Allergic Rhinitis

Allergic rhinitis (AR) is an IgE-mediated Type I hypersensitivity inflammation of the nasal mucosa, presenting with the classic tetrad of sneezing, rhinorrhoea, nasal obstruction, and itching. It is the commonest chronic respiratory allergy and a favourite NEET PG topic for its immunology, the ARIA classification, and its tight link with asthma and nasal polyposis.

Definition & classification

Allergic rhinitis is a symptomatic disorder of the nose induced after allergen exposure by an IgE-mediated inflammation of the nasal mucosal lining. It is the nasal component of the "one airway, one disease" concept that links the upper and lower respiratory tracts (the unified airway hypothesis).

Older clinical classification:

Type	Allergen	Timing
Seasonal AR (hay fever)	Pollens (grasses, trees, weeds), outdoor moulds	Specific seasons
Perennial AR	House dust mite (Dermatophagoides), animal danders, cockroach, indoor moulds	Round the year
Occupational AR	Latex, flour (baker's), wood dust, chemicals	At workplace

High-yield: The single most important perennial allergen worldwide is the house dust mite (Dermatophagoides pteronyssinus / farinae); its faecal pellets carry the major allergen Der p 1.

ARIA (Allergic Rhinitis and its Impact on Asthma) classification — a WHO initiative that replaced the seasonal/perennial split because patients often overlap. It classifies AR on two independent axes: duration and severity.

Axis	Categories	Criteria
Duration	Intermittent	< 4 days/week OR < 4 consecutive weeks
	Persistent	≥ 4 days/week AND ≥ 4 consecutive weeks
Severity	Mild	Normal sleep, no impairment of daily activities/sport/work, no troublesome symptoms
	Moderate–severe	One or more of: abnormal sleep, impaired daily activity/sport, impaired school/work, troublesome symptoms

High-yield: Remember the ARIA cut-off as "4 and 4" — intermittent = both criteria below 4; persistent = both at or above 4. Severity is "mild" only if all quality-of-life items are normal; any single abnormality makes it moderate–severe.

Etiology & pathophysiology

AR is a textbook Type I (immediate, anaphylactic) hypersensitivity reaction mediated by IgE bound to mast cells and basophils. The response unfolds in two temporally distinct phases.

Sensitisation (first exposure): Allergen is taken up by dendritic cells → presented to naïve T cells → drive a Th2 response. Th2 cells secrete IL-4 and IL-13 (drive B-cell class-switching to IgE) and IL-5 (eosinophil maturation/recruitment). The IgE produced binds to high-affinity FcεRI receptors on mast cells. The patient is now "sensitised" but asymptomatic.

Early-phase response (re-exposure, within minutes): Allergen cross-links adjacent IgE molecules on the mast cell → degranulation. The pivotal preformed mediator is histamine, with newly synthesised leukotrienes (LTC4, LTD4, LTE4 — the cysteinyl leukotrienes), prostaglandin D2, and tryptase.

The early-phase flow: Allergen → IgE cross-linking on mast cell → degranulation → histamine release → sensory nerve stimulation (sneezing, itching), vasodilatation & glandular secretion (watery rhinorrhoea), and vascular permeability (early congestion).

High-yield: Sneezing, itching and watery rhinorrhoea are predominantly histamine-mediated (early phase) and respond well to antihistamines. Nasal blockage/obstruction is largely a late-phase, eosinophil-driven effect and responds best to intranasal corticosteroids — this clinical-pharmacology pairing is repeatedly tested.

Late-phase response (4–12 hours later): Cytokines and chemokines recruit inflammatory cells, chiefly eosinophils, along with basophils, Th2 lymphocytes and neutrophils. Eosinophils release major basic protein, eosinophil cationic protein and leukotrienes, sustaining mucosal oedema and producing the dominant persistent nasal obstruction. Repeated late-phase reactions cause the "priming effect", where progressively smaller allergen doses trigger symptoms, and non-specific nasal hyper-reactivity to irritants like smoke and cold air.

Mnemonic for Th2 cytokines: "IgE needs FOUR; eosinophils need FIVE" → IL-4 drives IgE, IL-5 drives eosinophils.

Clinical features

The classic tetrad: paroxysmal sneezing (often in bouts), watery anterior rhinorrhoea, nasal obstruction (frequently alternating between sides), and nasal/palatal/ocular itching. Associated allergic conjunctivitis (watery, itchy red eyes) is common, reflecting shared mucosal allergy.

Signs in children — examination favourites:

• Allergic shiners — dark circles/infraorbital venous congestion under the eyes.
• Allergic salute — a transverse rubbing of the nose with the palm.
• Allergic (transverse nasal) crease — a horizontal groove across the lower nasal dorsum from repeated saluting.
• Dennie–Morgan lines (folds) — accentuated creases below the lower eyelid.
• Adenoid (allergic) facies — open-mouth breathing, high-arched palate, elongated face from chronic obstruction.
• Cobblestone appearance of the posterior pharyngeal wall from lymphoid hyperplasia.

