The pathophysiology of allergic rhinitis: Impact of therapeutic intervention

Abstract

In individuals with allergic rhinitis, exposure to antigens, such as pollens, can activate the nasal mast cells to initiate the allergic process. During this process, the patient develops symptoms and mediators are released (including histamine, prostaglandin D 2, thromboxane B 2, and leukotriene C 4) to produce the inflammation characteristic of allergic rhinitis. The allergic process can be divided into three phases: early, occurring within minutes of allergen challenge; late, occurring in about half those challenged about 3 to 10 hours later; and rechallenge, occurring 12 to 24 hours after the first exposure. Mediators are released in each phase; in the late and rechallenge phases, cells, including basophils, eosinophils, neutrophils, and mononuclear cells, enter the nose in large numbers. The basophils can release mediators, increasing the allergic response. Pretreatment of patients with allergic rhinitis with systemic steroids, such as prednisone, prevents the late and rechallenge phases of the allergic process. However, with the exception of kinin generation, such pretreatment has no effect on the early phase. In contrast, pretreatment with the topical steroid flunisolide prevents many more aspects of the allergic process: the production of symptoms and the release of mediators in the early phase and the further development of symptoms and mediator release in the late and rechallenge phases. Flunisolide pretreatment also prevents the influx into the nose of mediator-releasing cells, including basophils. Therefore, physicians should consider pretreating their patients with allergic rhinitis with flunisolide several days before the pollen season begins. Early response to the antigen will be reduced, and the inflammation associated with chronic allergic rhinitis will be suppressed.