyme, are proposed.

Aspirin desensitisation for Chinese patients with coronary artery disease

“…[1][2][3] Cutaneous reactions to NSAIDs occur in 0.1 to 3% of patients consuming these drugs. 4 Specific cyclo-oxygenase (COX)-2 inhibitors or other classes of drugs, such as paracetamol, can be used as alternative pain killers. 5,6 However, in the subgroup of patients with coronary artery disease (CAD), the use of aspirin as secondary prophylaxis appears more compelling.…”

Hypersensitivitet ved bruk av ikke-steroide antiinflammatoriske legemidler

“…Meloksikam og nimesulid hemmer COX-2 i større grad enn COX-1 (fortrinnsvise COX-2-hemmere) (7). Koksiber (selektive COX-2-hemmere) utgjør en nyere gruppe NSAID-preparater som ikke hemmer COX-1 i terapeutiske doser (5,6). Paracetamol er en svak cyklooksygenasehemmer, men klassifiseres ikke som et NSAIDpreparat på grunn av manglende antiinflammatorisk effekt (6,8).…”

“…Dette medfører økt danning av cysteinylleukotriener som er potente mediatorer av inflammasjon, bronkospasme og ødem (5). Overproduksjon av cysteinylleukotriener er i kliniske studier bekreftet ved bruk av ulike laboratorieundersøkelser (4).…”

Approach to “Aspirin Allergy” in Cardiovascular Patients

“…13 Additionally, NSAIDs exacerbate urticaria in one third to two thirds of patients with chronic idiopathic urticaria. 14 The postulated mechanism for cutaneous reactions, just as for the respiratory reactions, is the increased production of leukotrienes resulting from COX-1 inhibition. 14 One support of this "cyclooxygenase theory" is the demonstration that pretreatment with leukotriene-receptor antagonists can block NSAID-induced urticaria and angioedema reactions.…”

“…14 One support of this "cyclooxygenase theory" is the demonstration that pretreatment with leukotriene-receptor antagonists can block NSAID-induced urticaria and angioedema reactions. 14 In addition to NSAIDs class-related urticaria and angioedema, Stevenson et al 15 describe single-drug anaphylaxis and blended reactions. In single-drug anaphylaxis, after the initial drug exposure and sensitization, subsequent drug exposure leads to cutaneous reactions plus respiratory symptoms.…”