Allergic Rhinitis
Treatment
Allergen avoidance
Avoidance of allergens which trigger the inflammatory cascade is preventive measure to avoid symptoms of allergic rhinitis.
Pharmacotherapy
- Antihistamines
- Decongestants
- Nasal corticosteroids
- Immunotherapy
1. Antihistamines
Histamine H1-receptor antagonists bind to H1 receptors without activating them, preventing histamine binding and action. They are more effective in preventing the histamine response than in reversing it.
Oral antihistamines can be divided into two major categories:
- Nonselective (first-generation or sedating antihistamines)
- Peripherally selective (second generation or non-sedating antihistamines)
However, individual agents should be judged on their specific sedating effects because variation exists among agents within these broad categories. The central sedating effect may depend on the ability to cross the blood brain barrier. Most older antihistamines are lipid soluble and cross this barrier easily. The peripherally selective agents have little or no central or autonomic nervous system effects.
Symptom relief is caused in part by anticholinergic properties, which are responsible for the drying effect that reduces nasal, salivary, and lacrimal gland hypersecretion.
Antihistamines antagonize increased capillary permeability, wheal and flare formation, and itching. Drowsiness is the most frequent side effect, and it can interfere with driving ability or adequate functioning at the workplace. Sedative effects can be beneficial in patients who have difficulty sleeping because of rhinitis symptoms.
Although anticholinergic (drying) effects contribute to efficacy, adverse effects such as dry mouth, difficulty in voiding urine, constipation, and potential cardiovascular effects may occur. Antihistamines should be used with caution in patients predisposed to urinary retention and in those with increased intraocular pressure, hyperthyroidism, and cardiovascular disease.
Other side effects include loss of appetite, nausea, vomiting, and epigastric distress.
Antihistamines are more effective when taken approximately 1 to 2 hours before anticipated exposure to the offending allergen.
Azelastine is an intranasal antihistamine that rapidly relieves symptoms of seasonal allergic rhinitis. However, patients should be cautioned about its potential for drowsiness because systemic availability is approximately 40%. Patients may also experience drying effects, headache, and diminished effectiveness over time.
Levocabastine and olopatadine are ophthalmic anti-histamines that can be used for allergic conjunctivitis that is often associated with allergic rhinitis. However, systemic antihistamines are usually effective for allergic conjunctivitis, making an ocular product unnecessary.
They may be a logical addition to nasal glucocorticoids when ocular symptoms occur.
2. Decongestants
Topical and systemic decongestants are sympathomimetic agents that act on adrenergic receptors in the nasal mucosa to produce vasoconstriction, shrink swollen mucosa and improve ventilation. Decongestants work well in combination with antihistamines when nasal congestion is part of the clinical picture.
Topical decongestants are applied directly to swollen nasal mucosa via drops or sprays. They result in little or no systemic absorption.
Prolonged use of topical agents (more than 3 to 5 days) can result in rhinitis medicamentosa, which is rebound vasodilation with congestion. Patients with this condition use more spray more often with less response.
Abrupt cessation is an effective treatment, but rebound congestion may last for several days or weeks. Nasal steroids have been used successfully, but they take several days to work. Weaning the patient off the topical decongestant can be accomplished by decreasing the dosing frequency or concentration over several weeks. Combining the weaning process with nasal steroids may be helpful.
Other adverse effects of topical decongestants include burning, stinging, sneezing, and dryness of the nasal mucosa.
These products should be used only when absolutely necessary (e.g., at bedtime) and in doses that are as small and infrequent as possible. Duration of therapy should always be limited to 3 to 5 days.
Pseudoephedrine is an oral decongestant that has a slower onset of action than topical agents but may last longer and cause less local irritation. Also, rhinitis medicamentosa does not occur with oral decongestants. Doses up to 180 mg produce no measurable change in blood pressure or heart rate. However, higher doses (210 to 240 mg) may raise both blood pressure and heart rate.
