Non-allergic rhinitis and Local allergic rhinitis.pdf

Nonallergic rhinitis and
Local allergic rhinitis
Suravat Homvises

Outline
• Definitions
• Classifications and subtypes
• Triggers
• Pathophysiology
• Diagnosis
• Investigations
• Local allergic rhinitis
• Nasal allergen provocation test
• Treatment
• Prognosis

Definition
• Rhinitis: inflammation of the membranes lining the nose, characterized by nasal
symptoms
• Classification: Allergic rhinitis, Nonallergic rhinitis (NAR), Mixed rhinitis (MR)
• Non-allergic rhinitis: Periodic and perennial symptoms of rhinitis that are not result
of IgE-dependent events
- Greiwe JC, Bernstein JA. J Clin Med. 2019;8(11)
- Wallace DV, et al. J Allergy Clin Immunol. 2008;122(2 Suppl):S1-84.

Phenotypes of chronic rhinitis
Hellings PW, et al. Allergy. 2017;72(11):1657-65.

Manifestations
• Nasal symptoms: rhinorrhea, nasal congestion, itching, sneezing, post-nasal drainage
• Cough
• Eye symptoms: itching, redness and swelling of the white of the eye, watering,
lid swelling, periorbital oedema
• Other symptoms: snoring, sleep problems, repeated sniffing, nasal intonation of
the voice
Scadding GK, et al. Clin Exp Allergy. 2017;47(7):856-89.

Chronic rhinitis

• Infectious rhinitis
• May be acute or chronic
• Acute rhinitis usually result of viruses, but secondary bacterial infection with sinus
involvement may be complication
• Symptoms include nasal congestion, mucopurulent discharge, pain and pressure, headache,
olfactory disturbance, postnasal drainage, cough
Subtypes
- Sur DKC, Plesa ML. Am Fam Physician. 2018;98(3):171-6.

• Non-allergic rhinopathy
• Most common subtype of chronic nonallergic rhinitis
• Known as vasomotor rhinitis or idiopathic nonallergic rhinitis
• Nasal symptoms that are triggered by environmental conditions such as strong smells or
changes in temperature, humidity, or barometric pressure
• Typically, no nasal and palatal itching or bursts of sneezing
• Usually not associated with nasal eosinophilia
Subtypes

• Nonallergic rhinitis with nasal eosinophilia syndrome (NARES)
• Inflammatory type of rhinitis with increased eosinophils in the secretions and on nasal
biopsy
• Gustatory rhinitis
• Watery rhinorrhea after ingestion specific foods (spicy foods) or liquids (alcohol)
• It is believed to be induced by a gustatory reflex associated with a hyperactive,
nonadrenergic, noncholinergic, or peptidergic neural system
• Often overlaps with senile rhinitis
Subtypes
- Hellings PW, et al. Allergy. 2017;72(11):1657-65.

• Occupational rhinitis
• Defined as an inflammation of the nasal mucosa due to exposure to a particular work
environment such as latex, flour, chemicals, and substances (HMW and LMW)
• Typically worsen throughout the work week and improve with time off
• HMW agents may induce a typical IgE-mediated allergic inflammation, giving rise to
occupational allergic disease
• Prolonged exposure to occupational agents, patients may progress to asthma
• Nonspecific nasal hyperreactivity to occupational triggers can also be found in the absence of
mucosal inflammation (occupational nonallergic rhinopathy)
• Determining and avoiding the trigger are key to treatment
Subtypes

• Hormonal-induced rhinitis
• Including menstrual cycle, puberty, pregnancy, menopause, and specific endocrine disorders
such as hypothyroidism and acromegaly
• Estrogens
• Exert vascular engorgement effect in the nose
• Lead to nasal obstruction and/or nasal hypersecretion
• Beta-estradiol and Progesterone
• Increase the expression of histamine H1-receptors on human nasal epithelial and
microvascular endothelial cells
• Induce eosinophil migration and/or degranulation
Subtypes

