• Allergic rhinitis (AR) is the most common chronic dis-
ease in children
• Often being mistaken for recurrent episodes of the com-
mon cold
• It is one of the major reasons for visits to pediatricians
and is associated with a number of significant comorbidi- ties
• AR is a hypersensitivity reaction to specific allergens that
occur in sensitized patients
• It is mediated by immunoglobulin E (IgE) antibodies and
results in inflammation (Table 1)
Classification
• Intermittent disease with symptoms < 4 days/week or for
duration < 4 weeks usually related to outdoor allergens, e.g., pollens
• Persistent disease with symptoms > 4 days/week and are
present for > 4 weeks, usually related to indoors allergens, e.g., molds
Clinical presentation
• Nasal congestion may be reported by parents as mouth
161 Allergic and Immunologic Disorders
• Paroxysmal sneezing, nasal and palatal pruritus, nose
blowing, sniffing, snorting, and occasional coughing
• Nasal pruritus often produces the classic sign of the aller-
gic salute
• Itchy eyes and postnasal drip
• Seasonality, progression of symptoms, identifiable trig-
gers, alleviating factors, and responsiveness to allergy medication
• Comorbid conditions such as headaches, sleep distur-
bance, fatigue, and impaired concentration and attentive- ness at school
• Nasal turbinates may appear edematous, with a pale to
bluish hue
• Cobblestoning from lymphoid hyperplasia may be seen
on the posterior oropharynx
• Dark discolorations underneath the eyes, “allergic shin-
ers,” are due to venous engorgement and suborbital edema
• Dennie lines are folds under the eyes due to edema
• A transverse nasal crease is seen across the bridge of the
nose in children who chronically push their palms upward
under their noses (allergic salute; Fig. 1)
• Chronic mouth breathing from nasal obstruction may
cause “allergic facies,” with an open mouth, receding chin, overbite, elongated face, and arched hard palate
Diagnosis
• History and physical examination are keys to diagnosing
AR
• Percutaneous (prick or puncture) skin testing remains the
most specific and cost-effective diagnostic modality
• ELISA immunology testing also may be used
• These tests can help to identify the offending allergen,
and specific avoidance can be recommended
• Nasal smear for eosinophils with eosinophil count of
greater than 4 % in children may be help to distinguish AR from viral infections and nonallergic rhinitis
Management
• Allergen avoidance, whenever possible
• Intermittent disease (Outdoor environmental control)
− Staying inside (5 am to 10 am)
− Keep air-conditioning on during the spring, fall, and pollen seasons
• Persistent disease (Indoor environmental control)
− Avoiding molds include humidity control < 51 % in the home by using a dehumidifier
− Use dust mite covers on the bed and pillows − Use hypoallergenic pillows and comforters Table 1 Types of hypersensitivity
Hypersensitivity type Associated disorders Mediators Description Type I: Allergy (immediate) Atopy
Asthma Anaphylaxis
IgE Fast response which occurs in minutes
Free antigens cross link the IgE on mast cells and basophils, which causes a release of vasoactive biomolecules
Testing can be done via skin test for specific IgE Type II: Cytotoxic,
antibody-dependent Autoimmune hemolytic anemiaThrombocytopenia Rheumatic heart disease Membranous nephropathy
IgM or IgG Complement MAC (membrane attack complex)
Antibody (IgM or IgG) binds to antigen on a target cell, which is actually a host cell that is perceived by the immune system as foreign, leading to cellular destruction via the MAC
Testing includes both the direct and indirect Coombs test
Type III: Immune complex
disease Serum sicknessLupus PSGN
IgG Complement Neutrophils
Antibody (IgG) binds to soluble antigen, forming a circulating immune complex. This is often deposited in the vessel walls of the joints and kidney, initiating a local inflammatory reaction
Type IV: Delayed-type hyper- sensitivity cell-mediated immune memory response, antibody-independent
Contact dermatitis TB skin test
Chronic transplant rejection
T-Cell T cells find antigen and activate macrophages
Fig. 1 A child with allergic rhinitis showing the transverse nasal
162 O. Naga
− Wash linens in hot water to denature dust mite allergen − If allergic to pets get rid of them entirely or removing
pets from the bedroom may help decrease exposure to their danders
• Intranasal corticosteroids (INS)
− The first-line treatment and most effective for patients who have AR
− Onset of action has been shown to be within 12 h − Can be used as needed
− Epistaxis is most common side effect
− Generally has no effect on growth over 1 year of treat- ment in pediatric patients
• H1 antihistamine
− The most popular
− Decreased sneezing, itching, and rhinorrhea, but oral antihistamines are notoriously ineffective in treating nasal congestion
− Adverse effects include sedation, which can lead to reduced school and cognitive performance
− Sedation effect can be avoided by using second-gen- eration antihistamines that have low or no sedation effects
• Decongestants side effects
− Cardiac-related events such as palpitations and tachycardia
− Prolonged use of topical decongestant can lead to rhi- nitis medicamentosa (rebound nasal congestion)
• LTRA such as montelukast can be used
• Allergy immunotherapy
− It is not used routinely for management of typical AR − Its use is reserved for severe cases
• Comorbidities
− AR also is one of the risk factors associated with otitis media
− 20 % of children who have AR have otitis media with effusion and that 50 % of the children who have chronic otitis media with effusion have AR
− Poorly controlled rhinitis symptoms may exacerbate coexisting asthma
− Allergic rhinitis may increase the risk of development of sinusitis