Systemic decongestants should be avoided in hypertensive patients unless absolutely necessary. Severe hypertensive reactions can occur when pseudoephedrine is given concomitantly with mono- amine oxidase inhibitors. Pseudoephedrine can cause mild CNS stimulation, even at therapeutic doses.
Phenylephrine has replaced pseudoephedrine in many nonprescription antihistamine decongestant combination products because of the legal restriction on pseudoephedrine sales.
Use of combination oral products containing a decongestant and antihistamine is rational because of the different mechanisms of action.
3. Nasal corticosteroids
Intranasal corticosteroids effectively relieve sneezing, rhinorrhea, pruritus, and nasal congestion with minimal side effects. They reduce inflammation by blocking mediator release, suppressing neutrophil chemotaxis, causing mild vasoconstriction, and inhibiting mast cell mediated, late phase reactions.
These agents are an excellent choice for perennial rhinitis and can be useful in seasonal rhinitis, especially if begun in advance of symptoms. Some authorities recommend nasal steroids as initial therapy over antihistamines because of their high degree of efficacy when used properly along with allergen avoidance.
Side effects include sneezing, stinging, headache, epistaxis, and rare infections with
Candida albicans
Some patients improve within a few days, but peak response may require 2 to 3 weeks. The dosage may be reduced once a response is achieved.
Blocked nasal passages should be cleared with a decongestant or saline irrigation before administration to ensure adequate penetration of the spray.
Cromolyn sodium, a mast cell stabilizer, is available as a nonprescription nasal spray for symptomatic prevention and treatment of allergic rhinitis. It prevents antigen-triggered mast cell degranulation and release of mediators, including histamine.
The most common side effect is local irritation (sneezing and nasal stinging).
The dosage for individuals at least 2 years of age is one spray in each nostril three to four times daily at regular intervals. Nasal passages should be cleared before administration, and inhaling through the nose during administration enhances distribution to the entire nasal lining.
For seasonal rhinitis, treatment should be initiated just before the start of the offending allergen’s season and continue throughout the season.
In perennial rhinitis, the effects may not be seen for 2 to 4 weeks; antihistamines or decongestants may be needed during this initial phase of therapy.
Ipratropium Bromide is an anticholinergic agent useful in perennial allergic rhinitis.
It exhibits antisecretory properties when applied locally and provides symptomatic relief of rhinorrhea associated with allergic and other forms of chronic rhinitis.
The 0.03% solution is given as two sprays (42 mcg) two to three times daily. Adverse effects are mild and include headache, epistaxis, and nasal dryness.
Montelukast is a leukotriene receptor antagonist approved for treatment of seasonal allergic rhinitis. It is effective alone or in combination with an antihistamine.
The dosage for adults and adolescents older than 15 years is one 10 mg daily. Children aged 6 to 14 years may receive one 5-mg daily. Children aged 2 to 5 years may be given one 4-mg daily. The timing of administration can be individualized. The dose should be given in the evening if the patient has combined asthma and seasonal allergic rhinitis.
Although leukotriene antagonists represent a new therapeutic alternative, published studies to date have shown them to be no more effective than peripherally selective antihistamines and less effective than intranasal corticosteroids. However, combined use with antihistamines is more effective than antihistamine treatment alone.
4. Immunotherapy
Immunotherapy is the slow, gradual process of injecting increasing doses of antigens responsible for eliciting allergic symptoms in a patient with the intent of increasing tolerance to the allergen when natural exposure occurs.
The effectiveness of immunotherapy may result from diminished IgE production, increased IgG production, changes in T lymphocytes, reduced inflammatory mediator release from sensitized cells, and diminished tissue responsiveness.
In general, very dilute solutions are given initially once or twice per week.
The concentration is increased until the maximum tolerated dose is achieved. This maintenance dose is continued every 2 to 6 weeks, depending on clinical response. Better results are obtained with year-round rather than seasonal injections. Common mild local adverse reactions include induration and swelling at the injection site. More severe reactions (generalized urticaria, broncho- spasm, laryngospasm, vascular collapse, and death from anaphylaxis) occur rarely. Severe reactions are treated with epinephrine, antihistamines, and systemic corticosteroids.
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