Residency · Residency · Otolaryngology
Allergic Rhinitis: Pathophysiology and Treatment
Introduction
Allergic rhinitis is a chronic inflammatory condition of the nasal mucosa mediated by IgE-dependent immune responses to inhaled allergens. It affects approximately 20-30% of the adult population and significantly impacts quality of life, work productivity, and sleep. Understanding the underlying immunologic mechanisms and treatment hierarchy is essential for the otolaryngologist.
Classification
By Temporal Pattern
Seasonal allergic rhinitis: triggered by outdoor aeroallergens (tree, grass, weed pollens, mold spores). Perennial allergic rhinitis: triggered by year-round allergens (dust mites, pet dander, cockroach, mold).
ARIA Classification (Allergic Rhinitis and its Impact on Asthma)
| Duration | Severity |
|---|---|
| Intermittent: <4 days/week OR <4 consecutive weeks | Mild: Normal sleep, daily activities, work/school |
| Persistent: ≥4 days/week AND ≥4 consecutive weeks | Moderate-severe: Impairment in ≥1 domain |
Intermittent: symptoms <4 days/week or <4 consecutive weeks. Persistent: symptoms >4 days/week and >4 consecutive weeks. Mild: normal sleep, daily activities, work/school performance. Moderate-severe: impairment in one or more of the above domains.
Pathophysiology
Early Phase (Minutes)
Allergen exposure leads to cross-linking of IgE on mast cells in the nasal mucosa. Mast cell degranulation releases histamine, tryptase, leukotrienes, prostaglandins. Results in: sneezing, rhinorrhea, pruritus, congestion within minutes.
Late Phase (4-8 Hours)
Recruitment of eosinophils, basophils, T-helper 2 (Th2) lymphocytes to the nasal mucosa. Release of cytokines: IL-4, IL-5, IL-13 perpetuate inflammation. Prolonged nasal congestion, mucosal edema, mucus hypersecretion. Accounts for persistent symptoms and nasal priming (increased sensitivity to lower allergen doses).
Immunologic Basis
Type I hypersensitivity reaction (Gell and Coombs classification). Antigen-presenting cells process allergen and present to Th2 cells. Th2 cells produce IL-4 (promotes B-cell class switching to IgE) and IL-5 (eosinophil recruitment). IgE binds to high-affinity receptors (FcepsilonRI) on mast cells and basophils.
Clinical Presentation
Cardinal symptoms: rhinorrhea (clear, watery), nasal congestion, sneezing, nasal pruritus. Associated symptoms: postnasal drip, eye symptoms (itching, tearing, redness), palatal pruritus, ear fullness. Physical findings: pale, boggy, bluish turbinates; clear rhinorrhea; allergic shiners (infraorbital darkening); transverse nasal crease (allergic salute); Dennie-Morgan lines. Comorbidities: asthma (up to 40% of allergic rhinitis patients), sinusitis, otitis media with effusion, nasal polyposis, sleep disturbance.
Diagnostic Workup
Skin Prick Testing
Gold standard for identifying specific allergen sensitivities. Rapid results (15-20 minutes), high sensitivity, Must withhold antihistamines for 5-7 days before testing, Tests common regional aeroallergens.
Serum-Specific IgE (ImmunoCAP)
Alternative when skin testing is not feasible (dermatographism, severe eczema, inability to stop antihistamines). Comparable specificity to skin testing; slightly lower sensitivity.
Nasal Endoscopy
Assess for turbinate hypertrophy, nasal polyposis, septal deviation, adenoid hypertrophy (children). Rule out other causes of nasal obstruction.
Treatment
Environmental Control and Allergen Avoidance
Dust mite avoidance: encasements, HEPA filters, humidity control (<50%). Pet dander: removal from bedroom, HEPA filters. Pollen: window closure during high pollen counts, nasal saline irrigation. Evidence for avoidance measures alone is modest but recommended as adjunctive therapy.
Pharmacotherapy
Intranasal corticosteroids (INCS): most effective single agent for all symptoms; fluticasone, mometasone, budesonide; onset in 12 hours, peak efficacy in days-weeks. Second-generation oral antihistamines: loratadine, cetirizine, fexofenadine; effective for sneezing, rhinorrhea, pruritus; minimal sedation. Intranasal antihistamines: azelastine, olopatadine; rapid onset; can be combined with INCS. Combination sprays: azelastine/fluticasone (Dymista) — superior to either agent alone. Leukotriene receptor antagonists: montelukast; less effective than INCS; useful for comorbid asthma. Oral/topical decongestants: short-term use only; risk of rhinitis medicamentosa with topical use >3-5 days. Intranasal anticholinergics: ipratropium bromide; targets rhinorrhea specifically. Nasal saline irrigation: adjunctive therapy for all patients.
Immunotherapy
Subcutaneous immunotherapy (SCIT): escalating doses of allergen extract; 3-5 year course; disease-modifying. Sublingual immunotherapy (SLIT): tablets or drops; FDA-approved for grass, ragweed, dust mite. Indications: moderate-severe symptoms, inadequate response to pharmacotherapy, desire to reduce medication burden. Only treatment that alters the natural disease course and prevents new sensitizations.
Surgical Options
Inferior turbinate reduction: for medication-refractory nasal obstruction due to turbinate hypertrophy. Techniques: submucosal resection, radiofrequency ablation, microdebrider-assisted turbinoplasty. Surgery addresses obstruction, not the allergic inflammatory process.
Key Clinical Pearls
Intranasal corticosteroids are the most effective monotherapy for allergic rhinitis and should be first-line for moderate-severe disease. Allergic rhinitis is a risk factor for asthma development — the unified airway concept supports treating nasal disease to improve lower airway outcomes. Immunotherapy is the only treatment that modifies the natural history of allergic disease. Persistent unilateral nasal symptoms should prompt investigation for alternative diagnoses (neoplasm, CSF leak, foreign body). Topical decongestant use beyond 3-5 days risks rhinitis medicamentosa.
References
- Bousquet J, Khaltaev N, Cruz AA, et al. Allergic Rhinitis and its Impact on Asthma (ARIA) 2008 Update. Allergy. 2008;63(Suppl 86):8-160.
- Seidman MD, Gurgel RK, Lin SY, et al. Clinical practice guideline: allergic rhinitis. Otolaryngol Head Neck Surg. 2015;152(1 Suppl):S1-S43.
- Wheatley LM, Togias A. Clinical practice: allergic rhinitis. N Engl J Med. 2015;372(5):456-463.
- Durham SR, Penagos M. Sublingual or subcutaneous immunotherapy for allergic rhinitis? J Allergy Clin Immunol. 2016;137(2):339-349.