Aspirin-induced asthma

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Samter's triad
Classification and external resources
Regular strength enteric coated aspirin tablets.jpg
Aspirin in tablets
ICD-10 J45.1, J45.8
ICD-9 493.1
OMIM 208550
MeSH D055963

Samter's triad is a medical condition consisting of asthma, aspirin and NSAID sensitivity, and nasal/ethmoidal polyposis.[1] It usually begins in young adulthood[2] (twenties and thirties are the most common onset times)[3] and may not include any other allergies.

Signs and symptoms[edit]

Most commonly the first symptom is rhinitis (inflammation or irritation of the nasal mucosa), which can manifest as sneezing, runny nose, or congestion. The disorder typically progresses to asthma, then nasal polyposis, with aspirin sensitivity coming last. The reactions to aspirin vary in severity, ranging from mild nasal congestion and eye watering to lower respiratory symptoms including wheezing, coughing, an asthma attack, anaphylaxis, and urticaria in some cases. In addition to aspirin, patients usually also react to other NSAIDs such as ibuprofen, and to any medication that inhibits the cyclooxygenase-1 (COX-1) enzyme, although paracetamol (acetaminophen) in low doses[4] is generally considered safe.

Anosmia (lack of smell) is also common, as inflammation within the nose and sinuses likely reaches the olfactory receptors.

In addition to aspirin and NSAIDs, consumption of even small amounts of alcohol also produces uncomfortable respiratory reactions in many patients.[5]

Cause[edit]

The disorder is caused by an anomaly in the arachidonic acid cascade which leads to 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, production of thromboxane and some prostaglandins is decreased, and in patients with aspirin-induced asthma this results in the overproduction of leukotrienes and produces the severe asthma and allergy-like effects.[6] The underlying cause of the disorder is not fully understood, but there have been several important findings:

  • Abnormally low levels of prostaglandin E2 (PGE2), which is protective for the lungs, has been found in patients with aspirin-induced asthma and may worsen their lung inflammation.[7]
  • Overexpression of both the cysteinyl leukotriene receptor 1[8] and the leukotriene C4 synthase[9] enzyme has been shown in respiratory tissue from patients with aspirin-induced asthma, which likely relates to the increased response to leukotrienes and increased production of leukotrienes seen in the disorder.
  • The attachment of platelets to certain leukocytes in the blood of patients with aspirin-sensitive asthma has also been shown to contribute to the overproduction of leukotrienes.[10]
  • There may be a relationship between aspirin-induced asthma and TBX21, PTGER2, and LTC4S.[11]

Treatment[edit]

Medication[edit]

The preferred treatment for many patients 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,[12] the Massachusetts General Hospital in Boston, MA,[13] the Brigham and Women's Hospital in Boston, MA,[14] National Jewish Hospital in Denver [15] 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 and while on daily aspirin they often have reduced need for supporting medications, fewer asthma and sinusitis symptoms than previously, and many have an improved sense of smell. Desensitization to aspirin reduces the chance of nasal polyp recurrence, and can slow the regrowth of nasal polyps. Even patients desensitized to aspirin may continue to need other medications including nasal steroids, inhaled steroids, and leukotriene antagonists.

Leukotriene antagonists and inhibitors (montelukast, zafirlukast, and zileuton) are often helpful in treating the symptoms of aspirin-induced asthma. Some patients require oral steroids to alleviate asthma and congestion, and most patients will have recurring or chronic sinusitis due to the nasal inflammation.

Surgery[edit]

Often surgery is required to remove nasal polyps,[16] although they typically recur, particularly if aspirin desensitization is not undertaken.

Diet[edit]

A diet low in omega-6 oils (precursors of arachidonic acid), and high in omega-3 oils, may also help.[citation needed]

Some people have reported relief of symptoms by following a low-salicylate diet such as the Feingold diet. However, there is little evidence that a low-salicylate diet is beneficial for patients with AERD,[17] and current clinical trials are underway to determine whether or not the difficult dietary changes truly provide worthwhile therapeutic improvement for these patients.[18]

Alternate and related names[edit]

Samter's triad goes by several other names:

  • Acetylsalicylic acid triad [19]
  • Widal's triad
  • Francis' triad
  • Aspirin triad
  • Aspirin-exacerbated respiratory disease (AERD).[20]
  • Aspirin-induced asthma and rhinitis (AIAR)[21]

A sufferer who has not yet experienced asthma or aspirin sensitivity might be diagnosed as having:

History[edit]

It is named for Max Samter.[22]

Initial reports on the link between asthma, aspirin and nasal polyposis were made by Widal in 1922.[23] Further studies were done by Samter & Beers in reports published in 1968.[24]

