#Allergic #rhinitis is very common. Seasonal
#allergicRhinitis is most commonly caused by pollens and spores. Flowering shrub and tree pollens are most common in the spring, flowering plants and grasses in the summer, and ragweed and molds in the fall. Dust, house-hold mites, air pollution, and pet dander may produce year-round symptoms, termed “perennial rhinitis.”
Allergic rhinitis is caused by exposure to an airborne allergen in a predisposed individual. Activation of both humoral (B-cell) and cytotoxic (T-cell) immune responses with subsequent allergen-specific IgE responses causes release of inflammatory mediators. The response is
increased as antigen is passed to regional lymph nodes for greater T-cell activation. Interleukin and cytokine release causes specific activation of mast cells, eosinophils, plasma cells, basophils and other T-cells. Many of these circulating cells then migrate into the nasal and ocular epithelium
where they contribute directly to symptoms through proinflammatory mediators, including histamine, prosta-glandins, and kinins.
Clinical Findings
The symptoms of “hay fever” are similar to those of viral rhinitis but are usually persistent and may show seasonal variation. Nasal symptoms are often accompanied by eye irritation, pruritus, conjunctival erythema, and excessive tearing. Many patients will note a strong family history of atopy or allergy.
The clinician should be careful to distinguish allergic rhinitis from nonallergic or vasomotor rhinitis. Vasomotor rhinitis is caused by increased sensitivity of the vidian nerve and is a common cause of clear rhinorrhea in the elderly. Often patients will report that they have troubling rhinorrhea in response to numerous nasal stimuli, includ-ing warm or cold air, odors or scents, light, or particulate matter. On physical examination, the mucosa of the turbinates is usually pale or violaceous because of venous engorge-ment. This is in contrast to the erythema of viral rhinitis. Nasal polyps, which are yellowish boggy masses of hyper-trophic mucosa, are associated with long-standing allergic rhinitis.
Treatment
A. Intranasal Corticosteroids
Intranasal corticosteroid sprays have revolutionized the treatment of allergic rhinitis. Evidence-based literature reviews show that these are more effective—and frequently less expensive—than nonsedating antihistamines. Patients should be reminded that there may be a delay in onset of relief of 2 or more weeks. Corticosteroid sprays may also
shrink hypertrophic nasal mucosa and nasal polyps, thereby providing an improved nasal airway and osteomeatal com-plex drainage. Because of this effect, intranasal corticos-teroids are critical in treating allergy in patients prone to recurrent acute bacterial rhinosinusitis or chronic rhi-nosinusitis. There are many available preparations, including beclomethasone (42 mcg/spray twice daily per nostril), flunisolide (25 mcg/spray twice daily per nos-tril), mometasone furoate (200 mcg once daily per nos-tril), budesonide (100 mcg twice daily per nostril) and fluticasone propionate (200 mcg once daily per nostril). All intranasal corticosteroids are considered equally effective. Probably the most critical factor is compliance with regu-lar use and proper introduction into the nasal cavity. In order to deliver medication to the region of the middle
meatus, proper application involves holding the bottle straight up with the head tilted forward and pointing the bottle toward the ipsilateral ear when spraying. Side effects are limited and the most annoying is epistaxis. Some experts believe that this is related to incorrect delivery of the drug to the nasal septum.
