3. RHINITIS
Rhinitis is characterized by 1 or more of the
following symptoms: nasal congestion,
rhinorrhea (anterior and posterior), sneezing,
and itching.
Nonallergic rhinitis is characterized by periodic
or perennial symptoms of rhinitis that are not a
result of IgE-dependent events.
Dana V. Wallace, Mark S. Dykewicz, The diagnosis and management of rhinitis: An updated practice parameter, J Allergy Clin Immunol 2008
4. Nonallergic Rhinitis
NAR is defined as a symptomatic inflammation of the
nasal mucosa with the presence of a minimum of two
nasal symptoms such as nasal obstruction, rhinorrhea,
sneezing, and/or itchy nose, without clinical evidence of
endonasal infection and without systemic signs of
sensitization to inhalant allergens.
Symptoms of NAR may have a wide range of severity
and be either continuously present and/or induced by
exposure to unspecific triggers, also called nasal
hyperresponsiveness.
P. W. Hellings , Non-allergic rhinitis: Position paper of the European Academy of Allergy and Clinical Immunology , Allergy. 2017
5. P. W. Hellings , Non-allergic rhinitis: Position paper of the European Academy of Allergy and Clinical Immunology , Allergy. 2017
The ratio of allergic to pure nonallergic rhinitis 3:1
Data suggest that 44%-87% of patients with rhinitis may have
mixed rhinitis.
Dana V. Wallace, Mark S. Dykewicz, The diagnosis and management of rhinitis: An updated practice parameter, J Allergy Clin Immunol 2008
6. P. W. Hellings , Non-allergic rhinitis: Position paper of the European Academy of Allergy and Clinical Immunology , Allergy. 2017
7. Classification of nonallergic rhinitis subtype
Nonallergic rhinopathy: previously known as vasomotor rhinitis,
irritant-induced rhinitis, and idiopathic rhinitis
Nonallergic rhinitis with eosinophila
Drug-induced rhinitis (ie, rhinitis medicamentosa)
Hormonal-induced rhinitis
Atrophic rhinitis
Senile rhinitis
Gustatory rhinitis (rhinorrhea associated with eating)
Cerebral spinal fluid leak manifesting as rhinorrhea
Justin Greiwe, MDa,b, Jonathan A. Bernstein, MD , Nonallergic Rhinitis Diagnosis , Immunol Allergy Clin N Am ,2016
8. Type of Rhinitis
Dana V. Wallace, Mark S. Dykewicz, The diagnosis and management of rhinitis: An updated practice parameter, J Allergy Clin Immunol 2008
9. Nonallergic Rhinitis Allergic Rhinitis
Onset of symptoms later in life Usually presents in
childhood
Perennial symptoms in nature
with very little seasonal
variation
Most have seasonal
exacerbation of symptoms
Negative aeroallergen skin
testing
And /or serum igE testing
Positive aeroallergen skin
test and/or serum igE
testing
Justin Greiwe, MDa,b, Jonathan A. Bernstein, MD , Nonallergic Rhinitis Diagnosis , Immunol Allergy Clin N Am ,2016
10. Nonallergic Rhinitis Allergic Rhinitis
Broad range of irritant triggers Aeroallergen triggers
Symptoms include
- Nasal congestion
- Postnasal drainage
Symptoms include
- Congestion , sneezing , rhinorrhea and
nasal itch
- Ocular conjunctivitis , watering and itch
Nasal mucosa can be normal with
increased clear watery secretions
, may be erythematous or atrophic
Nasal mucosa edematous ,pale
,and boggy
Allergic shiners
Justin Greiwe, MDa,b, Jonathan A. Bernstein, MD , Nonallergic Rhinitis Diagnosis , Immunol Allergy Clin N Am ,2016
11. Symptoms
Justin Greiwe, MDa,b, Jonathan A. Bernstein, MD , Nonallergic Rhinitis Diagnosis , Immunol Allergy Clin N Am ,2016
12. Testing for specific IgE antibody
- Skin tests are the preferred test for diagnosis of the
IgE-mediated sensitivity .
