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.
In summary:
- 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.
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