Rhinitis Alergi

01Pathophysiology

Allergic rhinitis is a Type I (IgE-mediated) hypersensitivity reaction occurring at the nasal mucosa. Understanding the two-phase immune response is critical for exam purposes.

On initial exposure to an inhaled allergen, antigen-presenting cells process the allergen and present it to Th2 helper T cells. Th2 cells release IL-4 and IL-13, which drive B-cell class switching to produce allergen-specific IgE antibodies. These IgE molecules bind to high-affinity FcεRI receptors on the surface of mast cells residing in the nasal mucosa. This is the sensitization phase, and no symptoms occur here.

Upon re-exposure, the allergen cross-links two adjacent IgE molecules on the mast cell surface, triggering mast cell degranulation. This is the early phase (occurring within minutes), releasing preformed mediators including histamine, tryptase, and newly synthesized mediators such as leukotrienes (LTC4, LTD4) and prostaglandin D2. Histamine acts on H1 receptors in the nasal mucosa, directly causing the hallmark triad of sneezing, pruritus, and watery rhinorrhea. Vascular permeability increases, glandular secretion ramps up, and sensory nerve endings are stimulated. This is why antihistamines are effective against sneezing and itching but less so against congestion.

The late phase follows 4 to 8 hours later and is driven by recruited inflammatory cells, particularly eosinophils, basophils, and Th2 lymphocytes. Eosinophils release major basic protein and eosinophilic cationic protein, perpetuating mucosal inflammation and edema. This late-phase inflammation accounts for the persistent nasal congestion that does not respond well to antihistamines alone but does respond to corticosteroids, which broadly suppress the inflammatory cascade at the transcriptional level. This is the mechanistic reason intranasal corticosteroids are superior to antihistamines for overall symptom control, particularly congestion.

With chronic allergen exposure, the nasal mucosa undergoes a process called nasal priming, where progressively lower doses of allergen trigger progressively stronger responses. This explains why patients notice worsening symptoms as the allergy season progresses even without increased allergen exposure.

02Classification and Clinical Manifestation

The classification follows the ARIA (Allergic Rhinitis and its Impact on Asthma) framework, which replaced the older "seasonal vs. perennial" terminology. Exam questions may use either system.

ARIA Classification by Duration

ARIA Classification by Severity

By Allergen Trigger (Traditional Classification)

Clinical Manifestations by Mediator

The critical exam point: sneezing, itching, and rhinorrhea are early-phase, histamine-driven symptoms (respond to antihistamines). Nasal congestion is predominantly a late-phase, eosinophil-driven symptom (responds best to intranasal corticosteroids).

03Diagnostic Workup

The diagnosis of allergic rhinitis is primarily clinical. A patient presenting with the characteristic history of episodic or chronic sneezing, clear watery rhinorrhea, nasal congestion, and pruritus, with identifiable triggers and an atopic background, can be diagnosed on history and physical examination alone. The physical exam findings of pale, boggy (edematous) nasal turbinates with clear secretions and the external signs of chronicity (allergic shiners, Dennie-Morgan lines, transverse nasal crease) reinforce the diagnosis.

When confirmation of the causative allergen is needed, particularly before starting allergen immunotherapy, the skin prick test is the gold standard. It is rapid (results in 15-20 minutes), cost-effective, and has high sensitivity. A positive test produces a wheal-and-flare response. Important caveats: patients must discontinue first-generation antihistamines for 3 to 5 days and second-generation antihistamines for 7 days before testing to avoid false negatives. Patients with severe dermatologic conditions (e.g., widespread eczema or dermatographism) are poor candidates for SPT.

Serum allergen-specific IgE testing (formerly known as RAST, now performed via ImmunoCAP) is the alternative when skin testing is not feasible. This is the appropriate test in patients who cannot stop antihistamines, have diffuse skin disease, or are at elevated risk for anaphylaxis. It is less sensitive than SPT but offers the advantage of no risk for systemic reaction and no interference from medications.

A nasal smear showing eosinophils supports the diagnosis and helps distinguish allergic rhinitis from non-allergic rhinitis (which may show neutrophils instead). However, this finding alone is not confirmatory, as non-allergic rhinitis with eosinophilia syndrome (NARES) also demonstrates nasal eosinophilia.

04Management and Treatment

Step 1: Allergen Avoidance. All patients should receive counseling on environmental control measures. For dust mite allergy, this includes mattress and pillow encasements, washing bedding in hot water (≥ 60 degrees C) weekly, reducing indoor humidity below 50%, and removing carpets from bedrooms. For pollen allergy, keeping windows closed during high-pollen days, showering after outdoor activity, and monitoring pollen counts are recommended. While evidence for individual measures is modest, the combined approach reduces allergen load meaningfully.

