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Patients with aspirin sensitivity, asthma, and nasal polyps exhibit increased synthesis of cysteinyl leukotrienes—both basally and in response to exogenous aspirin—and increased responsiveness to inhaled cysteinyl leukotrienes, in contrast to patients with aspirin tolerant asthma. The authors hypothesised that the latter effect reflects overexpression of the cysteinyl leukotriene receptor CysLT1.
Nasal biopsy specimens were obtained from 22 aspirin sensitive and 12 aspirin tolerant patients with chronic rhinosinusitis and nasal polyposis. The absolute number (and percentage of CD45+ leucocytes) of cells expressing the CysLT1 (but not LTB4) receptor was increased in the aspirin sensitive group, despite no overall difference in numbers of leucocytes. Subsequently, nasal application of lysine aspirin to aspirin sensitive patients caused a reduction in the percentage of CD45+ leucocytes expressing the CysLT1 receptor compared with placebo.
This study raises intriguing questions about the pathogenesis of aspirin sensitive syndromes, providing evidence for overexpression of the CysLT1 receptor in addition to increased leukotriene production. This overexpression is reduced by aspirin desensitisation. Further studies are warranted of leukotriene antagonists and aspirin desensitisation in patients with nasal polyposis with aspirin sensitivity. Variation in the response to leukotriene antagonists may well be related to differences in CysLT1 expression in inflammatory cells in the upper and lower airway.
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