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    Current Diagnosis

    • Rhinitis presents as nasal congestion, sneezing, itching, rhinorrhea, and postnasal drainage.

    • Patients with palatal and nasal itching should be considered for allergic disease.

    • Allergic rhinitis is confirmed by positive skin-prick testing and IgE reactivity.

    •   Nonallergic rhinitis patients lack allergic evidence for disease.

    •   Nonallergic rhinitis conditions have multiple presentations.

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    Current Therapy

    • Avoidance therapy should be first-line treatment for all forms of rhinitis.

    • Second generation oral antihistamines have good therapeutic efficacy for allergic rhinitis.

    • Intranasal corticosteroids are the mainstay of treatment for nonallergic rhinitis and moderate-to-severe allergic rhinitis.

    • Consultation with an allergy specialist should be considered in cases with multiple treatment failures.

    • Patients whose allergic rhinitis is uncontrolled on multiple therapies should be considered for immunotherapy.

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    Rhinitis is defined as inflammation of the nasal mucous membranes. Rhinitis presents as nasal congestion, sneezing, itching, rhinorrhea, and postnasal drainage; it can be divided into allergic and nonallergic rhinitis. Mixed rhinitis has components of both allergic and nonallergic disease. Allergic rhinitis is nasal inflammation that is mediated by IgE to environmental allergens. Nonallergic rhinitis is defined by non–IgE-mediated perennial symptoms. Nonallergic rhinitis shares symptoms with allergic rhinitis, but is only distinguishable by negative allergy tests. Nonallergic rhinitis is also known as perennial nonallergic rhinitis, idiopathic rhinitis, and vasomotor rhinitis.

    Most research still classifies allergic rhinitis according to its seasonality or its perennial nature. Seasonal allergic rhinitis is commonly caused by pollen allergens; perennial allergic rhinitis is mainly caused by dust mites and animal dander. Allergic rhinitis can be further classified as mild, moderate, or severe. Mild rhinitis is rhinitis that does not impair work, school, daily functioning, or sleep. Moderate to severe rhinitis interferes with activities of daily living, quality of life, and/or sleep. Severe rhinitis is so marked that normal functioning cannot take place without treatment. Episodic allergic rhinitis occurs with sporadic inhalant aeroallergen exposure not typically encountered by the patient’s usual indoor and outdoor environments. An example of episodic allergic rhinitis is a child who is allergic to cats but is not normally exposed, but then visits a household with cats and develops symptoms.

    The Allergic Rhinitis and its Impact on Asthma Guidelines: Revised 2010 (ARIA) discouraged the use of the terms seasonal and perennial rhinitis in favor of intermittent and persistent rhinitis. Intermittent rhinitis can be defined as nasal symptoms lasting less than 4 weeks’ duration and fewer than 4 days per week. Persistent rhinitis is rhinitis lasting more than 4 weeks’ duration or more that 4 days per week.

    No standard classification exists for nonallergic rhinitis. A variety of conditions present with similar symptoms and are called nonallergic rhinitis. Nonallergic rhinitis includes vasomotor rhinitis, gustatory rhinitis, nonallergic rhinitis with eosinophilia syndrome (NARES), occupational rhinitis, hormonal rhinitis, drug-induced rhinitis, and atrophic rhinitis. Another entity classified in or out of nonallergic rhinitis is infectious rhinitis.

    Local allergic rhinitis is a newly defined entity found in nonatopic patients. Local allergic rhinitis is characterized by local inflammatory reactions including local eosinophils and localized IgE in response to aeroallergens. Local allergic rhinitis does not show significant skin- prick testing reactions, and patients have negative systemic IgE reactions to aeroallergens.

    Rhinitis may be viewed by some as a trivial disease, but it places a significant financial burden on society. The estimated direct and indirect costs to society of rhinitis were around $11.58 billion in 2002.