- In vitro assays for specific IgE – The precise
sensitivity of specific IgE immunoassays compared
with skin prick/puncture tests is approximately 70%-
75%
Dana V. Wallace, Mark S. Dykewicz, The diagnosis and management of rhinitis: An updated practice parameter, J Allergy Clin Immunol 2008
13. Justin Greiwe, MDa,b, Jonathan A. Bernstein, MD , Nonallergic Rhinitis Diagnosis , Immunol Allergy Clin N Am ,2016
14. Mechanism of Action
Inflammation (A Th2 cytokine inflammatory pattern is found in AR
patients, as well as in those with occupational allergic rhinitis induced by
high molecular weight (HMW) allergens , LAR )
Neurogenic Mechanism including rhinitis of the elderly, gustatory
rhinitis, some forms of occupational rhinitis, some forms of drug induced
rhinitis, and IR )
P. W. Hellings , Non-allergic rhinitis: Position paper of the European Academy of Allergy and Clinical Immunology , Allergy. 2017
16. clinical evaluation and nasal cytology
two groups: patients without inflammation
(symptomatic patients without evidence for nasal cytology with
a cellular inflammatory infiltrate);
patients with inflammation
(symptomatic patients with evidence for nasal cytology with a
cellular inflammatory infiltrate).
into 4 subgroups according to the results of the cytological
nasal smear:
• NAR with eosinophils (NARES): eosinophils > 20% of total cells.
• NAR with neutrophils (NARNE): neutrophils > 50% of total cells.
• NAR with mast cells (NARMA): mast cells > 10% of total cells.
• Mixed NAR with eosinophils and mast cells (NARESMA): eosinophils > 20% and
mast cells > 10% of total cells
Eugenio De Corso , Role of inflammation in non-allergic rhinitis ,Rhinology 52: 142-149, 2014
17. Eugenio De Corso , Role of inflammation in non-allergic rhinitis ,Rhinology 52: 142-149, 2014
18. Dennis Shusterman , Nonallergic Rhinitis Environmental Determinants , Immunol Allergy Clin N Am 36 (2016) 379–399
NEUROGENIC MECHANISM
20. VASOMOTOR RHINITIS
(idiopathic rhinitis)
Heterogenous group , not immunologic or infection in
origin and is usually not associated with nasal
eosinophilia .
Rhinorrhea – enhanced cholinergic glandular
secretory activity , atropinelike agents effectively
reduce secretions .
Dana V. Wallace, Mark S. Dykewicz, The diagnosis and management of rhinitis: An updated practice parameter, J Allergy Clin Immunol 2008
21. Rhinitis from foods and alcohol
After ingestion of foods or alcoholic products .
Gustatory rhinitis is characterized by watery
rhinorrhea after ingestion of hot and spicy food.
induced by a gustatory reflex associated with a
hyperactive, nonadrenergic, noncholinergic, or
peptidergic neural system.
Result of vagally mediated mechanism .
Response to intranasal cholinergic agents
Dana V. Wallace, Mark S. Dykewicz, The diagnosis and management of rhinitis: An updated practice parameter, J Allergy Clin Immunol 2008
P. W. Hellings , Non-allergic rhinitis: Position paper of the European Academy of Allergy and Clinical Immunology , Allergy. 2017
22. Occupational rhinitis
Response to air-borne substances in the workplace.
Allergic and nonallergic factors
In case of prolonged exposure to occupational
agents, patients may progress to asthma.
Dana V. Wallace, Mark S. Dykewicz, The diagnosis and management of rhinitis: An updated practice parameter, J Allergy Clin Immunol 2008
P. W. Hellings , Non-allergic rhinitis: Position paper of the European Academy of Allergy and Clinical Immunology , Allergy. 2017
23. Dennis Shusterman , Nonallergic Rhinitis Environmental Determinants , Immunol Allergy Clin N Am 36 (2016) 379–399
24. Dennis Shusterman , Nonallergic Rhinitis Environmental Determinants , Immunol Allergy Clin N Am 36 (2016) 379–399
25. Dennis Shusterman , Nonallergic Rhinitis Environmental Determinants , Immunol Allergy Clin N Am 36 (2016) 379–399
26. NARES
Nasal eosinophil in patients , perennial symptoms
and occasional reduced sense of smell .
Middle ages
NARES may precede the development of nasal
polyposis and aspirin sensitivity .