B. Antihistamines
Treatment of allergic and perennial rhinitis has improved in recent years. Antihistamines offer temporary, but imme-diate, control of many of the most troubling symptoms of allergic rhinitis. Over-the-counter antihistamines include nonsedating
#loratadine (10 mg orally once daily) and minimally sedating cetirizine (10 mg orally once daily). Brompheniramine or chlorpheniramine (4 mg orallyevery 6–8 hours, or 8–12 mg orally every 8–12 hours as asustained-release tablet) and clemastine (1.34–2.68 mg
orally twice daily) may be less expensive, although usually associated with some drowsiness. Prescription oral H1-receptor antagonists include fexofenadine (60 mgtwice daily or 120 mg once daily) and desloratadine (5 mg once daily). Fexofenadine appears to be nonsedating;
desloratadine is minimally sedating. Also shown to be effective in randomized trials are ebastine (10–20 mg orally once daily) and misolastine (10 mg orally once daily). The H1-receptor antagonist antihistamine nasal spray azelastine (1–2 sprays per nostril daily) has also been shown to be effective in a randomized trial. Topical
#nasalsprays are particularly useful in patients who experience
side effects, mostly xerostomia and sedation, of oral anti-histamines. Many patients who find initial benefit from an antihistamine complain that allergy symptoms eventually return after several months of use. In such patients, typi-cally with perennial allergy problems, antihistamine toler-ance seems to develop and alternating effective antihistamines periodically can control symptoms over the long term.
C. Adjunctive Treatment Measures
In addition to intranasal corticosteroid sprays and anti-histamines, including H1-receptor antagonists, the litera-ture supports the use of antileukotriene medications such as montelukast (10 mg/d orally) alone or with
#cetirizine (10 mg/d orally) or loratadine (10 mg/d orally). There are
proinflammatory effects of cysteinyl leukotrienes in upper airway disease, including allergic rhinitis, and hyperplas-tic polyposis, and sinusitis. Improved nasal rhinorrhea, sneezing, and congestion are seen with the use of leukot-riene receptor antagonists, often in conjunction with
antihistamines. Cromolyn sodium and sodium nedocro-mil are also useful adjunct agents for allergic rhinitis.
They work by stabilizing mast cells and preventing proin-flammatory mediator release. They are not absorbed by the gastrointestinal tract but do function topically and have very few side effects. The most useful form of cro-molyn is probably the ophthalmologic preparation; the nasal preparation is not nearly as effective as inhaled cor-ticosteroids. Intranasal cromolyn is cleared rapidly and must be administered four times daily for continued relief of symptoms.
Intranasal anticholinergic agents, such as ipratropium bromide 0.03% or 0.06% sprays (42–84 mcg per nostril three times daily), may be helpful adjuncts when rhinor-rhea is a major symptom. Ipratropium nasal sprays are not as effective as intranasal corticosteroids for treating
allergic rhinitis but are useful for treating vasomotor rhinitis. Avoiding or reducing exposure to airborne allergens is the most effective means of alleviating symptoms of aller-gic rhinitis. Depending on the allergen, this can be extremely difficult. Maintaining an allergen-free environment by
covering pillows and mattresses with plastic covers, substi-tuting synthetic materials (foam mattress, acrylics) for animal products (wool, horsehair), and removing dust-collecting household fixtures (carpets, drapes, bedspreads,wicker) is worth the attempt to help more troubled
patients. Air purifiers and dust filters may also aid in main-taining an allergen-free environment. Nasal saline irriga-tions are a useful adjunct in the treatment of allergic rhinitis to mechanically flush the allergens from the nasal cavity. Though debated, there is no clear benefit to hyper-tonic saline over commercially available normal saline preparations (eg, Ayr or Ocean Spray). When symptoms are extremely bothersome, a search for offending allergens may prove helpful. This can either be done by serum radio-allergosorbent test (RAST) testing or skin testing by an
allergist.In some cases, allergic rhinitis symptoms are inade-quately relieved by medication and avoidance measures. Often, such patients have a strong family history of atopy and may also have lower respiratory manifestations such as allergic
#asthma. Referral to an allergist may be appro-priate for consideration of immunotherapy. This treat-ment course is quite involved, with proper identification of offending allergens, progressively increasing doses of allergen(s) and eventual maintenance dose administration over a period of 3–5 years. Immunotherapy has been proven to reduce circulating IgE levels in patients with allergic rhinitis and reduce the need for allergy medica-tions. While oral allergen exposure is actively being inves-tigated, currently the primary mode of allergen exposure is by subcutaneous injection. Treatments are given at a suitable medical facility with monitoring following treat-ment because of the risk of anaphylaxis during dose esca-lation. Local reactions are common and usually self-limited.
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