Unit
- Type I hypersensitivity: Allergic rhinitis is an IgE-mediated inflammatory condition triggered by inhaled allergens such as pollen, dust mites, or pet dander. Initial sensitization involves allergen presentation by dendritic cells to naive T cells, promoting a Th2 response.
- Th2 cytokine cascade: Activated Th2 cells produce interleukins IL-4, IL-5, and IL-13. IL-4 and IL-13 stimulate B cells to class-switch and produce allergen-specific IgE, while IL-5 recruits eosinophils to the nasal mucosa.
- Mast cell degranulation: Upon re-exposure, allergens cross-link IgE on mast cells, triggering release of histamine, leukotrienes, and prostaglandins. These mediators cause immediate sneezing, itching, rhinorrhea, and nasal congestion.
- Late-phase response: Four to six hours after allergen exposure, eosinophils, basophils, and T cells infiltrate the tissue, releasing mediators that sustain inflammation. This leads to persistent nasal obstruction and hyperreactivity.
- Eosinophilic inflammation: Eosinophils release major basic protein and eosinophil cationic protein, which damage nasal epithelium and contribute to remodeling. Chronic inflammation can lead to nasal polyp formation in susceptible individuals.
- Nasal hyperreactivity: Persistent inflammation lowers the threshold for nonspecific triggers like cold air, smoke, and strong odors. Patients become symptomatic even without allergen exposure.
- Systemic effects: Allergic rhinitis is not limited to the nose. Elevated systemic IgE and inflammatory markers correlate with asthma exacerbations, eczema flares, and conjunctival involvement.
- Genetics and epigenetics: Family history is a strong risk factor. Variants in genes encoding IL-4, IL-13, and FcεRI are linked to increased susceptibility. Epigenetic modifications from early-life exposure to allergens or microbes may influence disease expression.
- Clinical presentation: Patients typically present with sneezing, nasal itching, watery rhinorrhea, and congestion. Ocular symptoms like itchy, red eyes often accompany nasal complaints, especially in seasonal allergic rhinitis. Symptoms may worsen upon exposure to specific triggers such as grass or tree pollen.
- Diagnostic approach: Diagnosis is primarily clinical based on history and physical exam. Confirmation can be done via skin prick testing or serum specific IgE. A positive test correlates with clinical history, but false positives occur. Nasal endoscopy may be used to assess for polyps or other structural causes of obstruction.
- Stepwise pharmacotherapy: First-line treatment includes intranasal corticosteroids and oral antihistamines. For moderate to severe cases, leukotriene receptor antagonists or combination therapy can be considered. Intranasal antihistamines offer rapid relief. Oral decongestants should be avoided in patients with hypertension or cardiovascular disease.
- Allergen avoidance: Reducing exposure to triggers is critical. For dust mites, encase pillows and mattresses with allergen proof covers, wash bedding in hot water weekly, and reduce indoor humidity below 50 percent. Pollen avoidance includes keeping windows closed during peak seasons, using HEPA filters, and showering after outdoor exposure.
Terminology
- IgE
- Immunoglobulin E, the antibody class central to immediate hypersensitivity reactions.
- Th2
- Helper T cell subset that drives allergic inflammation through cytokine production.
- Mast cell
- Granulocyte that stores histamine and releases mediators upon IgE cross-linking.
- Eosinophil
- White blood cell involved in late-phase inflammation and tissue damage.
Scope of Practice
Role: Primary Care Provider in Allergy Diagnosis
Within scope:
- Recognizing classic symptoms of allergic rhinitis during history and physical exam.
- Educating patients about the basic pathophysiology of allergic reactions.
- Initiating first-line pharmacotherapy and recommending environmental changes.
Outside scope:
- Performing or interpreting skin prick tests without proper training.
- Managing complex cases with severe comorbidities like uncontrolled asthma.
- Administering allergen immunotherapy without specialist referral.
Quick Revision
- Allergic rhinitis is an IgE-mediated type I hypersensitivity reaction triggered by inhaled allergens.
- The immediate phase involves mast cell degranulation and histamine release.
- The late-phase response is driven by eosinophil and T-cell infiltration, causing persistent symptoms.
- Chronic inflammation can lead to nasal hyperreactivity and systemic effects like asthma.