NARES increased risk for the development of
obstructive sleep apnea.
Dana V. Wallace, Mark S. Dykewicz, The diagnosis and management of rhinitis: An updated practice parameter, J Allergy Clin Immunol 2008
27. Hormonal rhinitis
Pregnancy rhinitis , significant nasal congestion , starts after
second month of pregnancy , and usually disappears within 2
weeks after delivery.
Menstrual cycle-related rhinitis .
Estrogens exert a vascular engorgement effect in the nose,
which may 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 and induce eosinophil
migration and/or degranulation
Dana V. Wallace, Mark S. Dykewicz, The diagnosis and management of rhinitis: An updated practice parameter, J Allergy Clin Immunol 2008
P. W. Hellings , Non-allergic rhinitis: Position paper of the European Academy of Allergy and Clinical Immunology , Allergy. 2017
28. Dana V. Wallace, Mark S. Dykewicz, The diagnosis and management of rhinitis: An updated practice parameter, J Allergy Clin Immunol 2008
29. Dana V. Wallace, Mark S. Dykewicz, The diagnosis and management of rhinitis: An updated practice parameter, J Allergy Clin Immunol 2008
30. Drug-induced rhinitis
ACE inhibitors
Phosphodiesterase-5-selective inhibitors
Phentolamine
Aspirin
NSAIDS
α- receptor antagonists
Rhinitis medicamentosa – syndrome of rebound nasal congestion –
overuse of intranasal α- adrenergic decongestants(oxymetazoline and
phenylephrine) or cocaine . Benzalkonium chloride is vasoconstrictor
spray – develop rebound congestion , tachyphylaxis , reduced
mucociliary clearance .
Dana V. Wallace, Mark S. Dykewicz, The diagnosis and management of rhinitis: An updated practice parameter, J Allergy Clin Immunol 2008
31. Atrophic rhinitis
Empty nose syndrome – absence of identifiable turbinates
on sinus CT
Secondary atrophic rhinitis result of chronic sinusitis or
excessive surgery to the nasal turbinates .
Dana V. Wallace, Mark S. Dykewicz, The diagnosis and management of rhinitis: An updated practice parameter, J Allergy Clin Immunol 2008
32. Senile rhinitis or rhinitis in elderly
above 65 years of age
diagnosis of senile rhinitis most often refers to
those patients with late-onset, bilateral watery nasal
secretions without endonasal mucosal and/or anatomic
pathology.
A neurogenic dysregulation is considered the cause of the
symptoms as ipratropium bromide, that is, an anticholinergic
drug, is effective in reducing the severity and duration of the
rhinorrhea in these patients.
P. W. Hellings , Non-allergic rhinitis: Position paper of the European Academy of Allergy and Clinical Immunology , Allergy. 2017
33. Conditions that mimic rhinitis
Nasal polys
Anatomical abnormalities
Cerebral spinal fluid rhinorrhea ( β-2-transferrin ) giving
rise to (unilateral) watery discharge from the nose. CSF leakage should be
considered in those patients with a relevant history and rhinorrhea not responding
to nasal corticosteroids, ipratropium bromide, or capsaicin nasal treatment
Ciliary dysfunction
Dana V. Wallace, Mark S. DykP. W. Hellings , Non-allergic rhinitis: Position paper of the European Academy of Allergy and Clinical Immunology , Allergy. 2017
ewicz, The diagnosis and management of rhinitis: An updated practice parameter, J Allergy Clin Immunol 2008
34. LOCAL allergic rhinitis
Entopy
Localized nasal allergic response in patients with negative SPT and absence of
detectable specific igE (sIgE) to inhalant allergens in the blood
diagnosis of LAR can be confirmed by the detection of nasal sIgE, a positive NAPT
response, or both.
The NAPT is a key tool for the diagnosis although it is time-consuming. NAPT with
multiple aeroallergens (NAPT-M) in one session has proved to be specific, sensitive,
reproducible, and less time-consuming (75% reduction in the number of visits for
diagnosis of NAR, and a 55% for LAR).
Basophil activation test in peripheral blood is very specific and less time-consuming and
supports the diagnosis of LAR.
Medical management of LAR is similar to AR, with good response to nasal
corticosteroids.