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    Epidemiology/Risk Factors

    The National Health and Nutrition Survey (NHANES II and III) suggests that the overall prevalence of IgE sensitivity might be increasing. Of the patients evaluated for rhinitis in the United States, 43% (58 million people) have allergic disease, 23% (19 million people) have nonallergic disease, and 34% (26 million people) have mixed rhinitis. Seventy percent of allergic patients develop the disease in childhood (20 years and younger) as opposed to nonallergic rhinitis patients, 70% of whom develop disease in adulthood. Approximately two thirds of nonallergic rhinitis patients have vasomotor rhinitis, and one-third have NARES. Nonallergic rhinitis has a female predominance.

    The prevalence of local allergic rhinitis is largely unknown. In a small study of rhinitis patients, the prevalence of local allergic rhinitis was 25.7%, nonallergic rhinitis was 11.2%, and allergic rhinitis was 63.1%. Local allergic rhinitis is associated with asthma and conjunctivitis, and commonly begins in childhood.

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    Allergic rhinitis is the result of an IgE mediated, type I hypersensitivity allergic reaction in response to an inhaled allergen. Allergens are proteins derived from airborne particulate matter, including dust-mite feces, pollens, animal dander, and cockroach particles. Antigen-presenting cells (APCs) engulf allergens in the nose and break them into antigenic peptides. APCs present these peptides to naïve T cells (TH0). TH0 cells differentiate once activated, into the TH2 subtype. The TH2 lymphocytes generate cytokines that regulate B- lymphocytes and sequester inflammatory cells (including eosinophils).

    B-lymphocytes produce IgE. IgE attaches to mast cells and basophils and renders them sensitized. Once sensitized and cells are exposed to allergen, the mast cells and basophils degranulate.

    Degranulation of these cells releases a host of mediators including histamine and prostaglandin. Histamine stimulates histamine type I (H1) receptors on nerve endings that cause pruritus, sneezing and increased secretions. These symptoms constitute the early-phase response of allergic rhinitis. The early-phase response occurs within minutes of allergen exposure and dissipates within 1 hour.

    Eosinophils produce IL-5, which acts to promote activation and survival of other eosinophils. Eosinophils also produce toxic products that damage local mucosal cells. The damage done by these cells is what constitutes the late-phase reaction. The late-phase reaction occurs several hours after allergen exposure and is characterized by nasal congestion.

    Nonallergic Rhinitis

    The nasal mucosa has two major functions; one is trapping inhaled particles through mucus production and the second is humidifying inhaled air through a complex vascular system. The mucus glands and the vascular system are regulated by the parasympathetic and the adrenergic nervous systems. Sensory nerves are stimulated by irritants in the nose through the use of a sensory receptor called a nociceptor. The nociceptive signal generates a neural reflex in the central nervous system (CNS) controlling sympathetic and parasympathetic tone in the nasal mucosa. Parasympathetic stimulation results in mucus production. Sympathetic stimulation causes vasoconstriction, which empties venous cavities. Lack of sympathetic tone causes venous engorgement and nasal congestion.

    Symptomatic nonallergic rhinitis is an exaggeration of a normal defensive mechanism. Inflammation in the nose causes an upregulation of this neural activity, resulting in the exaggerated response (also known as neural hyperresponsiveness).

    Hyperresponsive parasympathetic efferent nerves trigger glandular activation in the nasal mucosa, leading to vasodilation and mucus production. Excessive mucus production anteriorly causes rhinorrhea and posteriorly causes postnasal drip. This hyperresponsiveness can be due to structural or functional components of the nasal mucosa altered through genetic or pathologic factors. The exact mechanisms of nonallergic rhinitis conditions are poorly understood because of their multiple presentations.

    Infectious Rhinitis/Rhinosinusitis

    Acute sinusitis (rhinosinusitis) most commonly occurs as a complication of viral upper-respiratory infections (URIs). Viral URIs cause nasal mucosal edema, which leads to obstruction of the sinus openings and ciliary impairment. Bacteria proliferate in the stagnant mucus as well as the low–oxygen-tension environment of the sinus cavities. Chronic rhinosinusitis is the result of long-term obstruction and/or dysfunction of the sinuses. Chronic inflammation leads to chronic low-grade infections.