• Hormonal-induced rhinitis
• In contrast, testosterone decreases eosinophil activation and viability
• Pregnancy rhinitis starts after the second month of pregnancy, and usually disappears within
2 weeks after delivery
• Late menarche (>13 years of age) was statistically significantly inversely related to allergic
rhinitis development
• Endogenous hormones, hormonal contraceptives might protect young women from allergies
and asthma after puberty
Subtypes

• Drug-induced rhinitis
• Adverse events of systemic treatment
• Prolonged oral intake of aspirin, ibuprofen, and other NSAID, beta-blockers, sedatives,
antidepressants, oral contraceptives, or drugs used to treat erectile dysfunction
• Peptidergic drugs activate human mast cells through a G-protein-coupled receptor, the
Mas-related G-protein-coupled receptor X2 (MRGPRX2)
• Abuse of decongestive nasal therapy (rhinitis medicamentosa)
• Prolonged use of potent decongestant sprays
• Abrupt arrest of the use of these sprays is recommended
Subtypes

• Tryptase released from degranulated MCs activates protease-activated receptor 2 (PAR2) on
sensory nerve endings
• Release of CGRP and SP, which interact with their receptors, CGRP1 and NK1
• Promote arteriolar dilation and venular permeability
• SP released from sensory nerve ending and activated MCs acts on MCs and promotes a vicious
cycle of MC activation through MRGPRX2
Subramanian H. J Allergy Clin Immunol. 2016;138(3):700-10.

• Senile rhinitis (Geriatric rhinitis)
• Defined as rhinitis in patients above 65 years of age
• Late-onset, bilateral watery nasal secretions without endonasal mucosal and/or
anatomic pathology
• Worsens in response to patient-identified triggers, including food, odors, or
environmental irritants
• Neurogenic dysregulation is considered the cause of the symptoms as ipratropium bromide
(an anticholinergic drug) is effective in reducing the severity and duration of the rhinorrhea
in these patients
Subtypes

• Atrophic rhinitis
• Atrophy of the nasal mucosa that can lead to nasal crusting and drying
Subtypes

Nonallergic rhinitis vs Allergic rhinitis

Triggers for nonallergic rhinitis
• Environmental changes: dry cold air, humidity, barometric pressure
• Airborne irritants: odors, fumes (cologne, perfume, cleaning products, cigarette smoke,
diesel, car exhaust)
• Medications: beta-blockers, aspirin, NSAIDs
• Dietary factors: spicy food, alcohol
• Sexual arousal
• Exercise
• Strong emotions or stress
• Hormone levels
Greiwe JC, Bernstein JA. J Clin Med. 2019;8(11)

Triggers for nonallergic rhinitis

Pathophysiology
• Mucosal inflammation
• Nasal cytology
• Hyperresponsiveness and Functional abnormalities
• Intranasal cold dry air provocation (CDA)
Middleton's’ Allergy: Principle and Practice, 9th edition

Mucosal inflammation
• Nasal cytology by inferior turbinate scraping
• Symptom score determination:
• VAS <3: mild symptoms
• VAS 3-7: moderate symptoms
• VAS >7: severe symptoms
• Total score: rhinorrhea, nasal obstruction, facial pain, sneezing, loss of smell,
nasal itching, difficulty falling asleep, lacrimation, nocturnal awakening
• Partial score (irritating nasal symptoms): sneezing, nasal itching, lacrimation, rhinorrhea
de Corso E, et al. Rhinology. 2014;52(2):142-9.

Mucosal inflammation
• Sub-categories
• Non-allergic rhinitis without inflammation (NAR-)
• Non-allergic rhinitis with inflammation (NAR+)
• Non-allergic neutrophil rhinitis (NARNE): neutrophil >50%
• Non-allergic rhinitis with eosinophilia syndrome (NARES): eosinophil >20%
• Non-allergic mast cell rhinitis (NARMA): mast cells >10%
• Non-allergic eosinophilic-mast cell rhinitis (NARESMA): eosinophil >20% and
mast cells >10%

• NAR with inflammation is associated with comorbidities (previously diagnosed
asthma, aspirin tolerance)
• Non-allergic neutrophil rhinitis is the most prevalent form of NAR with inflammation

• NARNE and NAR- was very high in patients with mild and moderate symptoms
• NARES, NARMA and NARESMA also behave similarly was higher in patients
with severe symptoms
• Significant difference was found especially partial score (sneezing, nasal itching,
lacrimation, rhinorrhea)

Innervation of nasal mucosa
Van Gerven L, et al. Rhinology. 2012;50(3):227-35.