P. W. Hellings , Non-allergic rhinitis: Position paper of the European Academy of Allergy and Clinical Immunology , Allergy. 2017
39. International Forum of Allergy & Rhinology, Vol. 7, No. 9, September 2017
Key findings of this study are that using
allergen sensitization (SPT, serum sIgE) alone can result
in a misdiagnosis occurring in 13.7% of AR patients and
24.7% of NAR
40. Nasal provocation testing
Clinical Indications for NPT
1. To identify specific allergen in the nasal target organ using allergen preparations.
2. To confirm the role of a special occupational agent
3. To confirm the clinical relevance of a specific allergen in patients with multiple positive
allergy skin tests.
4. To assess the role of allergens implicated by a patient’s history when allergy skin test and/or
RAST are negative or when the reactions of the nasal mucosa to an allergen are more
pronounced than those of skin.
5. To investigate food-induced rhinorrhea.
6. To determine if nasal application of allergen can induce symptoms in the conjunctiva,
middle ear, sinus, and lower respiratory airways.
7. To confirm the allergic nature of asthma, since positive nasal reactions may be obtained
when the corresponding bronchial provocation tests are negative or can not be safely
performed.
8. To confirm nasal reactivity before starting local nasal immunotherapy.
Ludmila I. Litvyakova , Ann Allergy Asthma Immunol 2001;86:355–365
41. Absolute Contraindications
1. Acute bacterial or viral rhinitis or sinusitis
2. Acute period or exacerbation of allergic disease
(rhinitis, food allergy, drug allergy, insect allergy, urticaria)
3. Previous anaphylactic reaction to an allergen
4. Severe general diseases or acute period of diseases,
especially severe asthma, obstructive bronchial diseases,
cardiopulmonary diseases with restricted lung capacity
5. Pregnancy
Ludmila I. Litvyakova , Ann Allergy Asthma Immunol 2001;86:355–365
43. Outcome measurement
True positive response at least two of the following three criteria: 5
sneezes, 50% fall in NPEFR, or rhinorrhea .
German guidelines, positive test flow reduction <40% and/or more than
three score points: secretion, 0 to 2 points (moderate, 1 point; severe, 2
points); sneezing, 0 to 2 points (0 to 2 sneezes = 0 point; 3 to 5 sneezes
=1 point; >5 sneezes = 2 points); additional symptoms such as tearing,
itching (eyes, throat) =1 point; conjunctivitis, cough, urticaria, and/or
dyspnea = 2 points.
Positive NPT with a decrease of 20% or more in NEPFR and occurrence
of nasal symptoms such as sneezes, rhinorrhea, nasal blockage and
itching. Changes in
the nasal temperature (using thermography) and the pH of nasal
secretions have also been proposed as endpoints
Ludmila I. Litvyakova , Ann Allergy Asthma Immunol 2001;86:355–365
44. Nasal Provocation. Unilateral administration of allergen or other materials may lead to local,
ipsilateral responses, and parasympathetic reflex effects
45.
46. Van Gerven et al.: Cold Dry Air Exposure for NHR DiagnosisLaryngoscope 122: December 2012
47. Van Gerven et al.: Cold Dry Air Exposure for NHR DiagnosisLaryngoscope 122: December 2012
52. Fig. 1. Changes in nasal specific IgE (nsIgE)/protein ratios after a nasal provocation test with Dermatophagoides pteronyssinus.
There were no differences in the mean nsIgE values between patients with local allergic rhinitis (LAR) or allergic rhinitis (AR),
but there was a statistically significant difference in comparison to the control group for all time points analyzed
(p < 0.001).
Anna Krajewska-Wojtys Jerzy Jarzab, Int Arch Allergy Immunol 2017;173:165–170
53. Fig. 2. Changes in nasal specific IgE (nsIgE)/protein ratios after a nasal provocation test with Alternaria.
Changes in the mean nsIgE values between patients with local allergic rhinitis (LAR)/allergic rhinitis (AR)
and controls for all time points analyzed (* p < 0.001–0.013).
