Allergic rhinitis refers to a symptom complex characterized by inflammation of the nasal mucosa that occurs when susceptible patients come into contact with a specific allergen.  Mediators of allergic rhinitis include histamine in the early phase and leukotrienes, prostaglandins, and cytokines in the late phase of the allergic reaction.  There are two seasons when allergy symptoms are prevalent, the early spring (tree and grass pollen) and late summer to early autumn covering August through October (ragweed pollen and mold spores).  Common household allergens include dust mites (Dermatophagoides pteronyssinus and D. farinae), cockroaches, pet dander, and fungi.  Women may develop symptoms of allergic rhinitis during pregnancy.  These symptoms result from an increase in the activity of nasal mucous glands and an increase in nasal blood flow which is a consequence of the elevated hormone levels associated with pregnancy.

     Symptoms generally begin with sneezing, nasal discharge (rhinorrhea), and ocular symptoms to include swelling, pruritus, and increased tearing.  If untreated, symptoms may progress to include congestion, postnasal drainage with resultant pharyngitis, headache, fatigue, ear popping, and/or pruritus of the auditory canal, nose, palate or throat.  Chronic cough is also a common symptom of allergic rhinitis.  Some patients present in an atypical fashion manifesting only a few symptoms; therefore, the clinician needs to always consider the diagnosis when evaluating patients with any of the above symptoms.  Consider this diagnosis when patients present with a “summer cold” or a cold that occurs during the same month every year.  Allergic rhinitis is associated with conditions such as asthma, sinusitis, and otitis media.

     The diagnosis is made clinically.  One lab abnormality that may suggest the diagnosis in patients who display symptoms, is the finding of eosinophilia on peripheral smear.  Although, this abnormality is not always present or specific.  Even when symptoms of rhinitis are present, the etiology is not always secondary to allergies.  Other causes of rhinitis include viral and bacterial sinus infections, NARES syndrome, gustatory rhinitis, vasomotor rhinitis, hormonally induced rhinitis, rhinitis medicamentosa (secondary to prolonged use of nasal decongestant sprays), drug induced rhinitis (ACE inhibitors, aspirin, beta blockers, and NSAIDs), atrophic rhinitis and the ciliary dyskinesia syndrome.  An empiric trial of therapy for allergic rhinitis is generally started in patients who present with symptoms.  If patients fail to respond to aggressive therapy, then one of the other potential etiologies should be suspected, and the appropriate evaluation should be initiated.

     The first step in therapy is to advise patients to discontinue any medications which may cause drug induced rhinitis and to avoid any identifiable allergens.  If household allergens are the cause of symptoms, limit the amount of upholstery and carpeting in the household.  Clean remaining carpets with a high-efficiency particulate air (HEPA) filter or a double thickness vacuum bag containing vacuum cleaner.  Other methods include frequent house cleaning, exposing bedding and furniture to heat or cold, controlling humidity, using chemicals that kill mites and cockroaches, covering bedding components (pillows, box springs, mattresses) with breathable microfine cotton fabrics or synthetic fabrics, washing bedding weekly in hot water with 1% tannic acid, counseling patients to exile all pets to living outdoors, limiting the amount of paraphernalia that collects dust, and eliminating standing water.  Chemicals which may be beneficial in reducing indoor allergens include benzyl benzoate (dust mites), hydramethylnon (cockroach), fipronil (cockroach), or boric acid (cockroach).  Small objects may be placed in a freezer to kill mites; whereas, in areas where the temperatures fall below freezing, larger objects may be placed outdoors for 3 days. While this advice is prudent, it is often labor intensive and therefore noncompliance is high. Many opt instead to initiate therapy first, and failing that, counsel patients on the above measures.

     Patients should be encouraged to comply with medical therapy for at least 1 to 2 weeks before deciding on the efficacy of a specific form of treatment.  Mild to moderate symptoms often respond to oral antihistamines, oral decongestants, leukotriene inhibitors, and intranasal therapy with either cromolyn sodium, ipratropium bromide,or steroids.  Intranasal steroids are a very effective form of therapy for most symptoms and are generally the drug of first choice.  Eye drops (patanol, crolom, or antihistamine drops) may be added to help combat ocular symptoms.  If symptoms are limited to nasal discharge or itching, nasal antihistamines or any of the above mentioned intranasal products may be sufficient.  Allergy induced cough may persist despite therapy with a second generation antihistamines; however, therapy with the first generation antihistamines chlorpheniramine or azatadine maleate may prove effective.  Cromolyn or nedrocromil sodium via metered dose inhalers may help with allergy induced variant cough.  If symptoms are refractory to therapy, a brief course of an oral steroid may help to control symptoms.  Immunotherapy (allergy shots) may be required for severe and refractory cases.  Referral to an allergy specialist for skin testing may be required in refractory cases.