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Aspirin in tablets
Samter's triad is a medical condition consisting of asthma, aspirin sensitivity, and nasal/ethmoidal polyposis. It occurs in middle age (twenties and thirties are the most common onset times) and may not include any allergies.
Signs and symptoms 
Most commonly, the first symptom is rhinitis (inflammation or irritation of the nasal mucosa), which can manifest with symptoms of sneezing, runny nose, or congestion. The disorder typically progresses to asthma, then nasal polyposis, with aspirin sensitivity coming last. The reactions to aspirin vary, but can be severe, ranging from mild nasal congestion and eye watering to lower respiratory symptoms including wheezing, coughing, an asthma attack, anaphylaxis, and urticaria in some cases. Patients typically react to other NSAIDs such as ibuprofen, and any medication that inhibits the COX-1 enzyme, although paracetamol (acetaminophen) in low doses is generally considered safe.
Anosmia (lack of smell) is also common, as the inflammation reaches the olfactory receptors in the nose.
The disorder is caused by an anomaly in the arachidonic acid cascade, which causes increased production of cysteinyl leukotrienes, a series of chemicals involved in the body's inflammatory response. When medications like NSAIDs or aspirin block the COX-1 enzyme, prostaglandin and thromboxane production is decreased, which causes the overproduction of leukotrienes and produces the severe asthma and allergy-like effects. Arachidonic acid can be metabolized through four major pathways namely cyclooxygenases (COX-1, COX-2), lipoxygenases (5-LOX, 15-LOX, and 12-LOX) cytochrome oxidases (hydrolase, epoxygenase) or non-enzymatic pathway. Reduced PGE2 production compared to aspirin tolerant asthmatics along with reduced baseline EP2 receptor expression and elevated PGD2(TH2/eosinophil chemoattractant) production in aspirin sensitive asthma cripples the COX pathway. This relive the inhibitory effects of PGE2 on cysteinyl leukotrienes shunting towards 5-LOX pathway. over expression of cysteinyl leukotriene receptor 1 and reduced production of cysteinyl leukotriene antagonists called lipoxins also contributes to the disease. Although the underlying cause is not fully understood, the attachment of platelets to certain leukocytes in the blood may contribute to the overproduction of leukotrienes.
In addition to aspirin, other vaso-dilators may induce the same reaction, such as alcohol.
The preferred treatment now is desensitization to aspirin, undertaken at a clinic or hospital specializing in such treatment. In the United States, the Scripps Clinic in San Diego, CA, the Massachusetts General Hospital in Boston, MA, the Brigham and Women's Hospital in Boston, MA, National Jewish Hospital in Denver  and Stanford University Adult ENT Clinic have allergists who routinely perform aspirin desensitization procedures for patients with aspirin-induced asthma. 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.
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 to aspirin reduces the chance of recurrence, and can slow the regrowth of the nasal polyps.
Occasionally surgery may be required to remove polyps, although they typically recur, particularly if desensitization is not undertaken.
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. 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. However, there is little evidence that a low-salicylate diet is beneficial for patients with AERD, and current clinical trials are underway to determine whether or not the difficult dietary changes truly provide worthwhile therapeutic improvement for these patients.
Samter's triad goes by several other names:
- Acetylsalicylic acid triad 
- Widal's triad
- Francis' triad
- Aspirin triad
A sufferer who has not yet experienced asthma or aspirin sensitivity might be diagnosed as having:
See also 
- Kim JE, Kountakis SE (July 2007). "The prevalence of Samter's triad in patients undergoing functional endoscopic sinus surgery". Ear, nose, & throat journal 86 (7): 396–9. PMID 17702319.
- "Current Management of Nasal Polyposis". Retrieved 2008-11-02.[dead link]
- Kevin C. Welch, M.D. "Aspirin Desensitization". American Rhinologic Society.
- Settipane RA, Schrank PJ, Simon RA, Mathison DA, Christiansen SC, Stevenson DD. Prevalence of cross-sensitivity with acetaminophen in aspirin-sensitive asthmatic subjects. Journal of Allergy and Clinical Immunology. 1995 Oct;96(4):480-5.
- Arun Narayanankutty, Juan Manuel Reséndiz-Hernández, Ramcés Falfán-Valencia, Luis M. Terán. Biochemical pathogenesis of aspirin exacerbated respiratory disease (AERD). Clinical Biochemistry. available online on 2012 Dec 13. http://dx.doi.org/10.1016/j.clinbiochem.2012.12.005. PMID 23246457.
- Laidlaw TM, Kidder MS, Bhattacharyya N, Xing W, Shen S, Milne GL, Castells MC, Chhay H, Boyce JA. Cysteinyl leukotriene overproduction in aspirin exacerbated respiratory disease is driven by platelet-adherent leukocytes. Blood. 2012 Jan 18.
- Online 'Mendelian Inheritance in Man' (OMIM) 208550
- McMains KC, Kountakis SE (2006). "Medical and surgical considerations in patients with Samter's triad". American journal of rhinology 20 (6): 573–6. doi:10.2500/ajr.2006.20.2913. PMID 17181095.
- Swain AR, Dutton SP, Truswell AS (August 1985). "Salicylates in foods". J Am Diet Assoc 85 (8): 950–60. PMID 4019987.
- Baxter GJ, Graham AB, Lawrence JR, Wiles D, Paterson JR (December 2001). "Salicylic acid in soups prepared from organically and non-organically grown vegetables". Eur J Nutr 40 (6): 289–92. doi:10.1007/s394-001-8358-x. PMID 11876493.
- Amar YG, Frenkiel S, Sobol SE (February 2000). "Outcome analysis of endoscopic sinus surgery for chronic sinusitis in patients having Samter's triad". The Journal of otolaryngology 29 (1): 7–12. PMID 10709165.
- Williams AN, Woessner KM (May 2008). "The clinical effectiveness of aspirin desensitization in chronic rhinosinusitis". Current allergy and asthma reports 8 (3): 245–52. doi:10.1007/s11882-008-0041-7. PMID 18589844.
- Bochenek G, Bánska K, Szabó Z, Nizankowska E, Szczeklik A (March 2002). "Diagnosis, prevention and treatment of aspirin-induced asthma and rhinitis". Current drug targets. Inflammation and allergy 1 (1): 1–11. doi:10.2174/1568010023345011. PMID 14561202.
- synd/2240 at Who Named It?
- Widal MF (1922). "Anaphylaxie et idiosyncraise". Press Med (in French) 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.