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Samter's triad

Last reviewed dd mmm yyyy. Last edited dd mmm yyyy

Authoring team

Samter's triad is association of (1,2,3):

  • bronchial asthma
  • nasal polyposis
  • aspirin intolerance

Nasal polyps

  • occur in 36-96% of patients with aspirin intolerance (3)
  • of all patients with nasal polyps - 12.8% have aspirin intolerance (3)

Patients with Samter's triad generally tend to have more severe symptoms of nasal polyposis and asthma, as well as rhinosinusitis, than do patients without the triad (3,4):

  • when their chronic sinusitis fails to respond to aggressive medical management, surgical intervention is indicated and has been found in a number of studies to reduce the severity of the asthma, but their postoperative course is often complicated by a recurrence of nasal polyps (3)

The pathogenesis of Samter's triad is unknown:

  • considered to be due, at least in part, to a disturbance of eicosanoid biosynthesis (3,4)
    • eicosanoids are rapidly synthesized and released products of arachidonic acid (AA) metabolism mainly via the cyclooxygenase (CO) and lipooxygenase (LO) pathway and, to a small extend, via the epoxygenase pathway (EO)
    • conversion of AA to prostaglandin (PGs) and thromboxanes (TXs) involves the CO pathway
    • conversion of AA to leukotriens (LTs) and hydroxyeicosatetranoic acid (HETEs) is via the LO pathway
    • aspirin competes with AA by irreversibly binding to the cyclooxygenase active site, thereby shifting AA to the LO pathway
      • inhibition of cyclo-oxygenases by aspirin results in the diversion of arachidonic acid products toward the lipo-oxygenase pathway, resulting in overproduction of leukotriens and other mediators, and a reduction of anti-inflammatory prostaglandins

Reference:


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