See also[edit]

References[edit]

  1. ^ Kim JE, Kountakis SE (July 2007). "The prevalence of Samter's triad in patients undergoing functional endoscopic sinus surgery". Ear Nose Throat J 86 (7): 396–9. PMID 17702319. 
  2. ^ "Current Management of Nasal Polyposis". Retrieved 2008-11-02. [dead link]
  3. ^ Welch, Kevin C. "Aspirin Desensitization". American Rhinologic Society. 
  4. ^ Settipane RA, Schrank PJ, Simon RA, Mathison DA, Christiansen SC, Stevenson DD (October 1995). "Prevalence of cross-sensitivity with acetaminophen in aspirin-sensitive asthmatic subjects". J. Allergy Clin. Immunol. 96 (4): 480–5. doi:10.1016/S0091-6749(95)70290-3. PMID 7560658. 
  5. ^ Cardet JC, White AA, Barrett NA, et al. (2014). "Alcohol-induced respiratory symptoms are common in patients with aspirin exacerbated respiratory disease". J Allergy Clin Immunol Pract 2 (2): 208–13. doi:10.1016/j.jaip.2013.12.003. PMID 24607050. 
  6. ^ Narayanankutty A, Reséndiz-Hernández JM, Falfán-Valencia R, Teran LM (May 2013). "Biochemical pathogenesis of aspirin exacerbated respiratory disease (AERD)". Clin. Biochem. 46 (7-8): 566–78. doi:10.1016/j.clinbiochem.2012.12.005. PMID 23246457. 
  7. ^ Picado C (2002). "Aspirin-intolerant asthma: role of cyclo-oxygenase enzymes". Allergy 57 (Suppl 72): 58–60. doi:10.1034/j.1398-9995.57.s72.14.x. PMID 12144557. 
  8. ^ Sousa AR, Parikh A, Scadding G, Corrigan CJ, Lee TH (November 2002). "Leukotriene-receptor expression on nasal mucosal inflammatory cells in aspirin-sensitive rhinosinusitis". N. Engl. J. Med. 347 (19): 1493–9. doi:10.1056/NEJMoa013508. PMID 12421891. 
  9. ^ Cowburn AS, Sladek K, Soja J, et al. (February 1998). "Overexpression of leukotriene C4 synthase in bronchial biopsies from patients with aspirin-intolerant asthma". J. Clin. Invest. 101 (4): 834–46. doi:10.1172/JCI620. PMC 508632. PMID 9466979. 
  10. ^ Laidlaw TM, Kidder MS, Bhattacharyya N, et al. (April 2012). "Cysteinyl leukotriene overproduction in aspirin-exacerbated respiratory disease is driven by platelet-adherent leukocytes". Blood 119 (16): 3790–8. doi:10.1182/blood-2011-10-384826. PMC 3335383. PMID 22262771. 
  11. ^ Online 'Mendelian Inheritance in Man' (OMIM) Asthma, Nasal Polyps, and Aspirin Intolerance -208550
  12. ^ "Frequently Asked Questions About Aspirin-Exacerbated Respiratory Disease (AERD) Treatment". Specialized Services: Aspirin Desensitization. Scripps Health. 
  13. ^ http://www.massgeneral.org/allergy/
  14. ^ "Aspirin Exacerbated Respiratory Disease/Samter’s Triad". Brigham and Women’s Hospital. 2012. 
  15. ^ "Aspirin Desensitization". 2013. National Jewish Health. Accessed 2013-10-15.
  16. ^ 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. 
  17. ^ "Salicylate-free diet in aspirin-exacerbated respiratory tract disease". American Academy of Allergy, Asthma & Immunology. 
  18. ^ ClinicalTrials.gov NCT01540032 Low Salicylate Diet in Aspirin Exacerbated Respiratory Disease
  19. ^ Amar YG, Frenkiel S, Sobol SE (February 2000). "Outcome analysis of endoscopic sinus surgery for chronic sinusitis in patients having Samter's triad". J Otolaryngol 29 (1): 7–12. PMID 10709165. 
  20. ^ 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. 
  21. ^ 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. 
  22. ^ Samter's syndrome at Who Named It?
  23. ^ Widal MF (1922). "Anaphylaxie et idiosyncraise". Press Med (in French) 119: 48–51. 
  24. ^ Samter M, Beers RF (1968). "Intolerance to aspirin. Clinical studies and consideration of its pathogenesis". Ann. Intern. Med. 68 (5): 975–83. doi:10.7326/0003-4819-68-5-975. PMID 5646829.