Anterior rhinoscopy classically shows a pale, bluish, boggy, oedematous nasal mucosa with bilateral swollen inferior turbinates and clear watery secretions — contrasting with the erythematous mucosa of infective rhinitis.

High-yield: A child with the allergic salute, transverse nasal crease, allergic shiners and a high-arched palate (adenoid facies) is the picture-perfect AR vignette.

Diagnosis & investigation of choice

Diagnosis is primarily clinical (history of typical symptoms with allergen exposure plus examination). Investigations confirm the allergic basis and identify the offending allergen.

Nasal smear cytology: Shows eosinophilia (> 10% eosinophils) in nasal secretions — a quick, supportive, classic finding. (Contrast: predominantly neutrophils suggest infective rhinitis.)

Peripheral blood: Absolute eosinophil count may be raised; total serum IgE is often elevated but is non-specific.

Test	What it detects	Notes / pitfalls
Skin-prick test (SPT)	Specific IgE in skin mast cells	Investigation of choice for identifying the allergen; cheap, rapid, sensitive. Stop antihistamines ~5–7 days before. Positive = wheal ≥ 3 mm over control.
Serum specific IgE (RAST / ImmunoCAP)	Allergen-specific IgE in serum	Used when SPT not feasible (dermographism, severe eczema, on antihistamines, risk of anaphylaxis). Costlier, slightly less sensitive.
Nasal smear	Eosinophilia	Supportive, not allergen-specific.
Total IgE	Overall atopy	Poor sensitivity/specificity alone.
Nasal provocation test	Mucosal response to allergen	Research / occupational AR confirmation.

High-yield: The skin-prick test is the investigation of choice to identify the causative allergen. Antihistamines must be withheld ~5–7 days before SPT (they blunt the wheal); systemic steroids generally do not need stopping for SPT.

Management & drug of choice

A stepwise, ARIA-guided approach. Allergen avoidance is first-line and underpins every step.

Stepwise approach:

1. Allergen avoidance & environmental control → dust-mite-proof bedding covers, washing linen in hot water, removing carpets/pets, reducing humidity, avoiding pollen exposure.
2. Pharmacotherapy tailored to ARIA category (see below).
3. Allergen-specific immunotherapy (SIT) for proven IgE-mediated disease not controlled by avoidance + drugs, or where long-term disease modification is desired.

Pharmacological agents:

Drug class	Best for	Key points
Oral 2nd-gen antihistamines (cetirizine, levocetirizine, loratadine, fexofenadine)	Sneezing, itching, rhinorrhoea	Non-sedating, preferred over 1st-gen (chlorpheniramine, diphenhydramine which cause sedation/anticholinergic effects).
Intranasal corticosteroids (INCS) — fluticasone, mometasone, budesonide	Nasal obstruction; most effective single agent overall	Drug of choice for moderate–severe persistent AR. Act on both early & late phases; onset over days.
Intranasal antihistamines (azelastine)	Rapid local relief	Faster onset than oral; azelastine + fluticasone combination is highly effective.
Leukotriene receptor antagonists (montelukast)	AR with coexisting asthma	Useful add-on, especially in the asthma–AR overlap.
Intranasal cromolyn (mast-cell stabiliser)	Prophylaxis	Needs frequent dosing; weaker; useful pre-exposure.
Intranasal anticholinergic (ipratropium)	Profuse watery rhinorrhoea	Targets secretions specifically.
Decongestants (oral pseudoephedrine; topical oxymetazoline)	Short-term congestion relief	Topical use > 5–7 days causes rhinitis medicamentosa (rebound congestion) — a classic exam trap.

High-yield: Intranasal corticosteroids are the single most effective drug class and the drug of choice for moderate–severe and persistent AR, because they suppress the eosinophil-driven late phase responsible for nasal blockage.

High-yield: Allergen-specific immunotherapy (SIT) — subcutaneous (SCIT) or sublingual (SLIT) — is the only treatment that can alter the natural course of the disease, induce long-lasting tolerance, and may prevent progression to asthma and development of new sensitisations. It works by shifting Th2 → Th1, inducing regulatory T cells and blocking IgG4 antibodies, and reducing IgE over time.

ARIA treatment logic:

• Mild intermittent → oral/intranasal antihistamine ± decongestant PRN.
• Moderate–severe intermittent / mild persistent → INCS or antihistamine; step up as needed.
• Moderate–severe persistent → INCS first-line, combine with antihistamine/LTRA; review in 2–4 weeks; consider immunotherapy.

Omalizumab (anti-IgE monoclonal) is reserved for severe refractory allergic disease/overlap with allergic asthma.

