Allergic Rhinitis: Brief Review

Author: V. Dimov, M.D., Allergist/Immunologist and Assistant Professor at University of Chicago
Reviewer: S. Randhawa, M.D., Allergist/Immunologist


Allergic rhinitis (AR) is an inflammation of the nasal mucosa characterized by pruritus, sneezing, discharge, and stuffiness. It is induced by an IgE-mediated response and shares many features with asthma. Both conditions involve the same allergens and specific IgE antibodies.

The nose of a healthy adult makes 1-2 L of secreations per day which are swallowed. There is an alternating pattern of congestion and decongestion in the nasal cavity -- when one side is congested the other side is patent. This cycle occurs in a period of 1-4 hours.

In allergic rhinitis, the nasal mucous membranes are pale and blue, whereas they are red in nonallergic (infectious) rhinitis. A transverse nasal crease caused by habitual nose pushing (allergic salute) can be present but is nonspecific. Infraorbital cyanosis (allergic shiners) is caused by venous stasis and is also nonspecific. Dennie-Morgan line, an extra infraorbital fold on the lower eyelid, is common in patients with AD but can also be seen in AR.

Prevalence and Significance of AR

AR is the most common allergic disease. Allergic rhinitis (hay fever) and conjunctivitis are very common conditions affecting 10-30% of adults and up to 40% of children, leading to an annual cost to U.S economy of $6 billion. Up to 40-60 million individuals in the US suffer annually from allergic rhinitis (1/5 of the population), and an additional 17 million persons are considered to have nonallergic rhinitis.

Prevalence of asthma is 8%, prevalence of AR is 3 times higher (24%). 40% of patients with AR have asthma, 80% of patients with asthma have AR.

Allergic rhinitis has been found to impair work and school performance, and learning ability. It is a major cause of school and work absenteeism. Symptomatic allergic rhinitis (AR) and use of rhinitis medications may lead to lower school grades in children.

AR is not seen until after age 4 or 5, it takes approximately 3 pollen season exposures. Peak age is 30 (decades 2, 3 and 4).

Fifty percent of children with otitis media with effusion have AR.

Pathogenesis of AR

Pollen (allergen) interacts with IgE on the surface of mucosal mast cells - an example of type 1 hypersensitivity. Mast cells release histamine and leukotrienes, which produce symptoms of AR.

Symptoms of SAR: CS DIES

Smell impairment

Discharge - watery nasal discharge
Eye symptoms

Gell and Goombs classification of hypersensitivity reactions: ACID

Anaphylaxis, angioedema, asthma, SAR, type I
Cytotoxic, antibody-mediated, type II, e.g AIHA, ITP, Graves'
Immune complex disease (CIC), type III, e.g. GN, serum sickness
Delayed, cell-mediated, type IV, e.g. contact dermatitis

The basis for the development of allergic rhinitis is the overexpression of IgE and the interaction between IgE and allergens. The CD40/CD40L interaction leads to induction of B cell switching and IgE synthesis.

New studies show that allergic rhinitis (AR) may be caused by local nasal IgE sensitization to aeroallergens in the absence of systemic evidence of IgE sensitization. This means that the skin prick test can be negative in a patient with AR.

Mast cells are derived from CD34+ hematopoietic progenitor cells that migrate to and mature in the peripheral tissues. Mast cells are categorized into 2 subpopulations based on the type of neutral proteases they express. The MCT subset contains only tryptase, and the MCTC subset contains chymase, cathepsin G, and carboxypeptidase in addition to tryptase. IL-4, although present in both subsets, is predominantly co-localized to the MCTC subset, whereas IL-5 and IL-6 are restricted to the MCT subset.

Blood cell lineage. Image source: Wikipedia.

Mast cells (mind map).

Mast cells are subdivided into 2 types based on proteinase content:
TC mast cells -- Tryptase and Chymase in granules
T mast cells -- Tryptase only granules


Tryptase only

Mast cells
Major cell (10 µm) -- 2 times bigger than basophils (5 µm)
Minute granules (0.2 µm)
More granules (1000) than basophils (80)
Monophorm (round) nucleus

Mast cells. Image source: Wikipedia.

When activated, mast cells release granule products and generate arachidonic acid products, such as prostaglandins and leukotrienes from the phospholipid cell membrane. The major prostanoid generated by mast cells is prostaglandin D2 (PGD2).

Eicosanoid synthesis. Image source: Wikipedia.