• Hyperinnervation of the nasal mucosa with increased expression of the
neuropeptides calcitonin gene related peptide (CGRP) and Substance P (SP) in
periglandular nerve fibers
• Neural regulation in the upper airways is maintained by the sympathetic (adrenergic)
and the parasympathetic (cholinergic) nervous systems
• Sympathetic nerve fibers innervate mainly the vascular structures and to a lesser
extent the secretory glands
• Release norepinephrine and neuropeptide Y (NPY)
• Vasoconstriction and a decrease in nasal secretion

• Parasympathetic fibers innervate both the blood vessels and the exocrine
(seromucous and serous) glands of the nasal mucosa
• Release predominantly acetylcholine and neuropeptide transmitters such as
vasoactive intestinal peptide (VIP)
• Increase nasal secretion and induce vasorelaxation leading to nasal congestion
under extreme conditions
• VIP mainly acts through VPAC1 and VPAC2 receptors leading to glandular
secretion

• Nonadrenergic noncholinergic (NANC) sensory nerve fibers
(intraepithelial and perivascular)
• Mainly unmyelinated sensory C-fibers contain various neuropeptides including
Substance P (SP), Calcitonin gene related peptide (CGRP), Neurokinin
A and B (NKA and NKB)
• Essential role in protective nasal clearing reflexes such as sneezing, mucus
production and congestion in response to noxious stimuli
• Considered to be responsible for the release of neuropeptides in
idiopathic rhinitis

• Intranasal cold dry air provocation (CDA)
• Preparation:
• Acclimatize to room temperature (20 C)
• Blew their nose gently to remove remaining secretions
• Nose was prerinsed with normal saline
• Cold dry air:
• Air is dried by passing column with silicon granules, filtered and entered
the nose at -10 C
Nasal hyperresponsiveness
Braat JP, et al. Am J Respir Crit Care Med. 1998;157(6 Pt 1):1748-55.

Intranasal cold dry air provocation (CDA)
• Provocation step: 1, 1, 2, 4, 8 and 16 minutes with each flow dosage
• Dosage: 12.5, 25, 50, 100, 200 and 400 L
• Inhale through the nose and exhale through the mouth
• Outcome parameters:
• Nasal patency reduction: using anterior rhinometry
• Mucus production: weighing the amount of secretions produced in preweighed
paper tissues

• CDA dose: The dose resulting in 40% reduction of nasal patency and/or 0.5 g
mucous production in 1 CDA
• 400 dose: The dose ≤400 L CDA resulting in 40% production of nasal patency
and/or 0.5 g mucous production in 1 CDA challenge
• 100 dose: The dose <100 L CDA resulting in 40% production of nasal patency
and/or 0.5 g mucous production in 1 CDA challenge

Sensitivity Specificity
Mean 100 dose 87% 71%
Mean 400 dose 94% 42%
• Cut-off point:

Diagnosis of NAR
• Based on medical history
• Duration and frequency of symptoms
• Hormonal state
• Occupational/environmental exposure to a list of triggers leading to nasal symptoms
• Systemic and nasal medication use
• Exclusion of clinically relevant sensitization to airborne allergens
• Exclusion of clinical signs of rhinosinusitis

Investigations
• Anterior rhinoscopy
• Check for signs of infection, endonasal crust formation, and/or significant
anatomic deformities
• Nasal endoscopy
• Evaluation of the whole endonasal cavity including the ostiomeatal complex
• Reveal the presence of CRSsNP or CRSwNP

