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Allergic rhinitis affects approximately 10-30% of adults and 40% of children globally, making it one of the most prevalent chronic conditions in clinical practice. It significantly impairs quality of life and is closely linked to comorbid asthma, chronic sinusitis, and allergic conjunctivitis.
Allergic rhinitis is an IgE-mediated type I hypersensitivity reaction. Repeat exposure to allergens (pollens, dust mites, pet dander, mold) causes mast cell degranulation in the nasal mucosa, releasing histamine, leukotrienes, and prostaglandins. This produces the early-phase response (sneezing, rhinorrhea, itching) within minutes. Late-phase inflammatory cell infiltration (eosinophils, basophils) perpetuates nasal congestion hours later.
Distinguishing allergic from non-allergic rhinitis guides management. Allergic rhinitis features clear rhinorrhea, nasal and palatal pruritus, sneezing, associated ocular symptoms, and a personal or family history of atopy. Skin prick testing or specific IgE (RAST) confirms sensitization. Treatment follows a stepwise approach: intranasal corticosteroids are first-line for persistent disease; second-generation antihistamines for intermittent symptoms; allergen immunotherapy for long-term disease modification. Key differentials include vasomotor rhinitis, chronic rhinosinusitis, and nasal polyps.