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    Environmental control of allergens can improve the severity of allergic rhinitis and can reduce the need for medications. Environmental control should be thorough if treatment is sought, but the full beneficial effects of the change may take weeks to months. Mild disease can usually be managed with avoidance measures. Complete avoidance of allergen, particularly pollen, is usually not feasible.

    Reduction of dust mite allergen exposure can be done in the following ways: remove carpets and soft toys, use covers impermeable to allergen for mattresses and pillows, vacuum beds weekly, and wash bedding at 60 degrees Celsius (140 degrees Fahrenheit). Pet dander avoidance can only be effectively managed by removing the pet and carefully cleaning all carpets, furniture and mattresses.

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    Clinical Manifestations

    If the patient presents with symptoms of palatal itching, nasal itching, ocular symptoms, or sneezing, consideration should be given to an allergic cause.

    The presentation of nonallergic rhinitis is dependent on the type of nonallergic rhinitis. Overall, patients with nonallergic rhinitis lack other allergic conditions.

    The vasomotor rhinitis patient will present with predominantly nasal obstruction and rhinorrhea. Typically, symptoms are triggered by temperature, exercise, and environmental stimuli (odors, smoke, and dust).

    NARES patients generally have more intense symptoms than vasomotor rhinitis or allergic disease patients. NARES patients present with paroxysms of flares to include sneezing, watery rhinorrhea, nasal itching, congestion, and some anosmia. NARES patients have eosinophils on a nasal smear, but lack other allergic evidence by skin-prick testing.

    Gustatory rhinitis sufferers complain of nasal congestion and rhinorrhea associated with ingestion of foods and, sometimes, alcoholic beverages.

    Nasal crusting, dryness, and fetor are the characteristics of atrophic rhinitis. These findings are due to glandular cell atrophy. Patients will have abnormally wide nasal cavities and may have squamous metaplasia.

    Occupational rhinitis patients have components of allergic and nonallergic disease. Patients present with nasal congestion and rhinorrhea triggered by an occupational exposure. Symptoms are present during duty and generally improve away from the work environment. Substances leading to symptoms include irritating chemicals, grain dust, ozone, lab animal antigens, and wood. Often occupational rhinitis co-exists with occupational asthma.

    Hormonal rhinitis manifests as nasal congestion during pregnancy or the menstrual cycle. Pregnant women are six times more likely to have rhinitis and sinusitis than nonpregnant women. Rhinitis usually resolves two weeks postdelivery.

    Drug-induced rhinitis occurs with certain medications. ACE inhibitors, phosphodiesterase-5 selective inhibitors, alpha-receptor antagonists, and phentolamine are common triggers. Patients present with rhinorrhea and nasal congestion.

    Rhinitis medicamentosa is a condition that presents with severe congestion. It is caused by prolonged and repetitive use of topical nasal decongestants. It can also be associated with cocaine use.

    Anatomic rhinitis is more likely in patients who present with unilateral nasal symptoms.

    Infectious rhinitis presents with sinus tenderness, erythema to the mucosa, postnasal drainage and sometimes periorbital edema.

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    The diagnosis of allergic rhinitis, nonallergic rhinitis, and infectious rhinitis is based largely on history and physical examination. Other diagnostic testing can be performed to aid in providing a more definitive diagnosis or to rule out other causes.

    Allergic rhinitis is confirmed by IgE reactivity to environmental allergen sensitivity through skin-prick testing. When skin-prick testing is difficult to interpret or if it is not feasible, serum–allergen- specific IgE testing can be used. Nasal smears looking for eosinophils are not recommended for routine use in the diagnosis of allergic rhinitis.

