Sensitivity to nonsteroidal anti-inflammatory drugs.
BACKGROUND
Aspirin can provoke reactions ranging from respiratory to cutaneous in susceptible individuals. There has been particular attention looking at the role of cyclo-oxygenase enzymes 1 and 2 and their role in aspirin-exacerbated respiratory disease.


OBJECTIVE
Patients who present with a spectrum of allergic and pseudoallergic reactions to aspirin pose a special challenge for the physician. This article discusses proposed classification system, clinical manifestations, pathogenesis of disease, and current treatment options of aspirin-related disease.


METHODS
Relevant articles in the medical literature were derived from searching the MEDLINE database with key terms aspirin-sensitive asthma, cyclo-oxygenase enzymes 1 and 2. Sources also include review articles, randomized control trials, and standard textbooks of allergy and immunology.


RESULTS
Aspirin-exacerbated respiratory disease remains a complex, heterogenous disease with varied clinical presentations. There have been many advances in trying to elucidate the pathogenesis of this disease. The classification system presented will provide greater ease when reading the literature and communicating with one another. Oral aspirin challenge remains the diagnostic test of choice for both respiratory and cutaneous reactions. Aspirin desensitization is an option for those with refractory respiratory disease or who require aspirin for other medical conditions.


CONCLUSIONS
This review discusses the challenges in classification, diagnosis, and treatment of those patients with a sensitivity to aspirin. Special attention is made to the possible mechanisms mediating disease progression and how specific therapies, such as leukotriene modifiers, may be helpful.
Namazy
Jennifer Altamura
JA
Division of Allergy, Asthma and Immunology, Scripps Clinic, La Jolla, California 92037, USA. janamazy@yahoo.com
Simon
Ronald A
RA
D000082:Acetaminophen / Q000009:adverse effects; D000328:Adult; D000707:Anaphylaxis / Q000139:chemically induced; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects* / Q000276:immunology; D001241:Aspirin / Q000009:adverse effects* / Q000276:immunology; D001249:Asthma / Q000139:chemically induced; D001760:Bleeding Time; D002648:Child; D002986:Clinical Trials as Topic; D003429:Cross Reactions; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors / Q000009:adverse effects* / Q000276:immunology; D003888:Desensitization, Immunologic; D004342:Drug Hypersensitivity / Q000145:classification / Q000175:diagnosis / Q000453:epidemiology / Q000209:etiology* / Q000628:therapy; D005260:Female; D006801:Humans; D007073:Immunoglobulin E / Q000276:immunology; D007527:Isoenzymes / Q000037:antagonists & inhibitors / Q000502:physiology; D020024:Leukotriene Antagonists / Q000627:therapeutic use; D008297:Male; D008565:Membrane Proteins; D009298:Nasal Polyps / Q000139:chemically induced; D015995:Prevalence; D011451:Prostaglandin-Endoperoxide Synthases / Q000502:physiology; D012130:Respiratory Hypersensitivity / Q000139:chemically induced / Q000175:diagnosis / Q000453:epidemiology / Q000276:immunology; D012220:Rhinitis / Q000139:chemically induced; D014581:Urticaria / Q000139:chemically induced
D000894:Anti-Inflammatory Agents, Non-Steroidal; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors; D007527:Isoenzymes; D020024:Leukotriene Antagonists; D008565:Membrane Proteins; D000082:Acetaminophen; D007073:Immunoglobulin E; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; C496511:PTGS1 protein, human; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases; D001241:Aspirin