Allergic Rhinitis

Allergic rhinitis is defined by the presence of nasal congestion, anterior

and posterior rhinorrhea, sneezing, and nasal itching secondary to Ig-E
mediated reaction of the immune system to any allergens that trigger allergic
inflammation of the nasal mucosa.

Allergic rhinitis (AR) affects patients of all ages. It affects 10-30% of

children and adults in the United States, and a 20% overall prevalence in the
Philippines according to the 2008 National Nutrition and Health Survey
(Abong, et.al.). Mainly pollens cause seasonal allergic rhinitis and as such the
clinical symptoms appear within the pollen season. Perennial allergic rhinitis
is caused by chronic exposure to allergens (such as house dust, molds,
certain food) and as such incites a permanent inflammation of the nasal
mucosa.

Risk Factors for Allergic Rhinitis include family history of atopic

diseases, increased serum Ig-E and presence of allergen specific Ig-E, male
sex, firstborn status, early use of antibiotics, and exposure to indoor
allergens. Patients with allergic rhinitis are also found to have other
symptoms of allergic diseases, mainly atopic dermatitis, conjunctivitis, and
asthma. More than 40% of patients with AR have asthma, and more than 80%
of asthmatic patients have concomitant rhinitis. Other co-morbidities
associated with AR include sinusitis, nasal polyposis, upper respiratory tract
infections, and otitis media with effusion; sleep disorders, and impaired
learning and attention in children, among others.

Pathogenesis

The nose has a large mucosal surface area and entrapment of allergens
especially during symptomatic season where the mucosa is already swollen
and hyperemic, triggers submucosal edema with eosinophil infiltration, along
with some basophils and neutrophils. IgE released by plasma cells binds with
mast cells, which generate and release mediators that trigger histamine,
PGD, and leukotrienes, capable of producing tissue edema and eosinophilic
infiltration.

Allergic diseases of the upper airways are frequently inherited in

autosomal-dominant pattern that predisposes an affected person to produce
high levels of allergen-specific IgE. These antibodies crosslinks with allergens
on mast cell surface resulting in degranulation and mediator release that
stimulates blood vessels, nerves, glands causing the clinical manifestations.
Mast cell mediators include histamine, which reproduces all acute symptoms
such as mucus secretion, vasodilation thus nasal congestion, increased
vascular permeability thus tissue edema and sneezing through stimulation of
sensory nerve fibers. Prostaglandins and leukotrienes are produced by the
crosslinking of IgE antibodies on mast cells. Prostaglandin D2 appears to be
more potent than histamine and LTB4 is the most potent chemotactic factor.
Other mediators like bradykinins are vasoactive and platelet-activating factor
is also a potent chemotactic factor.

Immediate allergic response is observed within seconds to minutes of

allergen exposure, peaking at around 15-30 minutes. Sneezing correlates
with histamine influx, as well as presence of prostaglandin and tryptase
reflect the role of mast cells. Late-phase allergic reactions develop in half of
patients with seasonal rhinitis. The late phase reaction is associated with the
recurrence of mast cell mediator release coincident with cytokine production.
The late-phase reaction is also theorized to be related to the chronicity of
symptoms.

Symptoms

According to the Philippine Society of Otorhinolaryngology-Head and

Neck Surgery Clinical Practice Guidelines for Allergic Rhinitis, the diagnosis of
Allergic Rhinitis is strongly considered in the presence of nasal itching,
sneezing, rhinorrhea, nasal congestion or obstruction, triggered by allergen
exposure. Supportive clinical information about frequency, duration, and
severity of symptoms; personal history of atopy manifestations; family history
of atopy; possible allergen identification; absence of symptoms upon change
in environment; previous allergy testing result; response to pharmacological
treatment and previous immunotherapy; must also be elicited. Anterior
rhinoscopy must be performed to support the diagnosis. Nasal endoscopy is
also strongly recommended for select patients. A complete ear, nose, and
throat examination must be performed on all patients with allergic rhinitis.
Detailed allergic work-up may also be performed for patients with
questionable diagnosis, unresponsive/intolerant to pharmacotherapy,
multiple target organ involvement, possible immunotherapy, or local allergic
rhinitis.

Local allergic rhinitis is a subset of patients where clinical history and

physical examination are consistent with allergic rhinitis but no evidence of
systemic atopy.

Treatment

Prevention is essential and individuals with allergic rhinitis are best

treated with less to nil exposure to allergen or triggers. Most patients though
would also require adjuvant pharmacotherapy as well.

Allergen avoidance measure would include humidity control, frequent

change of beddings, avoidance of carpeting, heavy curtains, clothed
upholstery, and the like. Use of dilute bleach solutions on nonporous surfaces
may reduce indoor fungal exposure.

Nasal saline irrigation may also serve as adjunctive treatment for

patients with allergic rhinitis. Moreover, systemic antihistamines are strongly
recommended for patients suffering from intermittent symptoms and short-
term allergen exposure. Alternative therapy for oral/systemic antihistamines
includes intranasal medications. Intranasal corticosteroids are more effective
than antihistamines for patients with moderate-severe, persistent symptoms,
and long-term allergen exposure. The duration of therapy can also be
individually based on patient follow-up findings. Anti-Leukotriene agents like
Montelukast can be given for patients with co-existing asthma. Cromolyn
sodium inhibits degradulation of sensitized mast cells thereby blocking
inflammatory and allergic mediator protein release, and though known for its
lesser side effects, it remains less effective than corticosteroids. Oral and
topical decongestants may be used by patients with prominent nasal
obstruction, but must be used judiciously. Allergen immunotherapy may
prevent new allergen sensitizations and reduce risk of progression of allergic
rhinitis to asthma.

Age-based Approach

Children less than 2 years of age, though uncommon to develop

allergic rhinitis, may benefit from Cromolyn sodium nasal spray and second-
generated antihistamines in liquid formulation. Pediatric patients with severe
symptoms that are unresponsive to either those previously mentioned,
glucocorticoid nasal spray may be administered.

Older children and adults with mild or episodic symptoms can be

managed with second-generation oral antihistamine, glucocorticoid nasal
spray, and cromolyn spray. Persistent or moderate to severe symptoms can
be best addressed with glucocorticoid nasal sprays.

Bibliography

Abong, J. (2012). Prevalence of Allergic Rhinitis in Filipino adults based on the

National Nutrition and Health Survey. Asia Pacific Allergy. Vol 2: pp. 129-
135

Clinical Practice Guidelines, PSO-HNS on Allergic Rhinitis in Adults. (2015).

Prepared by Philippine Academy of Rhinology.

de Shazo, R. and Kemp, S. (2016.) Allergic rhinitis: Clinical manifestations,

epidemiology, and diagnosis. UptoDate Wolters Kluver, retrieved 25 February
2017.
de Shazo, R. and Kemp, S. (2016.) Pathogenesis of allergic rhinitis (rhinosinusitis).
UptoDate Wolters Kluver, retrieved 25 February 2017.

de Shazo, R. and Kemp, S. (2016.) Pharmacotherapy of allergic rhinitis.

UptoDate Wolters Kluver, retrieved 25 February 2017.

Kasper, D.L. et al. (2015). Harrisons Principles of Internal Medicine, 19 th

Edition. McGraw-Hill Education, USA.

Probst, R. et. al. (2006). Basic Otorhinolaryngology, A Step by Step Learning

Guide. Thieme, New York, USA.