    Other testing available for evaluation of rhinitis includes nasal endoscopy, rhinomanometry, and radiologic imaging. Fiberoptic nasal endoscopy is reserved for those with atypical symptoms or an inadequate response to treatment. Rhinomanometry measures airflow obstruction in the upper airway. Rhinomanometry provides an objective measurement of nasal congestion. Rhinomanometry is used to evaluate clinical response to interventions and assess anatomic severity, such as in patients with obstructive sleep apnea. Radiologic imaging, such as computerized tomography (CT) and magnetic resonance imaging (MRI), is used to evaluate anatomic structure.

    Imaging may not correlate well with nasal function and is expensive.

    If a provider suspects a cerebrospinal fluid (CSF) leak, the rhinorrhea can be evaluated for beta transferrin protein, which is present only in CSF.

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    The best diagnostic tool in the evaluation of rhinitis is the history. Information regarding previous evaluation and treatment should be elicited. A positive family history of rhinitis points towards allergic disease. The history of symptoms should include questions regarding congestion; sneezing; rhinorrhea; sore throat; dry throat; cough; itchy, red, or tearing eyes; voice changes; sinus symptoms of drainage; pressure or pain; snoring; ear pain or loss of hearing; and smelling difficulty.

    When gathering the details of each symptom, evaluate the onset (such as those in childhood), frequency (episodic versus continual), pattern (seasonality), characteristics of secretions, triggers, severity (to include quality of life evaluation), and associated geographic location or environment (home versus work). Once a trigger is identified, history needs to be gathered even further to evaluate the possibility of modifying the exposure.

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    Physical Examination

    As with any disease process, the physical examination provides clues into the diagnosis. Although the physical examination in rhinitis patients should focus on the nasal mucosa, other body areas should be examined to rule out other processes. For example, the tympanic membranes should be examined for mobility, retraction, erythema, and Eustachian tube dysfunction.

    Examination of the eyes in allergic rhinitis might show that the conjunctiva have edema, erythema, and/or cobblestoning. Excessive lacrimation could be another finding. Darkening of the skin of the lower eyelids is prevalent in allergic disease and is also called “allergic shiners.”

    Allergic and nonallergic nasal mucosa may have a similar appearance. The nasal mucosa may appear boggy with a bluish appearance or be erythematous. Excessive watery-clear mucus might be present. Turbinate hypertrophy is another physical examination finding in rhinitis. Other nasal mucosa findings to look for are nasal polyps, sinusitis, septal deviation, septal perforation, and crusting.

    Looking for elongated facies, mouth breathing, and a high arch in the palate may provide a clue to the severity of the nasal obstruction. The tonsils and adenoids should be examined for enlargement.

    Posterior nasal drainage and cobblestoning in the oropharynx are common findings in rhinitis patients.

    The skin examination provides useful information in the patient with rhinitis. Atopic dermatitis or urticaria may be findings associated with allergic disease. The skin should be evaluated for dermatographism. Patients with dermatographism cannot be evaluated for allergic disease using skin-prick testing.

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    Differential Diagnosis

    Many different pathologic conditions can present similarly to rhinitis. Conditions to keep in mind while evaluating and treating a patient for rhinitis include: nasal polyps, ciliary dyskinesia syndrome, anatomic abnormalities such as deviated septum or tumors, nasal turbinate hypertrophy, cerebrospinal fluid rhinorrhea, pharyngonasal reflux, systemic disorders such as Wegener’s disease, aspirin intolerance, and other medication side effects.

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    Current guidelines in treatment of rhinitis do not take cost into consideration. However, the individual treatment goals should be based on factors such as age, route of administration preference (i.e., nasal versus oral), severity, seasonality, side effects, cost, benefit to comorbid conditions, and onset of action. For example, onset of action is an important consideration for an individual who has more episodic symptoms. Also, individual patients respond differently to treatment regimens within a given group.


