The presence of allergic rhinitis (seasonal or perennial) significantly increases the probability of asthma: up to 40% of people with allergic rhinitis have or will have asthma. Atopic eczema frequently precedes allergic rhinitis. Patients with allergic rhinitis usually have allergic conjunctivitis as well. The factors determining which atopic disease will develop in an individual person and the reasons why some people have only rhinitis and others have rhinitis after eczema or with asthma remain unclear.
The differential diagnosis includes forms of rhinitis that are nonallergic in origin such as a noninflammatory rhinopathy (also known as vasomotor rhinitis) and nonallergic chronic rhinosinusitis. Seasonal symptoms can be caused by viral infections, especially if the patient is a child or lives with children; rhinovirus has a marked peak in incidence in September and a smaller peak in the spring. The diagnosis of allergic rhinitis is often made clinically on the basis of characteristic symptoms and a good response to empirical treatment with an antihistamine or nasal glucocorticoid. Formal diagnosis is based on evidence of sensitization, measured either by the presence of allergen-specific IgE in the serum or by positive epicutaneous skin tests (i.e., wheal and flare responses to allergen extracts) and a history of symptoms that correspond with exposure to the sensitizing allergen. Epicutaneous skin testing and testing for allergen-specific IgE have similar sensitivity, although they do not identify sensitization in an entirely overlapping group of patients.
Pharmacologic treatment options include H1-antihistamines, intranasal glucocorticoids, and leukotriene-receptor antagonists. Therapy usually starts with oral antihistamines, frequently initiated by the patient. H1-antihistamines are also available as nasal sprays by prescription. The intranasal preparations appear to be similar to oral preparations in efficacy but may be less acceptable to patients owing to a bitter taste. The effect of antihistamines on symptoms, especially nasal congestion, is modest. They can be combined with oral decongestants, and the combination can improve nasal airflow in the short term (on the basis of data from trials lasting 2 to 6 weeks), at the cost of some side effects. Topical nasal decongestants are more effective than oral agents, but there are reports of rebound congestion (rhinitis medicamentosa) or reduced effectiveness beginning as early as 3 days after treatment, and only short-term use is recommended. In one study, adding an intranasal glucocorticoid reversed the reduced effectiveness of a topical decongestant. Intranasal glucocorticoids are the most effective pharmacotherapy for seasonal allergic rhinitis, yet the overall efficacy is moderate. Although the clinical effects appear within a day, the peak effect in cases of perennial rhinitis is not reached for several weeks. The superiority of intranasal glucocorticoids over antihistamines in the treatment of perennial allergic rhinitis is uncertain. The effect of leukotriene-receptor antagonists on the symptoms of allergic rhinitis is similar to or slightly less than that of oral antihistamines, and some randomized trials have shown a benefit of adding the leukotriene-receptor antagonist montelukast to an antihistamine. Although the majority of trials have favored intranasal glucocorticoids over this combination, data are inconsistent; this combination should be considered for patients whose symptoms are inadequately controlled with an antihistamine and who do not wish to use a glucocorticoid nasal spray. There is no significant benefit of adding an oral antihistamine or montelukast to a nasal glucocorticoid. However, in randomized trials, the combination of an intranasal antihistamine plus an intranasal glucocorticoid has been shown to be superior to either agent alone.
Although allergen immunotherapy has traditionally been administered subcutaneously in the United States, rapidly dissolving tablets for sublingual administration were recently approved by the FDA for treatment of grass and ragweed allergy. With immunotherapy, unlike pharmacotherapy, the effect persists after the discontinuation of therapy. If there is improvement in the first year, injections are generally continued for at least 3 years. Data from randomized trials are lacking to guide decisions about the duration of therapy. Subcutaneous immunotherapy carries a risk of systemic reactions, which occur in 0.1% of injection visits, in rare cases leading to life-threatening anaphylaxis (1 reaction per 1 million injection visits). Although subcutaneous immunotherapy has not been compared with sublingual immunotherapy in large head-to-head trials, indirect comparisons suggest that subcutaneous immunotherapy is more effective for symptom relief. However, sublingual immunotherapy has a clear advantage in terms of safety, with very few reports of anaphylactic reactions.
- Treat allergic rhinitis aggressively. Oral H1 antihistaminics +/- nasal steroids is a good first line approach.
- Oral or topical decongestants help to alleviate symptoms, but with some side effects and risk of tachyphylaxis and rebound effect. Therefore, use with caution and for short periods of time.
- Refer to allergy testing patient with severe symptoms, combination with asthma and/or atopic dermatitis.