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NARES (Nonallergic Rhinitis with Eosinophilia Syndrome)

Distinct subtype of nonallergic rhinitis defined by chronic perennial nasal symptoms (sneezing, watery rhinorrhea, congestion, anosmia) with negative allergy testing but >20 percent eosinophils in nasal cytology smear; often a precursor to chronic rhinosinusitis with nasal polyps and aspirin-exacerbated respiratory disease (Samter triad); treated with intranasal corticosteroids, antihistamine sprays, leukotriene receptor antagonists, and aspirin desensitization in select cases.

Written by: Saygı Hospital Health Guide Editorial Board
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This content has been compiled by the Saygı Hospital Health Guide Editorial Board and is periodically reviewed by a specialist physician.

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What is NARES (Nonallergic Rhinitis with Eosinophilia Syndrome)?

NARES (Nonallergic Rhinitis with Eosinophilia Syndrome) is a distinct clinical entity first described by Jacobs and colleagues in 1981, characterized by chronic perennial nasal symptoms (sneezing, watery rhinorrhea, congestion, hyposmia, anosmia, postnasal drip) in the absence of demonstrable IgE-mediated allergy but with significant eosinophilic inflammation in nasal mucosa. Prevalence approximately 15–33 percent of nonallergic rhinitis (NAR) cases, more common in adults than children, slight female predominance, mean age of onset 30–40 years.

Diagnostic criteria: (1) chronic perennial nasal symptoms for >12 weeks; (2) negative skin prick testing or absence of serum specific IgE for common aeroallergens; (3) nasal cytology smear (anterior or middle meatus, Hansel or Wright stain) demonstrating eosinophilic infiltration — most criteria require >20 percent eosinophils of total inflammatory cells (some use >25 percent or >5–10 percent thresholds), with >100 eosinophils per high-power field on average; (4) absence of overt nasal polyposis on initial examination (although nasal polyps often develop later), absence of asthma or aspirin sensitivity initially (which may develop later as part of progression to AERD).

Pathophysiology involves Th2-skewed inflammatory response with locally elevated IL-5, IL-13, eosinophil-active chemokines (CCL11/eotaxin-1, CCL24/eotaxin-2), with local eosinophil recruitment, activation, and degranulation despite negative systemic IgE responses. May represent: (a) localized allergic rhinitis (entopy) — local IgE production with negative systemic testing, (b) pre-polyp eosinophilic mucosal disease, (c) early manifestation of aspirin-exacerbated respiratory disease (AERD/Samter triad), (d) primary nonallergic eosinophilic rhinitis. Strong association with subsequent development of nasal polyposis (50 percent over years to decades), asthma, and aspirin/NSAID sensitivity (Samter triad).

Differential diagnosis of nonallergic rhinitis subtypes (each requires distinct workup): (1) NARES — eosinophils >20 percent on cytology; (2) Vasomotor rhinitis — autonomic dysfunction triggered by temperature, humidity, strong odors; (3) Idiopathic rhinitis — no identifiable trigger or eosinophilia; (4) Drug-induced rhinitis (rhinitis medicamentosa) — chronic decongestant overuse, antihypertensives (beta-blockers, ACE inhibitors); (5) Hormonal rhinitis — pregnancy, hypothyroidism; (6) Atrophic rhinitis — primary or post-surgical; (7) Gustatory rhinitis — food triggers; (8) Occupational rhinitis — irritant or allergic. NARES is distinguished by eosinophil count and clinical pattern.

Symptoms

Paroxysmal sneezing fits (often >5 sneezes in succession)
Copious watery rhinorrhea (often profuse, requiring frequent nose-blowing)
Nasal congestion and blockage with mouth breathing
Severe hyposmia or anosmia (loss of smell out of proportion to visible inflammation)
Postnasal drip with throat clearing or chronic cough
Itchy nose, eyes, or palate (less prominent than allergic rhinitis)
Facial pressure or fullness over sinuses
Symptoms perennial without clear seasonal variation
Symptoms not improved with antihistamines alone
Negative skin prick test or specific IgE despite allergic-appearing symptoms

Risk Factors

Adult onset (mean age 30–40 years)
Slight female predominance
History of asthma or aspirin sensitivity (Samter triad development)
History of nasal polyps or chronic rhinosinusitis with polyps
Family history of nasal polyposis or aspirin sensitivity
Tobacco smoke exposure
Air pollution and occupational irritant exposure
Frequent upper respiratory tract infections in childhood (possibly)
Concurrent eosinophilic conditions (eosinophilic esophagitis, atopic dermatitis)
Genetic factors (incompletely understood)

When to See a Doctor?