    Due to the lack of high-quality evidence, implementation of avoidance measures is largely based on panel recommendations. In addition, the ubiquitous nature of allergens may limit the effectiveness of the avoidance measures. For dust mites, encasing pillows and bedding in dust mite resistant materials may be beneficial. Pollen is seasonal and can be minimized by keeping the windows closed, using air conditioning, and limiting outdoor exposure. Using particulate filters in the home can also assist in reducing overall allergen load of pollens and dust. Avoiding basements and lowering household humidity may reduce the amount of mold exposure patients receive. Pet avoidance can only be reached by ridding the house of the pet altogether. Other, less-effective measures include limiting exposure of the pet to the house and/or bedroom.

    Intranasal Corticosteroid (INS)

    Intranasal corticosteroids are first-line treatment for moderate to severe allergic rhinitis and most nonallergic rhinitis conditions. All allergic rhinitis symptoms can be treated with INS. The intranasal corticosteroids budesonide aerosol (Rhinocort Aqua), fluticasone propionate aqueous (Flonase), and beclomethasone aqueous (Beconase AQ) preparations all have a Federal Drug Administration (FDA) treatment indication of nonallergic rhinitis. Intranasal corticosteroid side effects include irritation, bleeding, and perforation of the nasal septum; rarely, local candidiasis is seen with INS use.

    They are safe to use in pregnancy. No single INS preparation is more efficacious than, or has any relevant difference from, any other. INS has negligible hypothalamic-pituitary-adrenal axis suppression, and systemic burden is clinically insignificant.

    Intranasal Anticholinergic (IP)

    Ipratropium bromide (Atrovent), a specific intranasal anticholinergic, inhibits parasympathetic function in the nasal mucosa. The parasympathetic blockade reduces the output of secretions from seromucus glands in the nose. Ipratropium can be used in treatment of anterior watery rhinorrhea but has a very limited role in reducing postnasal drip, nasal congestion, or sneezing. Topical ipratropium prior to ingestion of food can be used as pretreatment of gustatory rhinitis and is effective in treatment of the common cold and skier’s nose. Side effects of IP include nasal dryness, burning, irritation, stuffy nose, headache, and dry mouth.

    Intranasal Antihistamine (INA)

    Azelastine (Astelin) is a nasal spray approved by the FDA for allergic and vasomotor rhinitis. Olopatadine (Patanase) intranasal spray has been approved for seasonal allergic rhinitis. INA has faster onset of action than intranasal corticosteroids. INA should be taken twice per day for maximum clinical benefit and may benefit those with nasal congestion. INA does not produce a significant amount of sedation, but side effects include headache, epistaxis, bitter taste, and nasal irritation.

    Nasal Cromolyn

    Cromolyn (NasalCrom) should be considered for early mild rhinitis, but should not be considered a first-line treatment in allergic rhinitis. Nasal cromolyn can be used prior to allergen exposure for prophylaxis of episodic allergic rhinitis. Cromolyn is mostly void of side effects. Cromolyn inhibits mast cell degranulation and is administered three to four times a day. Cromolyn has very limited usefulness for nonallergic rhinitis conditions.

    Nasal Saline

    Using nasal saline to irrigate the nasal cavities may remove mucus, enhance ciliary movement, improve sinus opening, and remove allergic and irritant particles. Several devices exist including: the neti pot, a nasally adapted plastic bottle, and a pulse irrigator. Evidence suggests that hypertonic saline provides modest benefit over isotonic saline, although it might be more irritating.

    Topical Decongestants

    Topical decongestants reduce congestion, but have no effect on itching, sneezing, or rhinorrhea. Oxymetazoline (Afrin), a common topical decongestant, causes nasal vasoconstriction. Vasoconstriction can cause tissue hypoxemia and inflammation, leading to severe rebound nasal congestion. Topical decongestants are not recommended for continued use because they can cause rhinitis medicamentosa.

    Oral Antihistamines

    Oral antihistamines block H1 receptors, thereby reducing nasal and palatal itching, rhinorrhea, sneezing, conjunctivitis, and urticaria.

