Clinical Immunology: Allergic Rhinitis
High-Yield Revision Notes for NEET PG / NEXT
Allergic Rhinitis is an IgE-mediated inflammatory disorder of the nasal mucosa triggered by allergen exposure. It represents a classic Type I Immediate Hypersensitivity reaction and is a core component of the “atopic march,” frequently coexisting with asthma and atopic dermatitis.
1. Pathophysiology
- Sensitization Phase: Initial allergen exposure activates Th2 cells, which drive B-cell class-switching to produce allergen-specific IgE antibodies. These antibodies bind to high-affinity receptors on mast cells and basophils.
- Early-Phase Response (Within minutes): Re-exposure causes allergen cross-linking of bound IgE, triggering mast cell degranulation. Preformed mediators like histamine, leukotrienes, and prostaglandins are released, causing immediate pruritus, paroxysmal sneezing, and watery rhinorrhoea.
- Late-Phase Response (4–8 hours): Driven by synthesized cytokines that recruit inflammatory cells, primarily eosinophils. This sustained inflammation causes chronic nasal congestion and mucosal hyperreactivity.
2. Clinical Signs & Stigmata
- Classic Symptoms: Paroxysmal sneezing, bilateral clear watery rhinorrhoea, nasal congestion, and severe nasal or palatal pruritus. (Note: Clear fluid that is sticky/viscous and contains eosinophils—differentiating it from the completely water-like CSF fluid).
- Anterior Rhinoscopy: Characterized by pale, bluish, edematous nasal mucosa with hypertrophied inferior turbinates, unlike the erythematous mucosa seen in infectious rhinitis.
- Allergic Shiners: Dark, bluish discoloration under the lower eyelids due to chronic venous stasis from nasal congestion.
- Dennie-Morgan Lines: Accentuated folds or wrinkles below the lower eyelid margins associated with atopic dermatitis/rhinitis.
- Allergic Salute & Crease: Habitual upward wiping of the nose with the palm (salute) to relieve itching, which eventually leaves a permanent transverse hyperpigmented line across the nasal bridge (crease).
3. Differential Diagnosis: Allergic Rhinitis vs. CSF Rhinorrhoea
| Feature | Allergic Rhinitis | CSF Rhinorrhoea |
|---|---|---|
| Laterality | Typically bilateral | Almost always strictly unilateral |
| Fluid Character | Clear, mucoid, slightly viscous; stiffens a handkerchief when dried due to protein content. | Completely watery, non-viscous; does not stiffen a handkerchief when dry (“Handkerchief Test”). |
| Associated Signs | Sneezing, itchy eyes/nose, pale turbinates. | Metallic/salty taste, positional gush (Reservoir sign), low-pressure headache, history of head trauma/FESS. |
| Diagnostic Assay | Nasal smear showing eosinophils; positive skin prick test or Specific IgE. | Positive Beta-2 Transferrin assay. |
4. Diagnostic Strategy
- Clinical Diagnosis: Primarily based on a thorough history and physical exam findings.
- Skin Prick Testing (SPT): The preferred in vivo method to identify specific offending IgE allergens. Highly sensitive and yields rapid results.
- In Vitro Specific IgE Assays (ImmunoCAP): Used if the patient has severe skin disease (eczema), is taking systemic antihistamines that interfere with SPT, or carries a high risk for anaphylaxis.
5. Evidence-Based Stepwise Management
Treatment combines allergen avoidance, pharmacotherapy, and targeted immunomodulation:
- Intranasal Corticosteroids (e.g., Fluticasone, Mometasone): The single most effective first-line monotherapy for moderate-to-severe or persistent allergic rhinitis. They downregulate mucosal inflammatory cytokine networks and effectively treat all symptoms, including nasal congestion.
- Oral or Intranasal Antihistamines (H1-receptor antagonists): Highly effective for sneezing, rhinorrhoea, and stitching, but minimal impact on congestion. Second-generation non-sedating agents (e.g., Cetirizine, Levocetirizine, Loratadine, Fexofenadine) are strongly preferred over first-generation agents (e.g., Diphenhydramine) due to blood-brain barrier penetration profiles.
- Leukotriene Receptor Antagonists (e.g., Montelukast): Beneficial as add-on therapy, particularly in patients with concomitant bronchial asthma.
- Intranasal Cromolyn Sodium: Mast cell stabilizer used as a prophylactic agent; requires frequent dosing (3–4 times daily), making compliance a limitation.
- Allergen Immunotherapy (AIT): Indicated for severe, refractory cases or patients who cannot tolerate standard pharmacotherapy. Administered via subcutaneous injections (SCIT) or sublingual tablets (SLIT). This is the only disease-modifying treatment modality capable of altering the underlying immunological course and preventing progression to asthma.