Complications

• Bronchial asthma — the strongest association; AR is an independent risk factor and frequent precursor (unified airway). Treating AR improves asthma control.
• Nasal polyposis — bilateral, bluish, mobile, insensitive (non-tender) grape-like masses; chronic mucosal oedema is the substrate.
• Chronic rhinosinusitis — ostial obstruction predisposes to recurrent/chronic sinusitis.
• Serous otitis media (otitis media with effusion) — Eustachian tube dysfunction, especially in children → conductive hearing loss.
• Sleep-disordered breathing, snoring, OSA, poor concentration and reduced quality of life.
• Rhinitis medicamentosa — iatrogenic, from prolonged topical decongestant abuse.

High-yield: The AR ↔ nasal polyp ↔ asthma triad is a recurrent NEET PG theme. Note: in the Samter's triad (aspirin-exacerbated respiratory disease) = asthma + nasal polyps + aspirin/NSAID sensitivity, the polyps are typically associated with non-allergic eosinophilic mechanisms — distinguish it from simple atopic polyposis.

Key differentials

Condition	Distinguishing features
Vasomotor (non-allergic) rhinitis	Triggered by temperature change, odours, spicy food; negative SPT, normal IgE, no eosinophilia; autonomic imbalance.
NARES (non-allergic rhinitis with eosinophilia)	Marked nasal eosinophilia but negative allergy tests (normal IgE, negative SPT); may precede aspirin-sensitive asthma.
Infective (viral/bacterial) rhinitis	Mucopurulent discharge, erythematous mucosa, neutrophils on smear, systemic symptoms, self-limiting.
Rhinitis medicamentosa	History of prolonged nasal decongestant use; rebound congestion.
CSF rhinorrhoea	Unilateral clear watery discharge, positive for beta-2 transferrin / glucose, increases on bending forward; trauma history.
Atrophic rhinitis (ozaena)	Nasal crusting, foul smell (merciful anosmia), roomy nasal cavity.
Hormonal / drug-induced rhinitis	Pregnancy, hypothyroidism, OCPs, beta-blockers, ACE inhibitors.

High-yield: NARES = eosinophils present but allergy tests negative; vasomotor rhinitis = neither eosinophilia nor positive allergy tests. Use the nasal smear + SPT/IgE pattern to separate them in single-best-answer questions.

Recently asked / exam angle

• Immunology: Type I hypersensitivity; IL-4 → IgE, IL-5 → eosinophils; early phase = histamine, late phase = eosinophils.
• ARIA classification numbers ("4 days/4 weeks") and the mild vs moderate–severe quality-of-life criteria — direct factual recall questions.
• Investigation of choice = skin-prick test; antihistamines stopped 5–7 days prior; nasal smear shows > 10% eosinophils.
• Drug of choice for moderate–severe persistent AR = intranasal corticosteroid; immunotherapy is the only disease-modifying therapy.
• Rhinitis medicamentosa from topical decongestant overuse (> 5–7 days) — pharmacology trap.
• Allergic salute, transverse nasal crease, allergic shiners, Dennie–Morgan lines, adenoid facies — clinical-sign image/vignette questions.
• AR–asthma–nasal polyp association and differentiation from Samter's triad.
• Differentiating NARES vs vasomotor rhinitis by eosinophilia and allergy testing.
• Major house dust mite allergen and Dermatophagoides as the chief perennial allergen.

Rapid revision

1. AR = IgE-mediated Type I hypersensitivity of nasal mucosa; classic tetrad = sneezing, rhinorrhoea, obstruction, itching.
2. Early phase = histamine (sneeze/itch/watery discharge); late phase = eosinophils (nasal blockage).
3. IL-4/IL-13 → IgE; IL-5 → eosinophils; mast-cell IgE on FcεRI receptors.
4. ARIA: Intermittent = < 4 days/wk or < 4 wk; Persistent = ≥ 4 days/wk and ≥ 4 wk.
5. ARIA severity is mild only if sleep, activity, work and symptoms are all normal — else moderate–severe.
6. Commonest perennial allergen = house dust mite (Dermatophagoides, allergen Der p 1).
7. Nasal smear shows > 10% eosinophils; mucosa is pale, boggy, bluish.
8. Skin-prick test = investigation of choice; stop antihistamines 5–7 days before; serum specific IgE if SPT not feasible.
9. Intranasal corticosteroid = drug of choice for moderate–severe persistent AR; 2nd-gen antihistamines preferred for sneeze/itch.
10. Immunotherapy (SCIT/SLIT) is the only disease-modifying treatment; works via Treg induction, Th2→Th1 shift, blocking IgG4.
11. Topical decongestant > 5–7 days → rhinitis medicamentosa (rebound congestion).
12. Complications/associations: asthma, bilateral nasal polyps, chronic sinusitis, otitis media with effusion; differentiate from NARES (eosinophils, negative tests) and vasomotor rhinitis (no eosinophils, negative tests).