Step 2: Pharmacotherapy. The cornerstone of treatment for moderate-severe or persistent allergic rhinitis is the intranasal corticosteroid (INCS). Per the ARIA 2024-2025 guidelines, INCS is recommended over oral antihistamines as first-line therapy because it addresses all symptoms including congestion, which antihistamines handle poorly. Fluticasone propionate (Flonase) 1-2 sprays (50 mcg/spray) per nostril once daily or mometasone furoate (Nasonex) 2 sprays (50 mcg/spray) per nostril once daily are the most commonly tested agents. Onset of effect takes several days to 2 weeks for full benefit; patients must be counseled that this is not a rescue medication. The proper technique is to aim the spray laterally (toward the ipsilateral ear), not toward the septum, to avoid septal irritation and epistaxis.

For mild intermittent disease, a second-generation oral antihistamine taken as needed is appropriate. The second-generation agents (cetirizine 10 mg daily, loratadine 10 mg daily, fexofenadine 180 mg daily) are preferred because they are non-sedating and have no anticholinergic side effects, unlike first-generation agents (diphenhydramine, chlorpheniramine). First-generation antihistamines cross the blood-brain barrier and cause sedation, impaired cognition, and urinary retention, making them a poor choice for routine use.

When INCS alone provides insufficient relief, the ARIA 2024-2025 guidelines recommend the combination of intranasal corticosteroid plus intranasal antihistamine (azelastine/fluticasone) over either agent alone. This fixed-dose combination provides faster onset (within 30 minutes from the azelastine component) while maintaining the broad anti-inflammatory effect of the steroid.

Leukotriene receptor antagonists (montelukast 10 mg daily) are less effective than INCS and are positioned below oral antihistamines in the treatment hierarchy. However, montelukast has a role in patients with concomitant asthma and allergic rhinitis, where a single agent can address both conditions. The FDA has added a black box warning for montelukast regarding neuropsychiatric events (mood changes, suicidal ideation), making this a high-yield testing point.

Intranasal decongestants (oxymetazoline 0.05%, 2 sprays per nostril BID) provide rapid congestion relief but must be limited to 3 to 5 days maximum. Prolonged use causes rebound congestion known as rhinitis medicamentosa, where the nasal mucosa becomes dependent on the decongestant and congestion worsens upon discontinuation. The mechanism involves downregulation of adrenergic receptors in the nasal vasculature.

Step 3: Allergen Immunotherapy. For patients with confirmed IgE-mediated allergic rhinitis who remain symptomatic despite optimal pharmacotherapy, allergen immunotherapy (either subcutaneous [SCIT] or sublingual [SLIT]) is indicated. This is the only treatment that modifies the natural history of the disease. The course is typically 3 to 5 years in duration. SCIT involves a build-up phase (weekly injections with incrementally increasing doses over 3-6 months) followed by a maintenance phase (monthly injections). SLIT tablets are taken daily at home. Immunotherapy induces immune tolerance by shifting the immune response from Th2-dominant to Th1/Treg-dominant, with production of blocking IgG4 antibodies. The principal risk of SCIT is anaphylaxis, which is why it must be administered in a supervised medical setting with a 30-minute observation period.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The most common way students lose points on allergic rhinitis questions is by selecting an oral antihistamine as first-line treatment for a patient with moderate-severe or persistent disease. The reflex to pick "antihistamine for allergy" is strong, but the correct answer for a patient whose chief complaint includes nasal congestion alongside sneezing and rhinorrhea is the intranasal corticosteroid. Antihistamines handle itching, sneezing, and rhinorrhea but do not adequately address congestion, which is the late-phase eosinophil-driven component.

A second common trap involves rhinitis medicamentosa. When a vignette describes worsening nasal congestion despite using "nasal spray" for several weeks, the test-writer is testing whether you recognize rebound congestion from decongestant overuse. The answer is discontinuation of the decongestant and initiation of INCS, not escalation to another decongestant or oral therapy.

Third, watch for the montelukast distractor. It will appear as an answer choice in an allergic rhinitis vignette, and while it is a real medication used in this condition, it is inferior to both INCS and oral antihistamines as monotherapy. The one scenario where it becomes a reasonable answer is when the patient has coexisting asthma, where a single agent addressing both airway and nasal inflammation is attractive.

Finally, be attentive to the distinction between allergic and non-allergic rhinitis. The test-writer will include or omit pruritus and sneezing deliberately. A middle-aged patient with chronic congestion and rhinorrhea but no itching, no sneezing, no atopic history, and symptoms triggered by cold air or strong odors is vasomotor rhinitis, not allergic rhinitis, and the workup and management differ accordingly.

The core competency being tested is the ability to match the pathophysiologic phase (early vs. late) to the correct pharmacologic intervention and to recognize the clinical and physical exam features that anchor the diagnosis against its closest mimics.