Pathophysiology of Allergic Rhinitis
1. Airborne allergens enter the nose during inhalation and are processed by lymphocytes, which produce antigen-specific IgE, sensitizing genetically predisposed hosts to those agents
2. On nasal reexposure, IgE bound to mast cells interacts with airborne allergens, triggering release of inflammatory mediators
3. Immediate reaction occurs within seconds to minutes, resulting in rapid release of preformed and newly generated mediators from the arachidonic acid cascade
4. Mediators of immediate hypersensitivity include histamine, leukotrienes, prostaglandin, tryptase, and kinins which cause vasodilation, increased vascular permeability, and production of nasal secretions
5. Late-phase reaction may occur 4 to 8 hours after initial allergen exposure due to cytokine release from mast cells and thymus-derived helper lymphocytes, causing persistent chronic symptoms including nasal congestion