Definitions

widal's

Samter's triad

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, aspirin induced asthma and rhinitis (AIAR) and according to the current allergy literature, aspirin-exacerbated respiratory disease (AERD).

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 paracetamol is generally considered safe.

Anosmia (lack of smell) is also typical, as the inflammation reaches the olfactory receptors in the nose.

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. 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.

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:

History

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

See also

References

  • Berges-Gimeno MP, Simon RA, Stevenson DD (2003). "Long-term treatment with aspirin desensitization in asthmatic patients with aspirin-exacerbated respiratory disease". J. Allergy Clin. Immunol. 111 (1): 180–6.
  • Berges-Gimeno MP, Simon RA, Stevenson DD (2002). "The natural history and clinical characteristics of aspirin-exacerbated respiratory disease". Ann. Allergy Asthma Immunol. 89 (5): 474–8.
  • Berges-Gimeno MP, Simon RA, Stevenson DD (2002). "The effect of leukotriene-modifier drugs on aspirin-induced asthma and rhinitis reactions". Clin. Exp. Allergy 32 (10): 1491–6.
  • Kim JE, Kountakis SE (2007). "The prevalence of Samter's triad in patients undergoing functional endoscopic sinus surgery". Ear Nose Throat J 86 (7): 396–9.
  • Kong JS, Teuber SS, Gershwin ME (2007). "Aspirin and nonsteroidal anti-inflammatory drug hypersensitivity". Clin Rev Allergy Immunol 32 (1): 97–110.
  • Mascia K, Haselkorn T, Deniz YM, Miller DP, Bleecker ER, Borish L (2005). "Aspirin sensitivity and severity of asthma: evidence for irreversible airway obstruction in patients with severe or difficult-to-treat asthma". J. Allergy Clin. Immunol. 116 (5): 970–5.
  • Parikh A, Scadding GK, Gray P, Belvisi MG, Mitchell JA (2002). "High levels of nitric oxide synthase activity are associated with nasal polyp tissue from aspirin-sensitive asthmatics". Acta Otolaryngol. 122 (3): 302–5.
  • Stevenson DD (2003). "Aspirin desensitization in patients with AERD". Clin Rev Allergy Immunol 24 (2): 159–68.
  • Stevenson DD, Zuraw BL (2003). "Pathogenesis of aspirin-exacerbated respiratory disease". Clin Rev Allergy Immunol 24 (2): 169–88.
  • Picado C (2002). "Aspirin intolerance and nasal polyposis". Curr Allergy Asthma Rep 2 (6): 488–93.

Wallace DV, Dykewicz MS, Bernstein DI et al. The diagnosis and management of rhinitis: an updated practice parameter. J Allergy Clin Immunol. 2008;122(2):S1-S84.

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