Allergic Rhinitis
Key statements
• Allergic rhinitis (AR) results from an IgE-mediated
inflammation of the nasal mucosa.
• The disease currently affects between 10% and 30 % of
the population.
• Studies indicate that prevalence rates are increasing
worldwide.
• The classification proposed in the Allergic Rhinitis and
its Impact on Asthma (ARIA) guidelines is useful for the
implementation of treatment.
• AR is a risk factor for asthma.
• Other co-morbidities of AR include: sinusitis, nasal
polyposis, conjunctivitis, otitis media with effusion, upper
respiratory infections, breathing through the mouth, and
sleep disorders.
• AR has a significant impact on patients based on
the degree of the severity of their symptoms. It has
psychological effects, interferes with social interactions,
and creates an economic burden not only for the affected
subject, but for the family and for the society at large.
• Management is based on patient education,
environmental control measures, pharmacotherapy and
specific immunotherapy
Introduction
Allergic rhinitis is defined by the presence of nasal
congestion, anterior and posterior rhinorrhea, sneezing,
and nasal itching secondary to IgE-mediated inflammation
of the nasal mucosa. It must be differentiated from other
non allergic forms of rhinitis with a similar clinical picture
Risk factors for the development of AR include a family
history of atopic diseases, increased total serum IgE
before 6 years of age, higher socio-economic class, and
the presence of positive immediate-type hypersensitivity
skin tests. The most common causative allergens include
pollens, dust mites, molds, and insects.
Atopic subjects inherit a predisposition to produce specific
IgE antibodies that bind to high-affinity receptors on mast
cells. In the nose, IgE-bound mast cells recognize the allergen
and degranulate, releasing preformed mediators (histamine,
tryptase, chymase, kininogenase, heparin, and other enzymes).
Newly formed mediators including prostaglandin D2 and
cysteinyl leukotrienes are released by mast cells, eosinophils,
basophils, and macrophages and produce edema, rhinorrhea,
mucosal hypertrophy, mucus secretion, and vasodilation leading
to nasal obstruction. Stimulation of sensory nerves results
in nasal itch, sneezing, and increased congestion. This early
allergic response is followed by a late-phase response starting
4 - 8 hours after allergen exposure, which is characterized
by congestion, postnasal mucous discharge, hyposmia, and
nasal hyperreactivity to non specific environmental stimuli.
Repeated mucosal exposure to allergens results in a priming
mechanism by which the amount of allergen required to induce
an immediate response decreases as a consequence of the
influx of inflammatory cells
Prevalence
Allergic rhinitis is the most common form of non-infectious
rhinitis, affecting between 10% and 30% of all adults and as
many as 40% of children. Epidemiologic studies show that the
prevalence of AR continues to increase worldwide. The World
Health Organization has estimated that 400 million people in
the world suffer from AR, and 300 million from asthma.
In the United States of America, the prevalence of AR ranges
from 3% to 19%. According to the Centers for Disease
Control and Prevention, 23.7 million cases were reported in
1996. Overall, it affects 30 to 60 million individuals annually. In
childhood, affected boys outnumber girls, but the sex ratio is
about equal in adults. AR develops before the age of 20 years
in 80% of cases. Increased prevalence is observed in non
whites, in some polluted urban areas, and in first-born children.
AR accounts for 16.7 million physician office visits annually.
In Europe, the European Community Respiratory Health Survey
established the prevalence of AR as being from 4% to 32%.
The International Study on Asthma and Allergies in Childhood
(ISAAC) reported the prevalence of allergic rhinitis in Latin
America.
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