    Nasal congestion is not treated well with oral antihistamines. First- generation oral antihistamines are poorly selective for H1 receptors. The sedative effects of these antihistamines result from crossing the blood–brain barrier; they have been linked to industrial accidents and contribute to loss of function at work and school. For these reasons, first-generation antihistamines have limited usefulness. Second generation H1 antagonists have excellent evidence for therapeutic efficacy. These medications may have some role in the treatment of nonallergic rhinitis because of their anticholinergic properties, but consideration must be given to these systemic properties, including dry mucous membranes, blurry vision, constipation, tachycardia, and urinary retention. A combination of intranasal corticosteroid treatment with oral antihistamines may be effective for sneezing and rhinorrhea in NARES.

    Leukotriene Receptor Antagonists (LTRA)

    Leukotriene receptor antagonists were originally studied in the treatment of asthma. The only LTRA approved by the FDA for treatment of allergic rhinitis is montelukast (Singulair). Montelukast is clinically efficacious in both perennial and seasonal allergic rhinitis.

    Montelukast is approved for children 6 months and older and has a pregnancy category B rating. The oral antihistamine loratadine (Claritin) and montelukast have similar efficacy, and can have additional benefit when used together. Although rare, montelukast has been associated with adverse psychiatric behavior, including suicidality. LTRA have no role in nonallergic rhinitis.

    Oral Decongestants

    Oral decongestants such as pseudoephedrine reduce nasal congestion. Oral decongestants have a sales restriction in many states. Side effects include insomnia, anorexia, irritability, and palpitations. Blood pressure elevation is rarely a concern in controlled hypertensive patients or in normotensive patients. Oral decongestants should be considered last-line treatment for nonallergic rhinitis conditions.

    Systemic Corticosteroids

    Few studies are available to support the use of systemic steroids in the treatment of rhinitis. Oral corticosteroids may have a role for severe resistive rhinitis, but not as first-line treatment. Short-term use of 5 to 7 days of oral corticosteroids is the standard, but they should not be used for longer than 3 weeks because of the risk for adverse effects.

    Oral steroids should be used as first-line treatment for severe nasal polyposis, a subset of anatomic rhinitis. Systemic steroids should not be used in children or pregnant women. Intraturbinate injections of corticosteroids have no role in the treatment of rhinitis. Parenteral corticosteroids are contraindicated because of long-term effects.


    Surgery can reduce nasal obstruction caused by septal deviation, turbinate hypertrophy, or adenoid hypertrophy. Procedures that can be performed include nasal polypectomy, septoplasty, reductive hypertrophic turbinate surgery, adenoidectomy, and endoscopic sinus surgery. Two nerves can be transected to decrease the parasympathetic nerve supply to the nasal mucosa: the vidian nerve, through endoscopic resection; and the anterior ethmoid nerve, through electrocoagulation, which leads to reduced nasal secretions.

    Anti IgE

    Omalizumab (Xolair) is a monoclonal antibody available for the treatment of poorly controlled asthma, but it might have a role in the treatment of allergic rhinitis.1 Omalizumab binds to IgE, hindering its relationship with inflammatory cells. Omalizumab only binds to circulating IgE and not bound IgE. Due to its high cost, reports of anaphylaxis, and its injectable only formulation, omalizumab has a limited role in allergic rhinitis treatment.


    Allergen extract immunotherapy has been used in the treatment of respiratory allergic disease since 1911, and its efficacy has been documented since the 1970s. The amount of allergen in each immunotherapy dose is slowly increased with each dose until a maintenance phase is reached. Immunotherapy is an effective treatment for allergic rhinitis and is the only treatment proven to alter the course of allergic disease. Debate exists regarding which form of immunotherapy is superior. Contraindications to immunotherapy include beta-blocker use, due to complications in treating anaphylaxis, and uncontrolled underlying diseases, such as uncontrolled asthma.