Eicosanoids are signaling molecules made by oxygenation of 20-carbon essential fatty acids. There are 4 families of eicosanoids (PP-LT): prostaglandins (PG), prostacyclins (PGI), leukotrienes (LT) and thromboxanes (TX).

Prostaglandin D2. Image source: Wikipedia.

What is the mediator typical of late-phase allergic reaction?
Leukotriene D4 (LTD4) released from basophils.

Role of IgE and mast cells in allergy. Image source: Wikipedia.

IL-4 and IL-13 are cytokines produced by Th2 cells. They up-regulate IgE production and thus increase allergic inflammation. IL-4 is much more potent than IL-13.

IgE production
Inflammation promoters

IL-4, IL-5, IL-13 potentiate the effects of TNF-α on the expression of vascular cell adhesion molecule-1 (VCAM-1) in the vascular endothelium. VCAM-1 interacts the very late antigen-4 (VLA-4) to induce recruitment of eosinophils, basophils, and lymphocytes.

Overview of adhesion molecules, 3 groups remembered by the mnemonic SIS.

Adhesion molecules, 3 groups = SIS
Superfamily Ig

Ig Superfamily = cell adhesion molecules (CAM)

VCAM (vascular cell adhesion molecule)
ICAM (intercellular adhesion molecule)
PECAM (platelet-endothelial cell adhesion molecule)

Intercellular adhesion molecule 2 (ICAM 2). Image source: Wikipedia.

Neurogenic mechanism of AR involves production on calcitonin gene related peptide (CGRP), the most potent vasodilator currently known. CGRP is primarily produced in nervous tissue, however, its receptors are expressed throughout the body. CGRP is currently a major target of migraine research. Calcitonin is a peptide hormone produced by the parafollicular (C-cells) of the thyroid. It reduces blood calcium, opposing the effects of parathyroid hormone.

Endothelial activation leads to recruitment of circulating cells. RANTES (regulated on activation, normal T cells expressed and secreted) cytokines (CCL5) are part of the process.

Chemokine (C-C motif) ligand 5 (CCL5, earlier called RANTES). Image source: Wikipedia, GNU Free Documentation license.

CCL5 (earlier called RANTES) is a small protein classified as a chemotactic cytokine or chemokine. CCL5 is chemotactic for T cells, eosinophils, and basophils, and plays an active role in recruiting leukocytes into inflammatory sites. It is also an HIV-suppressive factor released from CD8+ T cells.

Eosinophils are not a normally found in the nose. Immunohistochemical staining of nasal mucosa of patients with AR shows an abundance of eosinophils.

Allergic rhinitis mind map.

Classification of Rhinitis

There are several classifications of rhinitis and all of them are artificial. The pathophysiologic classification of rhinitis (not just allergic rhinitis) is shown below.

Rhinitis types, pathological classification.

Many people have both allergic and nonallergic rhinitis.

Eosinophilic Rhinitis

Rhinitis with nasal eosinophilia is one of the classic atopic diseases. The "united airway" concept implies that the same condition affects upper airway (rhinitis) and lower airways (asthma). The "allergic march" concept describes a progression from infantile atopic dermatitis followed by rhinitis and asthma. Early treatment of allergic rhinitis may prevent development of asthma.

Eosinophil. Image source: Wikipedia.

Eosinophil. Image source: Wikipedia.

Incidence of allergic rhinitis is 0.5-1%, annual prevalence is 5-22% of the population. Mean age of onset is 9-11 years.

Triggers of allergic rhinitis:
- pollens
- fungi
- dust mites
- cockroaches
- animal dander
- occupational allergens, prevalence 5-15%, latex in health care workers, flour in bakers, dander in animal care workers

Food allergy is not a common trigger of allergic rhinitis.

Pollen calendar

Pollen calendar: TGF W (similar to Tumor Growth Factor)

Tree pollens
Grass pollens
Fungal spores

Weed pollens

References: Clinical review: ABC of allergies, Summer hay fever. BMJ 1998;316:843, figure. Click here for Pollen Calendar for North America.

Symptoms of Allergic Rhinitis

Symptoms of SAR: CS DIES

Smell impairment

Discharge - watery nasal discharge
Eye symptoms

What is the most common symptom of AR?


What is the most bothersome symptom of AR?