Investigations
• Skin prick testing or determination of allergen-specific IgE
• Diagnosis of AR
• Clinical relevance of detected sensitization may be confirmed by history and/or
allergen provocation test
• Allergen provocation testing
• Confirm sensitization upon specific in patients that are likely to have LAR
• Microbiological analysis of the nasal content
• Not recommended in noninfectious rhinitis

Investigations
• Nasal cytology or biopsies
• Not recommended in NAR
• May help to distinguish between an inflammatory or neurogenic etiology of symptoms
• Detection of eosinophilic inflammation in cytology or biopsy in the absence of systemic
allergy may be attributed to LAR, NARES or to intolerance to drugs (such as aspirin), food
or preservatives
• Total IgE or allergen-specific IgE in nasal secretions
• Performed in a limited number of academic centers for the diagnosis of LAR
• CT scans of the sinonasal cavities
• Not recommended in rhinitis patients to exclude endonasal signs of sinonasal disease

• Localized nasal allergic response in patients with negative SPT and absence of
detectable specific IgE (sIgE) to inhalant allergens in the blood
• Characterized by
• Local production of sIgE
• Local production of Th2 cytokine pattern of mucosal cell infiltration
(eosinophils, basophils, mast cells, CD3+ T cells, and CD4+ T cells)
• Positive nasal allergen provocation test (NAPT) with release of inflammatory
mediators (tryptase and eosinophil cationic protein)
• Medical management of LAR is similar to AR, with good response to nasal
corticosteroid

IgE-mediated hypersensitivity response
Rondon C, et al. J Investig Allergol Clin Immunol. 2010;20(5):364-71

IgE-mediated hypersensitivity response
• Inhaled aeroallergens are deposited mainly in the nasal mucosa
• APCs are processed and presented to T cells
• T cells release of the mediators interleukin 4, 13
• Induction of IgE production via isotype switching in B cells
• Mast cells of the nasal mucosa induce higher levels of IgE synthesis than T cells
• IgE antibodies are synthesized by plasma cells in the nasal mucosa
• sIgE antibodies detected in the nasal secretions of patients
Rondon C, et al. J Investig Allergol Clin Immunol. 2010;20(5):364-71

• Diagnosis of LAR:
• Detection of nasal specific IgE
• Positive NAPT response, or both
• Investigations:
• NAPT with multiple aeroallergens (NAPT-M) in one session has proved to be
specific, sensitive, reproducible, and less time-consuming

Nasal allergen provocation test
Indications:
• Diagnosis of:
• Persisting allergic rhinitis
• Intermittent allergic rhinitis
• Local allergic rhinitis
• Occupational rhinitis
• Correlation with extranasal symptoms
• Differential diagnosis of ocular symptoms
• Further Evidence diagnosing food allergy
• To design allergen composition and to monitor clinical efficacy of immunotherapy
Auge J, et al. Allergy. 2018;73(8):1597-608.

Contraindications:
• Absolute contraindications:
• Previous anaphylactic reaction to the allergen
• During an acute inflammation of the nose or paranasal sinuses
• Severe comorbidities (cardiopulmonary diseases, impairment of lung capacity)
• Extremely high grade of sensitization (severe and uncontrolled bronchial asthma or
chronic obstructive pulmonary disease)
• Other severe systemic diseases (malignant tumors, autoimmune diseases)
• Systemic immunotherapy
• During pregnancy

Contraindications:
• Relative contraindications:
• Infants under the age of 5
• Unstandardized allergen extracts due to a lack of comparability and reproducibility
• Temporary contraindications:
• Acute allergic reactions in other organs
• Vaccination (wait 1 week)
• Acute viral or bacterial infection (wait 4 weeks)
• Surgery of the nose or paranasal sinuses (postpone for 6-8 weeks)
• Recent use of alcohol or tobacco for 24-48 hr before NAPT

Nasal allergen provocation test: Test day
• Performed a minimum of 4 weeks after the pollen season
• Allergen challenge should preferably be performed in the morning
• Patients should avoid any irritants (tobacco smoke, spicy food, or coffee) to minimize false results

