PATHOPHYSIOLOGY OF REACTIVE AIRWAY DISEASE AND SINUSITIS

The association between asthma and sinusitis was recognized more than a century ago. Since 1980, several studies have documented that severe asthma improved after coexisting sinusitis was effectively treated ei ther medically or surgically. Because the mechanism relating sinusitis to asthma is not known, several theories have been proposed: 1) aspir ation of infected sinus secretions into the lungs during sleep, 2) enh anced vagal stimulation in the infected sinus producing direct broncho spasm, 3) bronchospasm from excessive airway drying from mouth breathi ng, 4) production of bacterial toxins that induce partial beta blockad e, and 5) production in the infected sinus of cytokines and bronchocon strictive mediators. There are data to support each of these hypothese s, and any or all of them may be operative. In view of recent demonstr ations of activated lymphocytes and eosinophils in asthmatic airways, it is intriguing that biopsies of chronic hypertrophic sinusitis have revealed increased numbers of eosinophils and increased levels of gran ulocyte-macrophage colony stimulating factor, interleukin-3, and inter leukin-5 compared to control tissue. These findings suggest that sinus itis might induce asthma by stimulating eosinophil production and acti vation and thereby supplying peptidoleukotrienes (LTC4 and LTD 1) and other asthmagenic eosinophil products.