Classification of Allergic Rhinitis

1. Seasonal classification: episodic, perennial, seasonal, or perennial with seasonal exacerbations.

2. Allergic Rhinitis and its Impact on Asthma (ARIA) classification.

Eosinophilic rhinitis is compared to asthma by using the same categories - M MMS:
Mild intermittent
Mild persistent
Moderate persistent
Severe persistent

ARIA classification differs from asthma classification by having one more category for allergic rhinitis -- "moderate-severe intermittent."

Allergic Rhinitis and its Impact on Asthma (ARIA): Achievements in 10 years and future needs. ARIA has reclassified AR as mild/moderate-severe and intermittent/persistent. This classification closely reflects patients' needs and underlines the close relationship between rhinitis and asthma.


Intermittent - symptoms less than 4 d per wk, symptoms for less than 4 wks
Peristent - symptoms more than 4 d per wk, more than 4 wks


Moderate-severe - sleep disturbance, impairment of daily activities, school, work
Mild - no above sx

Diagnosis of AR

Rhinoscopy to exclude a structural problem
Skin prick test or RAST

A negative skin prick test (SPT) does not rule out AR. There is a local production of specific IgE in the nasal mucosa.

Most patients with asthma have rhinitis suggesting the concept of ‘one airway one disease’ or ‘united airways’. However, not all patients with rhinitis present with asthma.

The 1999 WHO workshop ‘Allergic Rhinitis and its Impact on Asthma’ recommended:

- patients with persistent allergic rhinitis should be evaluated for asthma by history, chest examination, and possibly assessment of airflow obstruction before and after bronchodilator

- history and examination of the upper respiratory tract for allergic rhinitis should be performed in patients with asthma

Comorbidities of allergic rhinitis (AR): asthma, sinusitis, and obstructive sleep apnea (OSA). The comorbidities may require evaluation with PFTs for asthma or a sleep study for OSA.

Emerging diagnostic procedure: acoustic rhinometry.

Treatment of AR

Allergic rhinitis mind map.

Early treatment of allergic rhinitis may prevent development of asthma. Stepwise approach to treatment of allergic rhinitis: OASIS

Omit (avoid) allergens
Antihistamines (oral and topical)
Steroids (topical)
Immunotherapy (SCIT, SLIT)

References: Clinical review: ABC of allergies, Perennial rhinitis. BMJ 1998;316:917, figure.

WHO and ARIA Workshop Report proposed stepwise treatment of allergic rhinitis analogous to asthma therapy.

The mainstay of treatment is allergen avoidance. Allergen immunotherapy (SCIT) is the only treatment to achieve clinical remission rather than transient symptom control.

Measures to avoid pollen exposure

Windows shut - car and buildings
Avoid open grassy places
Pollen filter in the car
Vacation by the sea during the peak season

See Video on Avoiding Allergies and Asthma. ICYou, 04/2008.

Medications for Allergic Rhinitis


Histamine H1-receptor antagonists alleviate most symptoms of allergic rhinitis but not nasal congestion. Decongestants may still be needed.

The first generation of antihistamines are not H1-selective and cross the blood-brain barrier, thus affecting alertness, cognitive function, and reaction time to stimuli. First generation antihistamines are the number one risk factor for occupational accidents. In 35 states, it is illegal to drive while on Benadryl (diphenhydramine). Studies showed that diphenhydramine affected driving ability more than being legally drunk by blood alcohol level.

Second generation antihistamines have greater H1-receptor specificity. Cetirizine, loratadine, and desloratadine have dose-related sedation which is not detectable in the FDA approved doses. Fexofenadine has no greater sedative effect than placebo in every dose studied

Free of sedation at any dose

The newer agents have a rapid onset of action and can be used as “reliever” therapy for acute symptoms given once daily.

Oral antihistamines are less effective for nasal congestion and INS are generally preferred for more severe AR.

Oral antihistamines are less effective than INS. However, they are similarly effective to INS for ocular symptoms in AR/AC.

Oral antihistamines are effective in reducing rhinorrhea, sneezing, and itching but have little effect on nasal congestion (this is where INS play the major role).

Oral antihistamines are ineffective for non-AR. They can achieve adequate control of moderate AR but INS are usually needed for severe AR.

Second-generation oral antihistamines fexofenadine, loratadine, and desloratadine do not cause sedation at recommended doses.

Second-generation antihistamines considered as safe agents during pregnancy (Zyrtec is pregnancy category B).

