Aspirin-induced asthma

Samter's triad
Classification and external resources
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 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.

Cause

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.

There may be a relationship between aspirin-induced asthma and TBX21, PTGER2, and LTC4S.

In addition to aspirin, other vaso-dilators may induce the same reaction, such as alcohol.

Treatment

Medication

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.

Leukotriene antagonists and inhibitors (montelukast, zafirlukast, and zileuton) are helpful in treating Samter's.

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.

Surgery

Occasionally surgery may be required to remove polyps, although they typically recur, particularly if desensitization is not undertaken.

Diet

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

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.

Alternate and related names

Samter's triad goes by several other names:

• Acetylsalicylic acid triad
• Widal's triad
• Francis' triad
• Aspirin triad

"AERD" ("aspirin-exacerbated respiratory disease") adds chronic rhinosinusitis to the triad. Similarly, "AIAR" ("aspirin-induced asthma and rhinitis") by definition includes rhinitis.

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)

History

It is named for Max Samter.

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

• Salicylate sensitivity
• Drug intolerance