    Subcutaneous immunotherapy uses the injectable form of allergen extract. Adequate treatment usually consists of a 3- to 5-year course of immunotherapy. Subcutaneous immunotherapy is indicated in those patients for whom medications and avoidance measures are inadequate, as well as those with only a few relevant allergens. The inherent risk of subcutaneous immunotherapy is systemic anaphylaxis, therefore it is dosed in the physician’s office. The rate of local reactions in subcutaneous immunotherapy is 0.6-58% and systemic reactions is 0.06 to 0.9%. The risk of death is 1 per 2.5 million injections. Subcutaneous immunotherapy is covered by most insurance plans.

    Studies for local-route immunotherapy (noninjected), many of which were carried out in Europe, have only been undertaken in adults. Local routes of immunotherapy include sublingual, local nasal, oral, and bronchial. Indications for local-route immunotherapy are the same as those for subcutaneous immunotherapy.

    Sublingual immunotherapy was approved by the FDA in April 2014. Sublingual immunotherapy formulations in the United States are low dose compared to those used in Europe, but have limited allergens available. The risk profile is low and therefore can be dosed at home. The rate of local reactions with sublingual immunotherapy is 0.2-97% and systemic reactions is 0.056%. No deaths have been reported with sublingual immunotherapy use. Some medical allergy providers use subcutaneous extracts (aqueous) as sublingual therapy, but this is an off-label use.

    Use of local nasal immunotherapy is used mostly in Europe. Oral and bronchial immunotherapy are not supported by evidence.

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    The provider should consider stepping down treatment when the patients’ symptoms have been controlled. The Total Nasal Symptoms Score [TNSS] is a subjective assessment of the patient’s specific symptoms, including rhinorrhea, nasal congestion, sneezing, and pruritus, and can be used to assess effectiveness of medications. The Rhinoconjunctivitis Quality of Life Questionnaire can also be used.

    Consideration for referral to an allergist might be extended to patients who have had a prolonged course, secondary infections, polyps, or other comorbid conditions including chronic sinusitis and asthma, or if immunotherapy is a consideration.

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    Rhinitis is associated with multiple complications including fatigue, decline in cognitive function, loss of productivity, headache, and disturbance of sleep. Patients with mild disease may experience these in mild form. Patients with moderate to severe disease may experience these complications in addition to impairment of activities, leisure, and work or school functioning.

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    Chaaban M., Corey J. Pharmacotherapy of rhinitis and rhinosinusitis. Facial Plast Surg Clin North Am. 2012;20:61–71.

    Cox L., Compalati E., Canonica W. Will sublingual immunotherapy become an approved treatment method in the United States? Curr Allergy Asthma Rep. 2011;11:4–6.

    Dykewicz M. Management of rhinitis: guidelines, evidence basis, and systematic clinical approach for what we do.

    Immunol Allergy Clin North Am. 2011;31:619–634.

    Greiner A., Meltzer E. Overview of the treatment of allergic rhinitis and nonallergic rhinopathy. Proc Am Thorac Soc.


    Rondon C., Campo P., Galindo L., et al. Prevalence and clinic relevance of local allergic rhinitis. Allergy. 2012;67:1282–1288. doi:10.1111/all.12002.

    Seidman M.D., Schwartz S.R., Bonner J.R., et al. Clinical practice guideline: allergic rhinitis. Otolaryngol Head Neck Surg.

    2015;152(1 Suppl.):S1–S43.

    Settipane R., Charnock D. Epidemiology of rhinitis: allergic and nonallergic. Clin Allergy Immunol. 2007;19:23–34.

    Sin B., Togias A. Pathophysiology of allergic and nonallergic rhinitis. Proc Am Thorac Soc. 2011;8:106–114.

    van Cauwenberge P., Bachert C., Passalacqua G., et al.

    Consensus statement on the treatment of allergic rhinitis. European Academy of Allergology and Clinical Immunology. Allergy. 2000;55:116–134.

    Wallace D., Dykewicz M. The diagnosis and management of rhinitis: an updated practice parameter. J Allergy Clin Immunol. 2008;122:S1–S84.

    Young-Yuen Wu A. Immunotherapy: vaccines for allergic disease. J Thorac Dis. 2012;4:198–202.

    1  Not FDA approved for this  indication.

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