Nasal allergen provocation test: Room conditions
• Environmental variations should be avoided
• Performed under standardized room conditions, including previous exposition, acclimation time,
room temperature, and humidity
• Room must not be contaminated by other substances (methacholine, test puffs of allergen spray
• Standardized room acclimation time of 15 minutes before baseline evaluation
• Room temperature of 20 +/- 1.5 C with a recommended humidity of 40%-60%

Nasal allergen provocation test: Medications
Tantilipikorn P, et al. Asian Pac J Allergy Immunol. 2010;28(4):225-31.

Emergency medicine:
• Antihistamines (oral/IM), Corticosteroids (oral/IM), Short acting beta-2 agonists (inhaled),
Adrenaline (IM/autoinjector), Nasal decongestants
Allergen:
• Application by spray bottles with a 50 µL/puff nozzle
• Allergen should be applied by giving 2 puffs (of 0.05 mL per puff) per nostril
(one in the inferior meatus and one on the direction of the middle turbinate)
• Avoided to spray toward the nasal septum to prevent mechanical irritation

Subjective measurement
• Symptom score: Sneezing, Nasal pruritus, Rhinorrhea, Nasal obstruction, and Ocular symptoms
Objective measurement of nasal patency
• Peak nasal inspiratory flow (PNIF)
• Easiest and cheapest
• Measure nasal airflow
• Strongly dependent on patients’ collaboration and lung function
• Intermeasurement variations can be significant
• Acoustic rhinometry (AcRh): quick and easy to preform
• Active anterior rhinomanometry (AAR): sensitive, highly specific method

Outcome interpretation

Procedures

Otolaryngology, Faculty of Medicine
Chulalongkorn University
• Nasal spray (metered-dose bottle) delivering a fixed volume of 0.125 mL/puff
• Nasal challenge test with diluents (buffered saline) was performed to exclude nasal
hyperreactivity
• Evaluation at 5 minutes after being challenged with diluents
• A positive NPT response was defined as an increase 3 of total VAS and a decrease 30% of the
average of bilateral MCA from baseline
• NPT response was evaluated at 5, 15, and 30 minutes after each challenge
• If the NPT was negative, the higher concentration of the allergen was challenged
Phothijindakul N, et al. Am J Rhinol Allergy. 2019;33(5):540-4.

• Therapeutic strategy links to the known or suspected underlying etiology
• Inflammatory rhinitis
• Anti-inflammatory treatment such as nasal/oral corticosteroids and/or
nasal/oral antihistamines
• RCTs evaluating local corticosteroids in NAR patients showed a lack of efficacy
• Drug-induced rhinitis
• Avoidance of the drug
• Noninflammatory rhinitis
• Depending on the presumed pathophysiology
Treatment

Treatment

• Irritant avoidance and smoking stop should be advised to all rhinitis patients
Treatment

Treatment

• Intranasal ipratropium
• Effective for watery rhinorrhea (level 1b)
• Topical capsaicin
• Desensitization reduced symptoms for several months in non-allergic,
non-infectious rhinitis
Treatment

• Topical corticosteroids
• Effect in skin prick test-negative rhinitis patients, probably on those with
underlying inflammation (level 1b)
• Relief was limited in subjects with low levels of nasal eosinophils in a recent study
• Topical nasal antihistamines
• Azelastine and Olopatadine (level 1b) and a combination of azelastine with
fluticasone (level 3)
• Reduced symptoms in skin prick test-negative patients over one year
Treatment

• Aspirin desensitization
• Nasal or oral aspirin challenge to establish the diagnosis of aspirin-sensitive
NAR before desensitization
• Montelukast
• Possible effect in SP-negative patients (low quality studies)
• Decongestants and oral antihistamines
• Ineffective
Treatment

Intranasal
corticosteroids
Segboer C, et al. Cochrane Database Syst Rev. 2019;2019(11).

