ABSTRACT
Sinusitis and asthma are commonly seen simultaneously in clinical practice (1-3). In fact, nearly 50% of asthmatics demonstrate upper airway symptoms and radiographic evidence of rhinosinusitis (4-11). Chronic sinusitis and asthma share several pathophysiological features: chemical mediators, e.g., histamine, cysteinyl leukotrienes, and prostaglandin D2; cytokines, e.g., interleukin-4 (IL-4), IL-5, IL-9, IL-13, and CCL11 (eotaxin); and cellular mediators, principally eosinophils and TH2 lymphocytes (12-14). These observations have led to the concept of ‘‘one airway . . . one disease’’ rather than the idea of isolated upper and lower airway disorders. At the same time, numerous clinical studies have demonstrated that aggressive medical or surgical treatment of sinusitis improves asthma, suggesting that upper airway inflammation may actually have a causative role in lower airway disease.
