Samter's triad
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Samter's triad is a medical condition consisting of asthma, aspirin sensitivity, and nasal/ethmoidal polyposis. It occurs in mid-life (twenties and thirties are the most common onset times) and may not include any allergies. It is also known as aspirin-sensitive asthma, aspirin triad, Widal's triad, and aspirin induced asthma and rhinitis (AIAR).
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[edit] Signs and symptoms
Most commonly, the first symptom is rhinitis (inflammation of the nose), which might be described as sneezing, a runny nose, or congestion. The disorder typically progresses to asthma, then polyposis, with aspirin sensitivity coming last. The aspirin reaction can be severe, including an asthma attack, anaphylaxis, and urticaria in some cases. Patients typically react to other NSAIDS such as ibuprofen, although Tylenol (acetaminophen or paracetamol) is generally considered safe.
Anosmia (lack of smell) is also typical, as the inflammation reaches the olfactory receptors in the nose.
[edit] Treatment
The preferred treatment now is desensitization to aspirin, undertaken at a clinic specilizing in such treatment. Patients who are desensitized then take a maintenance dose of aspirin daily; they have reduced need for supporting medications and fewer asthma and sinusitis symptoms than previously; many have an improved sense of smell. Treatment formerly focused on relieving the symptoms. Even desensitized people may continue to use nasal steroids, inhaled steroids, and leukotriene antagonists. Occasionally surgery may be required to remove polyps, although they typically recur, particularly if desensitization is not undertaken. Some patients require oral steroids to alleviate asthma and congestion, and most patients will have recurring or chronic sinusitis due to the nasal inflammation. Desensitization reduces the chance of recurrence.
The cause of Samter's triad is unknown, but it is widely believed that the disorder is caused by an anomaly in the arachidonic acid cascade, which causes undue production of leukotrienes, a series of chemicals involved in the body's inflammatory response. When prostaglandin production is blocked by NSAIDS like aspirin, the cascade shunts entirely to leukotrienes, producing the severe allergy-like effects.
Leukotriene antagonists and inhibitors (montelukast, zafirlukast, and zileuton) are helpful in treating Samter's. A diet low in omega-6 oils (precursors of arachidonic acid), and high in omega-3 oils, may also help.
Some people find relief of symptoms by following a low-salicylate diet such as the Feingold diet. They may need to eliminate the other salicylate-containing foods identified by Swain in 1985 as well.[1] For those who need them, these salicylates are listed in charts in the Feingold Handbook based on level of salicylate measured in the item. Unfortunately, any such list is only a rough guideline since amounts will vary depending on fruit/vegetable variety and where grown; in fact, organic foods have been shown to contain more salicylate than conventional produce because the plant is more likely to be under attack from pests, and salicylate is produced by the plant as protection.[2]
[edit] Alternate names
Samter's triad goes by several other names:
- AERD (aspirin-exacerbated respiratory disease)
- AIAR (aspirin-induced asthma and rhinitis)
- Widal's triad
- Francis' triad
- Aspirin triad
- Aspirin allergy (a misnomer)
- Aspirin intolerance
A sufferer who has not yet experienced asthma or aspirin sensitivity might be diagnosed as having:
- Non-allergic rhinitis
- Non-allergic rhinitis with eosinophilia syndrome (NARES)
[edit] History
Initial reports on the link between asthma, aspirin and nasal polyposis were made by Widal in 1922.[3] Further studies were done by Samter & Beers in reports published in 1968.[4]
[edit] See also
[edit] References
- ^ Swain AR, Dutton SP, Truswell AS (1985). "Salicylates in foods..". Journal of the American Dietetic Association. Aug;85(8): 950-60.. PMID 4019987.
- ^ Baxter GJ, Graham AB, Lawrence JR, Wiles D, Paterson JR. (2001). "Salicylic acid in soups prepared from organically and non-organically grown vegetables.". European Journal of Nutrition. Dec;40(6): 289-92.. PMID 11876493.
- ^ Widal MF (1922). "Anaphylaxie et idiosyncraise". Press Med 119: 48-51.
- ^ Samter M, Beers RF (1968). "Intolerance to aspirin. Clinical studies and consideration of its pathogenesis". Ann. Intern. Med. 68 (5): 975–83. PMID 5646829.
Berges-Gimeno MP, Simon RA, Stevenson DD J Allergy Long-term treatment with aspirin desensitization in asthmatic patients with aspirin-exacerbated respiratory disease.Clin Immunol. 2003 Jan;111(1):180-6
Berges-Gimeno MP, Simon RA, Stevenson DD.The natural history and clinical characteristics of aspirin-exacerbated respiratory disease.Ann Allergy Asthma Immunol. 2002 Nov;89(5):474-8.
Berges-Gimeno MP, Simon RA, Stevenson DD.The effect of leukotriene-modifier drugs on aspirin-induced asthma and rhinitis reactions. Clin Exp Allergy. 2002 Oct;32(10):1491-6.
Kim JE, Kountakis SE.The prevalence of Samter's triad in patients undergoing functional endoscopic sinus surgery.Ear Nose Throat J. 2007 Jul;86(7):396-9
Kong JS, Teuber SS, Gershwin ME.Aspirin and nonsteroidal anti-inflammatory drug hypersensitivity. Clin Rev Allergy Immunol. 2007 Feb;32(1):97-110. Review.
Mascia K, Haselkorn T, Deniz YM, Miller DP, Bleecker ER, Borish L; TENOR Study Group. Aspirin sensitivity and severity of asthma: evidence for irreversible airway obstruction in patients with severe or difficult-to-treat asthma.J Allergy Clin Immunol. 2005 Nov;116(5):970-5. Epub 2005 Oct 3.
Parikh A, Scadding GK, Gray P, Belvisi MG, Mitchell JA.High levels of nitric oxide synthase activity are associated with nasal polyp tissue from aspirin-sensitive asthmatics. Acta Otolaryngol. 2002 Apr;122(3):302-5
Stevenson, DD Aspirin desensitization in patients with AERD. Clin Rev Allergy Immunol. 2003 Apr;24(2):159-68. Review
Stevenson DD, Zuraw BL.Pathogenesis of aspirin-exacerbated respiratory disease. Clin Rev Allergy Immunol. 2003 Apr;24(2):169-88. Review.
- Picado C (2002). "Aspirin intolerance and nasal polyposis". Curr Allergy Asthma Rep 2 (6): 488–93. doi: . PMID 12428645.