Allergic Rhinitis

On this page
  1. Direct answer
  2. What you must remember
  3. Managing a persistent case from clinic to control
  4. Where students slip
  5. Frequently asked questions
  6. Related topics

Direct answer

Allergic rhinitis is an IgE-mediated type I hypersensitivity of the nasal mucosa to inhaled allergens — house dust mite and pollens in most Indian patients — producing the quartet of sneezing, watery rhinorrhoea, nasal obstruction and itching, classically with pale, boggy turbinates and a transverse nasal crease from the allergic salute. ARIA classifies it by duration and severity into intermittent versus persistent and mild versus moderate-severe, which decides therapy: intranasal corticosteroids are the single most effective treatment for anything beyond mild disease, second-generation oral antihistamines relieve sneezing and itch, and allergen immunotherapy is the only disease-modifying option for refractory or clearly allergen-driven disease. It is not a trivial complaint — the united airway links it to asthma, sinusitis, otitis media with effusion and sleep disturbance.

What you must remember

  • Mechanism in two phases: sensitisation followed by allergen-triggered mast-cell degranulation with histamine and leukotrienes (immediate sneeze and rhinorrhoea), then a late-phase eosinophilic inflammation sustaining obstruction — which is why antihistamines alone often disappoint.
  • ARIA classification: intermittent (symptoms under four days a week or under four weeks a year) versus persistent, each graded mild or moderate-severe by sleep disturbance, daily activity impairment and troublesome symptoms — an exam-standard definition pair.
  • Bedroom diagnosis: allergic salute (upward nose-rubbing creating the transverse nasal crease), shiners from venous stasis, mouth breathing, and pale bluish turbinates that glisten; nasal smear shows eosinophils.
  • Confirming tests: skin prick test (read at 15-20 minutes) or serum specific IgE for causally relevant allergens — house dust mite, cockroach, pollens and fungal spores dominate Indian panels; total IgE alone is neither sensitive nor specific.
  • Drug of choice: intranasal corticosteroid — fluticasone, mometasone or budesonide — used continuously for weeks, sprayed laterally aimed away from the septum; second-generation oral antihistamines (levocetirizine, desloratadine, furosemide-free bilastine) for sneeze and itch; nasal saline irrigation as adjunct; montelukast as add-on particularly with coexisting asthma.
  • Immunotherapy: subcutaneous or sublingual allergen immunotherapy over three to five years for patients with demonstrable single or few allergen sensitivity uncontrolled by drugs — the only therapy altering natural history.
  • Complications and associations: chronic rhinosinusitis, nasal polyposis, otitis media with effusion in children, adenoid hypertrophy, dental malocclusion, and asthma in the same atopic patient — one airway, one disease.

Managing a persistent case from clinic to control

A 24-year-old student from Delhi reports year-round sneezing bouts, early-morning nasal blockage and clear rhinorrhoea, worse while dusting her room, with summer aggravation; examination shows boggy pale turbinates, a transverse crease and throat findings of postnasal drip. Her symptoms exceed four days a week and disturb sleep, so this is persistent, moderate-severe allergic rhinitis by ARIA. Skin prick testing confirms house dust mite sensitivity with a strong positive wheel.

Stepwise care starts with allergen avoidance — mite-proof bedding, damp-dusting, washing soft toys — plus saline irrigation, and mometasone spray daily with correct technique, adding levocetirizine at night for two weeks. Review at four to six weeks: obstruction easing and sleep restored, the spray continues through the season and steps down gradually. If control fails despite adherence — or if asthma coexists, which is worth actively asking about — referral for sublingual immunotherapy against dust mite is discussed, a three-year commitment but the only option that changes the disease rather than suppressing it. Children with the same picture additionally need hearing assessment, for persistent effusion silently damages language and learning.

Where students slip

The commonest exam error is treating allergic and infective rhinitis as interchangeable: allergic secretions are profuse, watery and eosinophilic with itch, while infective rhinitis is mucopurulent without itch — mixing them loses the pathology mark. The second is underplaying intranasal steroids because "steroids have side effects": with correct technique they are the first-line for moderate-severe disease, far more effective than antihistamines for obstruction, since obstruction is late-phase inflammation, not histamine. Third, forgetting the united airway: any viva on allergic rhinitis can end with "and what else will you examine?" — the chest, for coexisting asthma.

Frequently asked questions

How does ARIA classify allergic rhinitis?

By symptom duration — intermittent (fewer than four days a week or four weeks a year) versus persistent — and by severity, mild versus moderate-severe, graded by impact on sleep, daily activities and symptom burden.

Which drug class is most effective for moderate-severe allergic rhinitis?

Intranasal corticosteroids, which address the late-phase eosinophilic inflammation responsible for obstruction; oral antihistamines control sneezing and itching but poorly relieve blockage.

What is the allergic salute and nasal crease?

The upward nose-rubbing gesture of allergic patients; repeated over years it produces a transverse skin crease across the nasal dorsum, a classical physical sign.

Which allergens dominate in Indian patients with allergic rhinitis?

House dust mite most commonly, followed by cockroach, pollens and fungal spores on skin prick testing; total serum IgE is supportive but non-specific.

What is the role of immunotherapy in allergic rhinitis?

Subcutaneous or sublingual allergen immunotherapy, given over three to five years to patients with demonstrable allergen sensitivity uncontrolled by pharmacotherapy, is the only disease-modifying treatment.

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