What is AERD/Samter’s Triad?

Aspirin tablet, 94084869Aspirin Exacerbated Respiratory Disease (AERD), also known as Samter’s Triad or Aspirin Sensitive Asthma, is a chronic medical condition that consists of asthma, recurrent sinus disease with nasal polyps, and a sensitivity to aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs). Approximately 10% of all adults with asthma and 40% of patients with asthma and nasal polyps are sensitive to aspirin and NSAIDs.

What are the symptoms?

Patients with AERD/Samter’s Triad usually have asthma, nasal congestion, and nasal polyps, and often do not respond to conventional treatments. Many have experienced chronic sinus infections and can lose their sense of smell. The characteristic feature of AERD/Samter’s Triad is that patients develop reactions triggered by aspirin or other NSAIDs.

These reactions can include:

  • Increased nasal congestion or stuffiness
  • Eye watering or redness
  • Cough, wheezing, or chest tightness
  • Frontal headache or sensation of sinus pain
  • Flushing and/or a rash
  • Nausea and/or abdominal cramping
  • General feeling of malaise, sometimes accompanied by dizziness

Latest News & Information
16 Dec 15

Zyflo CR (controlled-release zileuton)

Zyflo details

Zyflo CR is an asthma medication that inhibits the production of leukotrienes, inflammatory molecules that contribute to airway inflammation in patients with AERD. Zyflo CR is typically prescribed as two 600 mg pills that are taken twice a day; liver enzymes need to be checked periodically. If you are uninsured or your insurance does not cover the full cost of Zyflo CR, the new manufacturer will cover up to $2500 a month in out-of-pocket expenses. Recent backorder issues that patients may have experienced are now resolved. Please see the above link for more information.

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21 Sep 15

Patients with AERD who develop a skin rash and gastrointestinal symptoms with aspirin desensitization produce large amounts of prostaglandin D2.

Prostaglandin D2: A dominant mediator of aspirin-exacerbated respiratory disease.

The AERD Center at Brigham and Women’s Hospital in Boston, MA collected clinical characteristics and biologic specimens from 29 patients with AERD undergoing an aspirin desensitization procedure. In addition to the classical respiratory symptoms triggered by aspirin challenge in AERD, 6 of these 29 patients developed a red, flat, itchy rash that started on their hands and feet during aspirin exposure. 5 of the 6 also reported gastrointestinal symptoms including nausea, abdominal pain, vomiting or diarrhea. These patients were harder to desensitize and 5 of 6 failed to go on to tolerate high-dose aspirin. The presence of rash and gastrointestinal symptoms was associated not only with a rise in leukotrienes but also a dramatic increase in PGD2 when compared with the 23 patients with AERD who developed only the classical respiratory symptoms. Patients with AERD who did go on to be treated with high-dose aspirin therapy demonstrated a significant fall in PGD2 levels. These findings provide novel insight into the role PGD2 has in symptom generation during aspirin-induced reactions. Additionally, they offer a clue about the mechanism by which aspirin therapy provides clinical benefit in AERD. This study provides the foundation for the use of novel therapeutics, currently under development, which target PGD2 in AERD.

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