Anna Krajewska-Wojtys Jerzy Jarzab, Int Arch Allergy Immunol 2017;173:165–170
55. Special diagnostic technique
Fiber optic nasal endoscopy
CT and MRI
Rhinomanometry and acoustic rhinometry
Nasal provocation testing
Nasal cytology
Saccharin test and cilia biopsy
Dana V. Wallace, Mark S. Dykewicz, The diagnosis and management of rhinitis: An
updated practice parameter, J Allergy Clin Immunol 2008
61. Therapeutic strategy of nonallergic rhinitis
P. W. Hellings , Non-allergic rhinitis: Position paper of the European Academy of Allergy and Clinical Immunology , Allergy. 2017
Notes de l'éditeur
rhinitis of the elderly that mostly seems to be a dysregulation of the parasympathetic/sympathetic neural dysbalance.
rhinitis medicamentosa, resulting in dysregulation of adrenergic receptors in nasal mucosa and in a relative increase in the parasympathetic drive,leading to significant rhinorrhea and nasal obstruction
mall diameter nociceptive neurons(C- and Ad-fibers) constituting the terminal branches of the trigeminal nerve areinvested with wide variety of nociceptive ion channels with both thermal and chemicalresponsiveness.9–12 The C-fiber population also elaborates vasoactive neuropeptides,which in turn can be released locally as part of nociceptive reflexes. Classic examples include rhinorrhea occurring in response toconsumption of spicy foods (“gustatory rhinitis”) and cold air–induced rhinorrhea(“skier’s nose”), both of which can be blocked symptomatically by the topical application of a cholinergic antagonist.22,23 This clinical response, as well as the results ofnumerous nasal provocation experiments, have implicated a central parasympatheticreflex in most reflex rhinorrhea.
THE TRhe transient receptor potential (TRP) receptors, TRP vanilliod 1 (TRPV1)and TRP ankyrin 1 (TRPA1), are perhaps of particular note. TRPV1 is the receptor forcapsaicin. Several triggers activate TRPA1, including cold dry air as well as dietary isothiocyanates (mustard, wasabi, horseradish), allicin (garlic and onion), environmentalisothiocyanates, formalin, toluene, ozone, chlorite, and noxious components of smoke(acrolein, methacrolein, croton aldehyde).37–54 TRPV1 and TRPA1 sensitization andactivation patterns are summarized TRPV1 and TRPA1 sensitization and activation patterns. Inflammatory mediators,neurokinins, hormones including histamine, LT, acetylcholine, prostaglandins, proteasesincluding tryptase, bradykinin, MIP1 alpha, tumor necrosis factor (TNF) alpha, insulingrowth factor 1 (IGF-1), prolactin, nerve growth factor (NGF), somatostatin, and calcitoningene-related peptide (CGRP) act via their receptors to activate kinase and phospholipasesystems, which prime TRPV1. Priming of TRPA1 is less defined. Once primed, the receptorsbecome more susceptible to activation by endogenous and exogenous compounds. Activation results in a preferential influx of calcium and, in the case of sensory nerves, depolarization. This process promotes active exocytosis of neuromediators at the peripheral nerveterminals. The later process is reported to comprise the major component of neurogenicinflammation. BK, bradykinin; LT, Leukotriene; MIP1, Macrophage Inflammatory Protein;PC, phospholipase C; PG, prostaglandin; SP, substance P; VOC, volatile organic compound.
Nasal Provocation. Unilateral administration of allergen or other materials may lead to local,ipsilateral responses, and parasympathetic reflex effects. Allergen leads to mast cell degranulation withthe release of histamine, LTC4/D4/E4, tryptase, and other mediators. Histamine acts upon H1-receptorson endothelium to cause vascular permeability and exudation of an albumin-rich, watery discharge.H1-receptors on nociceptive nerves lead to the sensation of itch. The neural mechanism leading to thesensation of nasal congestion is not clearly understood. Nociceptive nerves may release neuropeptideswhen activated (“axon response” mechanism). Substance P may cause glandular secretion, whereascalcitonin gene-related peptide may cause vasodilation. Vasodilation with swelling of venous sinusoidsleads to thickening of the mucosa and obstruction to nasal airflow. Histamine, as well as other mediatorsand cytokines, plays a key role in regulating cellular infiltration as seen in the late phase response andclinical allergic rhinitis. Activation of nociceptive nerves recruits bilateral parasympathetic reflexes thatcause acetylcholine-mediated glandular exocytosis.