If you experience any of the following symptoms, seek medical attention promptly:

  • Chronic perennial nasal symptoms unresponsive to first-line antihistamines
  • Severe loss of smell with nasal congestion
  • Frequent paroxysmal sneezing fits with copious clear rhinorrhea
  • Negative allergy testing despite allergic-appearing nasal symptoms
  • Coexistence of asthma, nasal polyps, or aspirin sensitivity (suspect AERD/Samter)
  • Failed conventional rhinitis therapy after 4–6 weeks
  • Worsening symptoms with NSAID use
  • Need for diagnostic nasal cytology to differentiate rhinitis subtypes
  • Recurrent sinus infections in setting of chronic rhinitis
  • Consideration of biologic therapy in severe refractory cases

Treatment Methods

01
Diagnostic workup: detailed history (chronicity, triggers, NSAID use, asthma, smell loss), physical examination (anterior rhinoscopy and nasal endoscopy with topical anesthesia and decongestion to assess polyps, mucosal pallor and edema, drainage), nasal cytology smear (Hansel or Wright stain — eosinophils >20 percent diagnostic for NARES), comprehensive aeroallergen skin prick testing or serum specific IgE panel (negative for NARES), paranasal sinus CT (Lund-Mackay scoring for sinus opacification and polyp burden), spirometry to screen for asthma, baseline complete blood count with differential (peripheral eosinophilia in 30 percent), aspirin/NSAID challenge in controlled setting if AERD suspected (high risk; performed only by trained allergists)
02
Lifestyle and environmental: avoidance of nonspecific irritants (smoke, strong odors, air pollution), avoidance of nasal decongestant overuse (prevents rhinitis medicamentosa), saline nasal irrigation 1–2 times daily (high-volume large-particle), humidified air during dry seasons, smoking cessation
03
First-line pharmacotherapy: intranasal corticosteroid spray (fluticasone propionate 50–100 mcg twice daily, mometasone furoate 100 mcg twice daily, ciclesonide 200 mcg twice daily, beclomethasone, budesonide) — most effective single-agent therapy for NARES; onset 3–7 days, full effect 2–4 weeks; counsel on proper technique (head forward, point spray laterally, avoid septum to prevent epistaxis), monitor for nasal dryness, irritation, septal perforation (rare)
04
Second-line and add-on: intranasal antihistamine sprays (azelastine 0.1 percent, olopatadine 0.6 percent — useful add-on with rapid onset), oral leukotriene receptor antagonists (montelukast 10 mg daily — particularly useful in NARES given Th2 inflammation and AERD risk), oral antihistamines (less effective in pure NARES due to non-IgE mediated mechanism but may help itching), ipratropium bromide nasal spray for severe rhinorrhea
05
Refractory or severe disease: short oral corticosteroid course (prednisolone 30 mg/day tapered over 7–10 days for severe flares — avoid chronic use), endoscopic sinus surgery (FESS) if established CRSwNP (functional endoscopic sinus surgery with polypectomy, antrostomy, ethmoidectomy, frontal recess clearance); aspirin desensitization in confirmed AERD — initiated in hospital with incremental aspirin doses to achieve tolerance, then maintained on daily aspirin 325–650 mg or higher to suppress polyp regrowth and improve asthma control
06
Biologic therapy for severe CRSwNP with NARES progression or AERD: dupilumab (IL-4Rα antagonist — 300 mg every 2 weeks, FDA-approved for CRSwNP since 2019, dramatically improves polyp size, smell, and quality of life), mepolizumab and reslizumab (anti-IL-5 — for high eosinophilic disease), omalizumab (anti-IgE — selective benefit), benralizumab (anti-IL-5 receptor — emerging)
07
Dietary and aspirin/NSAID management: identify and document NSAID sensitivity, instruct strict NSAID avoidance unless desensitized (acetaminophen and selective COX-2 inhibitors generally tolerated), consider salicylate-low diet in some patients (limited evidence)
08
Comorbidity screening: asthma evaluation with spirometry every 6–12 months; periodic nasal endoscopy for polyp surveillance; vision examination if long-term oral corticosteroid use
09
Patient education: chronic disease nature, treatment adherence importance, NSAID avoidance, emergency action plan for AERD reactions, when to seek urgent care
10
Long-term: regular follow-up every 3–6 months for symptom and disease activity assessment, repeat nasal cytology if symptom change, watch for progression to nasal polyposis (FESS may be needed), recognize AERD development and refer for desensitization, multidisciplinary team (allergist-immunologist, otolaryngologist, pulmonologist) for complex cases

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