Allergic rhinitis (AR) is a common IgE-mediated hypersensitivity reaction of the nasal mucosa to airborne allergens. It is characterized by nasal obstruction, watery discharge, sneezing, and itching in the nose, often accompanied by itching in the eyes, palate, and pharynx. AR significantly affects the quality of life, necessitating proper understanding for diagnosis and management.
Types of Allergic Rhinitis
- Seasonal Allergic Rhinitis (SAR): Symptoms occur during specific seasons when particular pollens (e.g., from trees, grasses, weeds) are airborne.
- Perennial Allergic Rhinitis (PAR): Symptoms persist year-round, typically due to allergens like moulds, dust mites, cockroach allergens, and animal dander.
Aetiology
Airborne Allergens
- Seasonal Allergens: Pollens (trees, grasses, weeds) that vary geographically and seasonally.
- Perennial Allergens: Include dust mites (thriving in bedding and carpets), molds, animal dander, and cockroaches.
Genetic Predisposition. A strong familial association exists. Children with one allergic parent have a 20% risk, rising to 47% if both parents are allergic.
Pathogenesis. AR develops in genetically predisposed individuals exposed to inhaled allergens. Key steps include:
- Production of IgE antibodies specific to allergens.
- Binding of IgE to mast cells or basophils.
- Allergen exposure leads to degranulation of mast cells, releasing mediators like histamine, leukotrienes, prostaglandins, and cytokines.
- These mediators cause inflammation, vasodilation, mucosal edema, and nasal hypersecretion.
Phases of Allergic Reaction
- Acute Phase: Occurs within 5–30 minutes post-exposure due to preformed mediators like histamine. Symptoms include sneezing, nasal discharge, and obstruction.
- Late Phase: Develops 2–8 hours later, involving inflammatory cell infiltration (eosinophils, neutrophils, CD4+ T cells), leading to swelling and persistent symptoms.
Functions of mediators
Release mediators from mast cells play a crucial role in the body’s response to allergic or nonspecific stimuli. These mediators are responsible for various physiological effects that contribute to the inflammatory response. Below is an overview of the primary release mediators and their functions:
- Histamine – It causes vasodilation and bronchospasm and leads to increased blood flow to the affected area and constriction of the airways, which can contribute to symptoms such as redness, swelling, and difficulty breathing.
- Eosinophil Chemotactic Factor of Anaphylaxis (ECF-A) – ECF-A specifically functions as a chemotactic factor that attracts eosinophils to the site of an allergic reaction. Eosinophils are white blood cells that play a key role in combating parasitic infections and are also involved in allergic responses.
- Neutrophil Chemotactic Factor (NCF-A) – Similar to ECF-A, NCF-A serves as a chemotactic factor that attracts neutrophils, another type of white blood cell. Neutrophils are essential for the initial immune response and help combat infections.
- Heparin – Heparin is known for its role in enhancing phagocytosis, which is the process by which immune cells engulf and destroy pathogens. This mediator helps to improve the efficiency of the immune response during allergic reactions.
- Prostaglandins – Prostaglandins are vasoactive substances that also contribute to bronchospasm. They play a role in regulating inflammation, pain, and fever, thus amplifying the body’s response to allergens.
- Leukotrienes – Like prostaglandins, leukotrienes are vasoactive and bronchospastic mediators. They are involved in sustaining inflammatory responses and can lead to prolonged bronchoconstriction in asthma.
- Platelet Aggregating Factor (PAF) – PAF is significant for its ability to aggregate platelets and stimulate the release of histamine and serotonin from these cells. It also promotes chemotaxis, attracting neutrophils and eosinophils to the site of inflammation, thereby enhancing the immune response.
- Thromboxane A – Thromboxane A is recognized for its spasmogenic properties, contributing to bronchoconstriction and vasoconstriction, which can exacerbate allergic reactions.
- Tumor Necrosis Factor-alpha (TNF-α) – TNF-α plays a pivotal role in immune responses by facilitating the transmigration of neutrophils and eosinophils to sites of inflammation. It enhances the recruitment of these cells, thereby amplifying the body’s response to allergens.
Clinical Features
Age and Gender: This can occur at any age, typically between 12–16 years.
Symptoms:
- Seasonal AR: Paroxysmal sneezing (10–20 sneezes in a row), nasal obstruction, watery discharge, nasal itching, and sometimes bronchospasm.
- Perennial AR: Persistent nasal congestion, postnasal drip, loss of smell, chronic cough, and hearing impairment.
Signs
- Nasal Signs: Transverse nasal crease (from “allergic salute”), pale and oedematous mucosa, thin nasal discharge.
- Ocular Signs: Dark circles (“allergic shiners”), conjunctival congestion, eyelid oedema.
- Otologic Signs: Retracted tympanic membranes or serous otitis media.
- Pharyngeal Signs: Granular pharyngitis, mouth breathing.
- Laryngeal Signs: Hoarseness due to vocal cord oedema.
Diagnosis
History and Examination: Detailed history to identify allergens and exclude other causes of nasal congestion.
Investigations:
- Nasal Smear: Shows eosinophilia.
- Skin Tests: Prick or intradermal tests to identify allergens.
- RAST: Measures allergen-specific IgE levels.
- Nasal Provocation Test: Observes reactions after direct allergen exposure.
ARIA Classification of allergic rhinitis:
Duration of disease
- Intermittent: Symptoms <4 days/week or <4 weeks.
- Persistent: Symptoms >4 days/week or >4 weeks.
Severity of disease
- Mild: None of the following symptoms are present: Sleep disturbance/ Impairment of daily activities, leisure and sport/ Impairment of school or work/ Troublesome symptoms
- Moderate to severe: One or more of the above symptoms are present
Complications
- Recurrent sinusitis.
- Nasal polyps.
- Serous otitis media.
- Prolonged mouth breathing leads to orthodontic problems.
Treatment
1. Avoidance of Allergen: Remove pets, use allergen-proof bedding, and avoid specific food allergens.
2. Pharmacotherapy:
- Antihistamines: Control sneezing, itching, and discharge; side effects include drowsiness.
- Sympathomimetics: Reduce nasal congestion; prolonged use can cause rebound congestion.
- Corticosteroids: Effective for severe symptoms; topical forms minimize systemic side effects.
- Mast Cell Stabilizers (e.g., Sodium Cromoglycate): Prevent mast cell degranulation.
- Leukotriene Receptor Antagonists (e.g., Montelukast): Effective for both asthma and AR.
- Anti-IgE Therapy (e.g., Omalizumab): Reduces IgE levels, especially for coexisting asthma.
3. Immunotherapy: Administered subcutaneously or sublingually, immunotherapy reduces IgE levels and raises IgG levels over time. Recommended for refractory cases.
Stepwise Approach is recommended by ARIA for allergic rhinitis treatment:
- For Mild Intermittent Disease: Oral antihistamines or intranasal cromolyn.
- Moderate-Severe Disease: Intranasal corticosteroids as monotherapy or in combination with antihistamines.
- Severe Cases Disease: Oral steroids or immunotherapy for persistent symptoms.
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Reference Textbooks.
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Author:
Dr. Rahul Bagla
MBBS (MAMC, Delhi) MS ENT (UCMS, Delhi)
Fellow Rhinoplasty & Facial Plastic Surgery.
Renowned Teaching Faculty
Mail: msrahulbagla@gmail.com
India