Allergy and Immunology· Topic 1.3 Upper airway and ocular allergy· 1.3.1
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Allergic rhinitis

Allergic rhinitis is an IgE-mediated inflammation of the nasal mucosa causing sneezing, rhinorrhea, congestion, and itch on allergen exposure, classified as seasonal or perennial. Diagnosis is clinical, supported by skin or specific IgE testing to identify allergens, and treatment is allergen avoidance with intranasal corticosteroids first-line, escalating to combination therapy and allergen immunotherapy.

5 min readReviewed 2026-07-19

Key facts

Mechanism
IgE-mediated nasal mucosal inflammation (type I)
Cardinal symptoms
Sneezing, rhinorrhea, congestion, nasal/ocular itch
Classification
Seasonal vs perennial
First-line treatment
Intranasal corticosteroid (e.g., fluticasone)
Confirmatory test
Skin prick or allergen-specific IgE
Disease-modifying option
Allergen immunotherapy
Associations
Asthma, allergic conjunctivitis, atopic dermatitis

Overview

  • Definition: allergic rhinitis is an IgE-mediated inflammatory disorder of the nasal mucosa triggered by inhaled allergens.
  • Cardinal presentation: sneezing, watery rhinorrhea, nasal congestion, and nasal and ocular itching after allergen exposure.
  • Classification: seasonal (pollens) versus perennial (dust mite, animal dander, mold), which guides testing and treatment.
  • Why it matters: it is very common, impairs sleep and quality of life, and is closely linked to asthma and allergic conjunctivitis, so control benefits the whole atopic airway.

Epidemiology

  • Very common: among the most prevalent chronic conditions, often beginning in childhood or adolescence.
  • Atopic clustering: frequently coexists with asthma, allergic conjunctivitis, and atopic dermatitis.
  • Seasonal versus perennial: pollens drive seasonal disease; indoor allergens drive perennial disease.

Risk factors

  • Personal or family history of atopy: the strongest predictor.
  • Aeroallergen exposure: pollens, house dust mite, animal dander, and mold.
  • Early-life environmental exposures influencing sensitization.
  • Occupational allergen exposure in some adults.

Pathophysiology

  • Sensitization: inhaled allergen drives production of allergen-specific IgE that coats nasal mast cells.
  • Early-phase response: re-exposure cross-links IgE, releasing histamine and causing immediate sneezing, itch, and rhinorrhea.
  • Late-phase response: recruited eosinophils and other cells cause sustained congestion hours later.
  • Systemic atopy link: the same IgE mechanism underlies the associated conjunctivitis and asthma.

Clinical features

  • Nasal symptoms: paroxysmal sneezing, clear rhinorrhea, congestion, and itch.
  • Ocular symptoms: itchy, watery, red eyes (allergic conjunctivitis).
  • Examination signs: pale, boggy, edematous nasal turbinates and clear secretions; allergic shiners and a nasal crease in children.
  • Pattern: symptoms tracking with pollen seasons (seasonal) or persisting year-round (perennial).

Differential diagnosis

  • Nonallergic (vasomotor) rhinitis: nasal symptoms triggered by irritants, temperature, or odors with negative allergy testing.
  • Viral upper respiratory infection: self-limited with systemic symptoms and colored discharge, unlike the clear rhinorrhea and itch of allergy.
  • Chronic rhinosinusitis: facial pressure, purulent discharge, and hyposmia rather than sneezing and ocular itch.
  • Nasal polyps: obstruction and anosmia, often with aspirin sensitivity and asthma, not the paroxysmal itch-sneeze pattern of allergy.
  • Rhinitis medicamentosa: rebound congestion from overused topical decongestants, without the sneezing and itch of allergy.
  • Structural obstruction: septal deviation or, in children, a unilateral foreign body, causing fixed obstruction without itch or sneezing.
  • Hormonal or drug-induced rhinitis: pregnancy or medications such as ACE inhibitors, with congestion but no allergic itch.
  • Atrophic rhinitis: crusting and a wide nasal cavity in older adults.