INS vs Placebo: Total nasal symptom score <4 weeks

INS vs Placebo: Total nasal symptom score >4 weeks

INS vs Placebo: Change from baseline <4 weeks

INS vs Placebo: Epistaxis
Number needed to treat for an additional harmful outcome (NNTH) of 25

• Intranasal steroids reduced patient-reported severity in NAR patients
compared to placebo within 4 weeks of treatment
• No statistical significance difference in total nasal symptom score between
INS and placebo after 4 weeks to 3 months
• Intranasal steroids increased risk of epistaxis compared to placebo
INS vs Placebo

INS vs INS + Azelastine: TNSS >4 weeks

INS vs INS + Azelastine: Quality of life
• Combination of INS and intranasal azelastine reduced patient-reported severity and
improved quality of life in NAR patients compared to INS

Capsaicin
• Activate the transient receptor potential cation channel subfamily V, receptor 1 (TRPV1),
a nonselective cation channel functioning as a polymodal receptor in C-type fibers innervating
the human nasal mucosa
• TRPV1 activation leads to a cationic influx in the nerve terminals
• Neuronal excitation
• Antidromic release of neuropeptides
• Triggers a local inflammatory response
• Intranasal capsaicin induced by a strong excitation of the afferent C-fibers
• Defunctionalization and degeneration of nerve terminals by the massive Ca influx
Van Gerven L, et al. J Allergy Clin Immunol. 2014;133(5):1332-9, 9 e1-3.

Capsaicin and TRPV1 expression
• Patients with idiopathic rhinitis (IR) had higher baseline TRPV1 expression in the nasal
mucosa and higher concentrations of substance P (SP) in nasal secretions than healthy controls
• Expression of TRPV1 was reduced in patients with IR after capsaicin treatment.

Capsaicin
• Average VAS scores for major symptom
were significantly reduced at 4 and 12
weeks after capsaicin treatment
• Nasal obstruction and sneezing
decreased significantly at 4 and 12 weeks
• Rhinorrhea was significantly reduced
only after 12 weeks

Ipratropium bromide
• Double-blind, multicenter, randomized, parallel-group
• Trial compared the efficacy and safety of ipratropium bromide (Atrovent) nasal spray
0.03% with placebo (NSS vehicle) during a treatment period of 8 weeks in
224 patients with perennial nonallergic rhinitis
• Patients used two sprays per nostril three times a day (42 mcg of active drug)
Bronsky EA, et al. J Allergy Clin Immunol. 1995;95(5 Pt 2):1117-22.

• Both severity and duration of rhinorrhea decreased by at least 30% with ipratropium
• The reduction was significantly greater than that with the saline vehicle
Ipratropium bromide

• Significant reduction in the degree to which rhinorrhea interfered with their daily
activities and moods
(percentage of patients experiencing a significant improvement in quality of life)

Prognosis
• 180 patients who were given diagnoses of NAR in allergy clinic during 2000-2004
were re-evaluated in 2007 by using sociodemographic and clinical questionnaires,
spirometry, skin prick testing, and specific IgE to common aeroallergens
• NAR was defined by the presence of 2 or more nasal symptoms (sneezing, itching,
rhinorrhea, or nasal obstruction) plus a negative SPT response and serum specific
IgE level to aeroallergens
Rondon C, et al. J Allergy Clin Immunol. 2009;123(5):1098-102.

• Increase in the persistence (12%) and
severity of nasal symptoms (9%)
• Worsening disease (52%)
• Increase new comorbidities (24%)
• New sensitization to aeroallergens was
detected by SPT and/or specific IgE in
24% of the patients
Prognosis
Rondon C, et al. J Allergy Clin Immunol. 2009;123(5):1098-102.

