Allergic rhinitis, which affects approximately one in five Americans,1
is an inflammatory disease caused by an IgE-mediated immune response to inhaled allergens at the nasal mucosa. Onset of allergic rhinitis is most common in childhood with a mean age of onset of 8–11 years, but allergic rhinitis occurs in people of all ages.2
The disease affects boys more often than girls in childhood, but affects the sexes nearly equally in adulthood.2
Allergic rhinitis is characterized by nasal symptoms of congestion, rhinorrhea, sneezing, and ocular symptoms of redness, tearing, and itching,3
and it can be complicated by comorbidities including asthma, sinusitis, and otitis media.4
Symptoms disturb sleep, cause fatigue, and impair concentration. These effects may underlie the negative effects of allergic rhinitis on productivity and quality of life.1
Each year in the US, an estimated 3.5 million work days and two million school days are lost because of allergic rhinitis,1
and estimated annual direct and indirect costs of up to $4.9 billion and $9.7 billion, respectively, are incurred.9
Pharmacotherapy for allergic rhinitis includes intranasal corticosteroids and antihistamine-decongestant combinations, as well as the less commonly used decongestants alone, intranasal anticholinergics, oral, intranasal, and intraocular antihistamines, and mast cell stabilizers. Of these classes of therapy, intranasal corticosteroids are the preferred treatment for seasonal allergic rhinitis and are recommended in both the American Academy of Allergy, Asthma and Immunology guidelines and the World Health Organization Allergic Rhinitis and Impact on Asthma guidelines as the first line of pharmacotherapy for rhinitis with prominent nasal congestion, which is the most bothersome symptom of allergic rhinitis.3
Only intranasal corticosteroids have proven anti-inflammatory activity against the pathophysiologic aspects of both early- and late-phase allergic reactions and are effective for the range of nasal symptoms.10
In that intranasal corticosteroids inhibit the inflammatory process mediating nasal symptoms and consistently alleviate nasal congestion, they differ from oral antihistamines, which are not particularly effective for nasal congestion. In addition, systemic drug exposure and corresponding risk of systemic side effects are minimal with intranasal corticosteroids.
The enhanced-affinity intranasal corticosteroid fluticasone furoate nasal spray (GW685698X) is one of the newest additions to the armamentarium for allergic rhinitis. Fluticasone furoate was introduced in 2007 as Veramyst® in the US, where it is indicated for treatment of symptoms of seasonal and perennial allergic rhinitis in adults and children two years and older. In Europe, fluticasone furoate is marketed as Avamys® and is indicated for the treatment of symptoms of allergic rhinitis in adults and children six years and older. Fluticasone furoate is a new molecular entity that differs from other corticosteroid molecules, including fluticasone propionate and mometasone furoate. Important attributes of fluticasone furoate in seasonal allergic rhinitis include very low systemic bioavailability (<0.5%), onset of symptom relief as early as eight hours after initiation of treatment, 24-hour symptom relief with once-daily dosing, comprehensive coverage of both nasal and ocular symptoms, safety and tolerability with daily use, and availability in a novel, side-actuated delivery device designed to make medication delivery simple and consistent. This review summarizes the preclinical and clinical data on fluticasone furoate nasal spray and discusses its place in pharmacotherapy for allergic rhinitis.