Diagnosis

  • Diagnose clinically and confirm the allergen with IgE-based testing: allergic rhinitis is a clinical diagnosis based on characteristic symptoms with a temporal relationship to allergen exposure, confirmed and specified by skin prick testing or allergen-specific IgE to identify the culprit aeroallergens.
  • First step, history and examination: characterize seasonal versus perennial symptoms and identify likely triggers, examining for pale boggy turbinates.
  • Then perform skin prick testing (the preferred confirmatory test) to relevant aeroallergens; a positive test with a matching history establishes the sensitizing allergen.
  • Use allergen-specific IgE when skin testing is unavailable or antihistamines cannot be stopped.
  • Reserve imaging (CT sinuses) or nasal endoscopy for suspected chronic rhinosinusitis, polyps, or structural disease, not for uncomplicated allergic rhinitis.

Clinical pearl. Pale, boggy turbinates with clear discharge and itchy, watery eyes point to allergy, not infection; treat the whole atopic airway, because controlling allergic rhinitis improves coexisting asthma, and reach for a daily intranasal corticosteroid rather than layering oral decongestants that only cause rebound.

Management

  • First-line, an intranasal corticosteroid: for example fluticasone propionate 2 sprays (100 mcg) in each nostril once daily, the most effective single therapy, used regularly.
  • Add a second-generation oral or intranasal antihistamine for breakthrough symptoms: cetirizine 10 mg PO daily, or intranasal azelastine 1 to 2 sprays per nostril twice daily.
  • For persistent congestion, combine the intranasal corticosteroid (fluticasone) with an intranasal antihistamine (azelastine), and consider montelukast 10 mg PO daily when asthma coexists.
  • Then, if symptoms remain uncontrolled or medication is undesirable, offer allergen immunotherapy (subcutaneous or sublingual), the only disease-modifying treatment, over 3 to 5 years.
  • Use saline irrigation and allergen avoidance as adjuncts, and limit topical decongestants to a few days to avoid rebound.
  • Treat associated conjunctivitis with an ophthalmic antihistamine or mast cell stabilizer.

Complications

  • Impaired sleep, concentration, and quality of life.
  • Poor asthma control: untreated rhinitis worsens coexisting asthma.
  • Chronic rhinosinusitis and nasal polyps.
  • Otitis media with effusion in children.

Prognosis

  • Well controlled with therapy: most patients achieve good control with intranasal corticosteroids and antihistamines.
  • Disease-modifying immunotherapy: can induce lasting tolerance and reduce progression to asthma.
  • Often persistent: symptoms may continue for years, fluctuating with exposure.

Prevention

  • Reduce allergen exposure: dust-mite-proof bedding covers, humidity control, pet and pollen avoidance measures.
  • Use intranasal corticosteroids regularly during known allergen seasons rather than as needed.
  • Offer allergen immunotherapy over 3 to 5 years to modify disease and reduce the risk of new sensitizations and asthma.
  • Avoid overuse of topical decongestants to prevent rhinitis medicamentosa.

Key points

  • Allergic rhinitis is IgE-mediated nasal inflammation with sneezing, rhinorrhea, congestion, and itch, seasonal or perennial.
  • Diagnosis is clinical, confirmed by skin prick or specific IgE testing to identify allergens.
  • Intranasal corticosteroids are the most effective first-line therapy, with antihistamines added for breakthrough symptoms.
  • Allergen immunotherapy is the only disease-modifying treatment.
  • Treat the whole atopic airway, since controlling rhinitis improves coexisting asthma.

Practice questions

Board-style vignettes on this article, free with it. Pick an answer to see why each choice is right or wrong.

Vignette
A 28-year-old man is evaluated in the office for nasal symptoms that have recurred each April through early June for 3 years. Sneezing, clear rhinorrhea, congestion, and itching of the nose, eyes, and palate worsen after yard work and eased during a trip to another region last May. He has taken no medication. He had eczema as a child. Temperature is 36.8 C (98.2 F), blood pressure is 118/74 mm Hg, pulse rate is 70/min, respiration rate is 14/min, and oxygen saturation is 98% on ambient air. Conjunctivae are mildly injected. There is infraorbital darkening and a transverse nasal crease. Turbinates are enlarged, pale, and bluish. The pharynx is cobblestoned. Which of the following is the most appropriate treatment?

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Allergic rhinitis | Internal Medicine | Board Pearls