Reference 1
• Middleton's’ Allergy: Principle and Practice, 9th edition
• Greiwe JC, Bernstein JA. Allergic and Mixed Rhinitis: Diagnosis and Natural Evolution. J Clin Med. 2019;8(11)
• Hellings PW, Klimek L, Cingi C, Agache I, Akdis C, Bachert C, et al. Non-allergic rhinitis: Position paper of the European Academy of Allergy and Clinical Immunology.
Allergy. 2017;72(11):1657-65.
• Subramanian H, Gupta K, Ali H. Roles of Mas-related G protein-coupled receptor X2 on mast cell-mediated host defense, pseudoallergic drug reactions, and chronic
inflammatory diseases. J Allergy Clin Immunol. 2016;138(3):700-10.
• Wallace DV, Dykewicz MS, Bernstein DI, Blessing-Moore J, Cox L, Khan DA, et al. The diagnosis and management of rhinitis: an updated practice parameter. J Allergy
Clin Immunol. 2008;122(2 Suppl):S1-84.
• Sur DKC, Plesa ML. Chronic Nonallergic Rhinitis. Am Fam Physician. 2018;98(3):171-6.
• Scadding GK, Kariyawasam HH, Scadding G, Mirakian R, Buckley RJ, Dixon T, et al. BSACI guideline for the diagnosis and management of allergic and non-allergic
rhinitis (Revised Edition 2017; First edition 2007). Clin Exp Allergy. 2017;47(7):856-89.
• de Corso E, Battista M, Pandolfini M, Liberati L, Baroni S, Romanello M, et al. Role of inflammation in non-allergic rhinitis. Rhinology. 2014;52(2):142-9.
• Van Gerven L, Boeckxstaens G, Hellings P. Up-date on neuro-immune mechanisms involved in allergic and non-allergic rhinitis. Rhinology. 2012;50(3):227-35.
• Braat JP, Mulder PG, Fokkens WJ, van Wijk RG, Rijntjes E. Intranasal cold dry air is superior to histamine challenge in determining the presence and degree of nasal
hyperreactivity in nonallergic noninfectious perennial rhinitis. Am J Respir Crit Care Med. 1998;157(6 Pt 1):1748-55

Reference 2
• Rondon C, Fernandez J, Canto G, Blanca M. Local allergic rhinitis: concept, clinical manifestations, and diagnostic approach. J Investig Allergol Clin Immunol.
2010;20(5):364-71
• Auge J, Vent J, Agache I, Airaksinen L, Campo Mozo P, Chaker A, et al. EAACI Position paper on the standardization of nasal allergen challenges. Allergy.
2018;73(8):1597-608.
• Phothijindakul N, Chusakul S, Aeumjaturapat S, Snidvongs K, Kanjanaumporn J, Ruangritchankul K, et al. Nasal Cytology as a Diagnostic Tool for Local Allergic
Rhinitis. Am J Rhinol Allergy. 2019;33(5):540-4.
• Tantilipikorn P, Vichyanond P, Lacroix JS. Nasal provocation test: how to maximize its clinical use? Asian Pac J Allergy Immunol. 2010;28(4):225-31.
• Segboer C, Gevorgyan A, Avdeeva K, Chusakul S, Kanjanaumporn J, Aeumjaturapat S, et al. Intranasal corticosteroids for non-allergic rhinitis. Cochrane Database
Syst Rev. 2019;2019(11).
• Van Gerven L, Alpizar YA, Wouters MM, Hox V, Hauben E, Jorissen M, et al. Capsaicin treatment reduces nasal hyperreactivity and transient receptor potential cation
channel subfamily V, receptor 1 (TRPV1) overexpression in patients with idiopathic rhinitis. J Allergy Clin Immunol. 2014;133(5):1332-9, 9 e1-3.
• Bronsky EA, Druce H, Findlay SR, Hampel FC, Kaiser H, Ratner P, et al. A clinical trial of ipratropium bromide nasal spray in patients with perennial nonallergic rhinitis.
J Allergy Clin Immunol. 1995;95(5 Pt 2):1117-22.
• Rondon C, Dona I, Torres MJ, Campo P, Blanca M. Evolution of patients with nonallergic rhinitis supports conversion to allergic rhinitis. J Allergy Clin Immunol.
2009;123(5):1098-102.

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