Intranasal antihistamines

Intranasal antihistamines are considered the first line therapy of AR by some authors although intranasal steroids are the most effective one.

Olopatadine (Patanase) nasal spray form may provide an alternative to "unpleasant tasting" azelastine (Astelin) for seasonal allergic rhinitis. In a RCT of 544 patients, olopatadine was more effective than placebo and non-inferior to azelastine. The incidence of bad taste was much lower with olopatadine: 12.2% of patients taking olopatadine reported some degree of bitter taste, compared with 19.7% of those taking azelastine (P=0.05). Patanase was approved by the FDA in April, 2008.

Intranasal antihistamines have a rapid onset of action (3-4 hours) which makes them suitable for PRN use in episodic AR.

What nasal spray provides relief in 30 minutes in allergic rhinitis?

Patanase (olopatadine) is currently the only nasal spray to provide relief in 30 minutes in allergic rhinitis. The effect lasts for 12 hours.

Intranasal antihistamines are better than oral antihistamines for nasal congestion but yet not as effective as INS.

Intranasal antihistamines are also approved for vasomotor rhinitis (non-AR) which makes them a good option for patients with mixed rhinitis (AR/non-AR).

Patients often complain of bitter taste with intranasal azelastine but the newer intranasal olopatadine (Patanase) is better tolerated.


Topical decongestants such as oxymetazoline or phenylephrine are α-adrenergic receptor agonists with rapid onset of action, thus providing an immediate relief.

They should be used only for short periods (2-3 days) in intermittent rhinitis, because regular use causes rebound congestion and mucosal ischemia.

Oral decongestants (pseudoephedrine) do not produce substantial rebound congestion when stopped but they have systemic side effects such as tachycardia, hypertension, urinary retention, and insomnia.

Oral decongestants should be avoided in children younger than 6 years of age.

Intranasal steroids (INS)

Nasal CS are very effective for treatment of allergic rhinitis. They can be combined with nasal antihistamines.

Fluticasone 110 mcg qd is fast acting, with an 8-hour onset of action, and long-acting, with a 24-hour symptom control. It also helped the eye symptoms of SAR. Side effects: local irritation and epistaxis (in 5% of cases).

More than 90% or patients with AR achieve symptomatic relief with CS. Therapeutic efficacy is achieved within 1-3 days, but maximum efficacy may take up to 3 weeks.

Omnaris (ciclesonide) is a new steroid which seems to have no significant effect on hypothalamic-pituitary-adrenal axis. It was approved in 2006 for treatment of AR in adults and children 12 years of age and older.

Why ciclesonide has no significant effect on hypothalamic-pituitary-adrenal axis?

The medication is "activated" locally in the lungs. Carboxylesterases in bronchial epithelial cells convert ciclesonide to des-CIC in the lungs. Low systemic levels of des-CIC are a result of the high metabolic clearance by the liver following CIC inhalation.

Patients should be instructed to angle the spray towards the ear to direct it where the inflamed nasal mucosa is. Pumping it straight up will direct the medication to the nasal cartilage, leading to local side effects.

Single best drug in AR for
Stuffiness (congestion)

INS are the most effective therapy for AR

PRN use of INS may be effective for seasonal and episodic AR. New from the guidelines: intranasal corticosteroids (INS) are recommended for PRN use.

Typical onset of action of INS is within 12 hours which is slower than with oral or intranasal antihistamines (3-4 hours).

However, some patients report effect from INS within 3-h hourse (similar to antihistamines), hence the recommendation for PRN use.

INS are more effective than combination therapy with oral antihistamine and LTRA.

For ocular symptoms of AR, efficacy of INS is similar to that of oral antihistamines. INS may be used for symptoms of allergic conjunctivitis associated with rhinitis.

INS can be used for mixed rhinitis (AR and non-AR) -- similar to intranasal antihistamines.

INS do not cause growth suppression in children.

Systemic Steroids

Oral steroids may be used for very severe nasal symptoms when given as a short course (5 - 7 days). Single or repeated administration of intramuscular steroids should be discouraged.

Leukotriene Receptor Antagonists (LTRA)

Antagonists of the CysLT1 receptor (LTRA) are efficacious as controller therapy in asthma and montelukast is FDA-approved for treatment of seasonal allergic rhinitis.

LTRA have not been shown to be more efficacious than oral antihistamines for AR.

LTRA are approved for both AR and asthma and may be a good treatment option for patients who have both conditions.

