What is the pathophysiology and treatment of allergic rhinitis?

Pathophysiology and Underlying Mechanisms of Allergic Rhinitis

Allergic rhinitis occurs when disruption of the epithelial barrier allows allergens to penetrate the nasal mucosal epithelium, triggering a T-helper type 2 inflammatory response and production of allergen-specific IgE antibodies. 1

Pathophysiological Mechanism

The pathophysiology of allergic rhinitis involves a complex immunological cascade:

1. Initial Sensitization Phase:

   • Allergens penetrate the disrupted nasal epithelial barrier
   • Antigen-presenting cells process allergens and present them to T cells
   • T cells differentiate into T-helper type 2 (Th2) cells
   • Th2 cells produce cytokines that promote B cell production of allergen-specific IgE

2. Early Phase Response (minutes after allergen exposure):

   • IgE antibodies bind to high-affinity receptors on mast cells and basophils
   • Re-exposure to allergens causes cross-linking of IgE on these cells
   • Degranulation releases preformed mediators, primarily histamine
   • Histamine acts on H1 receptors causing:
     • Nasal itch and sneezing (neural response)
     • Rhinorrhea (glandular stimulation)
     • Nasal congestion (vascular dilation) 2

3. Late Phase Response (4-8 hours after exposure):

   • Recruitment of inflammatory cells (eosinophils, basophils, T cells)
   • Production of additional mediators:
     • Leukotrienes and prostaglandins (primarily causing nasal congestion)
     • Cytokines perpetuating inflammation
     • Kinins contributing to plasma protein exudation 2

Cellular Components

The nasal mucosa in allergic rhinitis shows:

• Increased mast cells in epithelium
• Accumulation of eosinophils in lamina propria and epithelium
• Increased tissue and cell surface basophils in activated states
• Increased T cells and Langerhans' cells in the epithelium 2

Mediators and Their Effects

1. Histamine: Primary mediator causing:

   • Nasal itch
   • Sneezing
   • Rhinorrhea
   • Partial contribution to nasal congestion
   • Accounts for approximately 40-50% of symptom manifestation 2

2. Leukotrienes, Prostaglandins, and Kinins:

   • Primarily responsible for nasal congestion
   • Act on nasal vasculature
   • Leukotrienes also induce plasma protein exudation contributing to nasal secretions 2

Clinical Manifestations

The pathophysiological changes result in characteristic symptoms:

• Nasal congestion (94.23% of patients)
• Rhinorrhea (90.38% of patients)
• Sneezing
• Nasal/ocular itching
• Postnasal drainage 1

Physical Examination Findings

• Seasonal allergic rhinitis: Edematous and pale turbinates
• Perennial allergic rhinitis: Erythematous and inflamed turbinates with serous secretions 1

Classification

• Intermittent: Symptoms occurring <4 consecutive days/week or <4 consecutive weeks/year
• Persistent: Symptoms occurring >4 consecutive days/week and >4 consecutive weeks/year 1

Epidemiology and Associations

• Affects approximately 15% of the US population (50 million individuals)
• Associated with asthma, eczema, chronic sinusitis, cough, and headaches
• Family history of allergic rhinitis, asthma, or atopic dermatitis increases risk
• Common sensitizing allergens include grass, dust mites, and ragweed 1, 3
• Approximately 10% of allergic rhinitis patients will develop asthma 3

The complex interplay between multiple immune cells, mediators, and cytokines explains why single-target therapies often provide incomplete symptom relief, necessitating combination approaches for optimal management of allergic rhinitis 4.