Intranasal anticholinergic

Intranasal anticholinergic (ipratropium) has a rapid onset of action (3-4 hours, similar to intranasal antihistamines) and can be used for for episodic rhinitis.

Ipratropium reduces rhinorrhea but is otherwise ineffective for congestion and other symptoms of AR.

Intranasal cromolyn

Intranasal cromolyn can be used for maintenance treatment of AR.

Onset of action is very slow (4-7 days) and the full benefit may not be evident for weeks.

Intranasal cromolyn is not as effective as INS.

Anti-IgE Therapy

Anti-IgE therapy with humanized mouse immunoglobulin against IgE is efficacious in allergic asthma and rhinitis and lowers total IgE levels dramatically. IgE levels rise again when therapy is stopped.

Anti-IgE (omalizumab, Xolair) is approved for treatment of severe persistent asthma. There are occasional case reports of anti-IgE (omalizumab) use as a new therapeutic approach for chronic rhinosinusitis.

With an annual cost of $ 8-10,000, omalizumab is considered "too expensive" by some experts for treatment of AR.


Contraindications to immunotherapy:
Age less than 5-6 years
Autoimmune disease
Uncontrolled asthma, FEV1 less than 70% of predicted

80-85% of patients achieve long-lasting symptomatic relief with immunotherapy. After 3-5 seasons with adequate relief, stopping should be considered.

There are 2 major reasons to consider immunotherapy:
1. To prevent sensitization to new allergens (from 1-2 at the beginning to 6-7 in a few years).
2. To prevent asthma development in the future.

Sublingual immunotherapy (SLIT) has been effective in Europe, where sensitization to monoallergens is common. In the U.S., where pollyargen sensititazion is more common, there have been 4 negative SLIT studies so far.


New treatments include beta-1,3-glucan, a mushroom product that induces T(H)1 response. T helper (Th) 2 cells play an important role in the development of IgE-mediated diseases such as AR, leading to local overproduction of Th2 cytokines (IL-4, IL-5 and IL-13). On the contrary, Th1 cytokines (IL-12 and IFN-gamma) are known to suppress this Th2 immune response. Beta-1,3-1,6-glucan (Glucan) is an immunomodulator stimulating particularly the Th1-mediated immune response.

Orally-administered yeast-glucan decreases levels of IL-4 and IL-5 while increasing the levels of IL-12. Glucan may have a role as an adjunct to standard treatment in patients with AR.

Emerging therapeutic procedure: radiofrequency volumetric tissue reduction.

Other Types of Rhinitis

There are different conditions which mimic AR but are of nonallergic etiology. “Gustatory” rhinitis, for example, describes nasal symptoms after eating. It is associated with the ingestion of hot spicy foods or alcohol, particularly wine, and is likely to represent an irritant response or chemical sensitivity.

Watery rhinorrhea in elderly men (“old man's drip”) is caused by testosterone deficiency. Hormonal rhinitis is seen in menopausal women, similarly to atrophic vaginitis, and may respond to the same topical treatment with estrogen cream.

The topical use of decongestant sprays leads to rebound hyperemia, producing progressively worse nasal obstruction and "rhinitis medicamentosa."

Although the most common agents implicated in "rhinitis medicamentosa" are topical decongestants, oral medications may also play a role, especially beta-blockers, clonidine, ACEi, and oral contraceptives.

Rhinitis types, pathological classification.

Nonallergic rhinitic eosinophilic syndrome (NARES)

Nonallergic rhinitis with eosinophilia (NARES) and eosinophilic nonallergic rhinitis (ENR) occur in patients without allergic triggers. NARES/ENR is idiopathic rhinitis and is a diagnosis by exclusion. NARES is considered similar to nonallergic, or intrinsic, asthma. Patients have substantial nasal eosinophilia and some may develop anosmia and polyps.

Noneosinophilic Rhinitis

Various conditions can cause noneosinophilic rhinitis. The most common infectious cause is the common cold, which is associated with more than 200 different viruses.

Non-infective, non-allergic rhinitis

The term “nonallergic rhinitis” is a misnomer. With the exception of idiopathic nasal eosinophilia (nonallergic rhinitic eosinophilic syndrome, NARES), these patients do not exhibit nasal inflammation. Therefore, there is thus no “-itis” to their disease and nasal biopsies show normal cell counts in the mucosa. The onset of the disease is in adult life and has been attributed to a neurovascular imbalance, thus the old term “vasomotor rhinitis.”

Capsaicin, the active principle of red hot pepper, stimulates sensory “C” fibers, inducing neuropeptide release. Repeated nasal capsaicin administration leads to tachyphylaxis and can improve symptoms in nonallergic rhinitis. The treatment is unpleasant because it induces burning pain, which can be modified by local anesthesia.

Nasal ipratropium is used in “vasomotor rhinitis” with variable effect. The concentration of nasal ipratropium is 0.03% compared to 0.06% for the inhaled product. The most common side effect is "too much drying" of the nasal mucosa.

Sinusitis and Nasal Polyps

Click here to read the review.

What is the triad of aspirin-exacerbated respiratory disease (AERD)?
Samter's triad include asthma, aspirin sensitivity, and nasal/ethmoidal polyposis.

Sensitivity to aspirin

Treatment Options for Allergic Rhinitis (AR) and Non-Allergic Rhinitis (NAR) (click to enlarge the image).


Diagnostic Tools In Rhinology - EAACI position paper - free full text, 2011.
Allergy and Immunology MKSAP, 3rd edition.
Chapter 76, Allergic and Nonallergic Rhinitis. Peter H. Howarth. Adkinson: Middleton's Allergy: Principles and Practice, 6th ed.
Clinical review: ABC of allergies, Summer hay fever. BMJ 1998;316:843.
Clinical review: ABC of allergies, Perennial rhinitis. BMJ 1998;316:917.
Rhinitis, Allergic. eMedicine, 2007.
Allergic Rhinitis. eMedicine, 2007.
Allergic rhinoconjunctivitis: Burden of disease. Blaiss, Michael S. Allergy and Asthma Proceedings, Volume 28, Number 4, July/August 2007 , pp. 393-397(5).
Fluticasone for seasonal allergic rhinitis (SAR). AllergyNotes, 2007.
Allergic Rhinitis May Lead to Lower School Grades. AllergyNotes, 2007.
Effect of acupuncture in the treatment of seasonal allergic rhinitis: a randomized controlled clinical trial. Am J Chin Med. 2002;30(1):1-11.
Anti-IgE (omalizumab): A new therapeutic approach for chronic rhinosinusitis. JACI, Volume 121, Issue 1, Pages 257-258 (January 2008).
Links between allergic rhinitis and asthma still reinforced. P. Demoly, P. J. Bousquet (2008). Allergy 63 (3), 251–254.

Related reading

Interactive Allergy Map by Greer Labs. Click your state to find region-specific, common airborne allergens there.
FIT Corner Questions. Chapter 76 of the 6th edition of Middleton’s Allergy Principles and Practice, edited by N. Franklin Adkinson, et al. Chapter 76 Questions: Allergic and Nonallergic Rhinitis. August 30, 2006.
New tools help MDs treat allergies. National Review, 03/2008.
Acute sinusitis: Are you following the rules you’ve set for supervising midlevels? March 2008 issue of Cortlandt Forum.
The Best Antihistamines for Sneezing and Nasal Congestion. Paul Enright, MD, 04/2008.
Advances in upper airway diseases and allergen immunotherapy in 2007. Saltoun C, Avila PC. J Allergy Clin Immunol. 2008 Aug 9.
Effects of glucan treatment on the Th1/Th2 balance in patients with allergic rhinitis: a double-blind placebo-controlled study. Eur Cytokine Netw. 2005 Jun;16(2):128-34.
Guidelines Updated for Diagnosis and Treatment of Rhinitis. Laurie Barclay. Medscape.
The Diagnosis and Management of Rhinitis: An Updated Practice Parameter. The Journal of Allergy and Clinical Immunology, Volume 122, Issue 2, Supplement (August 2008).
Rhinitis and asthma: united airway disease. Janet Rimmer and John W Ruhno. MJA 2006; 185 (10): 565-571.
FDA Approvals: Patanase, Actonel, Cimzia. Medscape, 2008.
Nasal carbon dioxide is a potentially efficacious treatment for the symptoms of allergic rhinitis

Audio and Video

Sinusitis Video from, 03/2008.
Video: Avoiding Allergies and Asthma. ICYou, 04/2008.

PowerPoint Presentations

Allergic Rhinitis,
Allergic Rhinitis in children,
Allergic Rhinitis,
Allergic Rhinitis in Children,

Published: 07/10/2007
Updated: 08/30/2012

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