Pediatric Allergic Rhinitis 

Although allergic rhinitis (AR) is a common disease, the impact on daily life cannot be underestimated. Some patients find allergic rhinitis to be just as debilitating and intrusive as severe asthma. Employees with untreated allergies are reportedly 10% less productive than coworkers without allergies, whereas those using allergy medications to treat allergic rhinitis were only 3% less productive.^[1] This suggests that effective medications may reduce the overall cost of decreased productivity.

Allergic rhinitis is caused by an immunoglobulin E (IgE)–mediated reaction to various allergens in the nasal mucosa. The most common allergens include dust mites, pet danders, cockroaches, molds, and pollens. For example, tree pollen allergen binds to IgE antibodies that are attached to a mast cell via Fce receptor. When 2 IgE molecules bind to the same tree pollen allergen, they cause the mast cell to fire off (degranurate), leading to release of various inflammatory mediators that cause the symptoms we feel as allergic rhinitis, including sneezing; nasal congestion; stuffiness; rhinorrhea (runny nose); cough; itching of the nose, eyes, and throat; sinus pressure; headache; and epistaxis (bloody nose).

The allergens present in the outdoor environment vary with the time of year and location. Knowing what allergens are in the environment at a specific time of year helps in diagnosing and treating allergic rhinitis and helps in excluding allergy as a cause of the patient's symptoms. For example, a patient who presents with nasal congestion in November in Boston, Massachusetts cannot have allergic rhinitis attributed to tree pollen allergy, which is prevalent in spring.

Allergen exposure likely causes both upper and lower airway inflammation, meaning that both the nose and the lungs may be involved. Many experts believe that a patient's airway needs to be evaluated as a total entity, not as individual parts. Studies have shown that most patients with asthma also have allergic rhinitis. Guidelines regarding the impact of allergic rhinitis on asthma have been established.^[2] Allergic reactions of the upper airway can trigger lower airway symptoms and vice versa. One study showed that patients with untreated allergic rhinitis and asthma have an almost 2-fold greater risk of having an emergency department visit and almost a 3-fold greater risk of being hospitalized for an asthma exacerbation, respectively.^[3] Similarly there are studies that reveal treatment of one disease entity improves the other.

The graphs below detail the significant impact of nasal allergies.

Understanding the function of the nose is important in order to understand allergic rhinitis. The purpose of the nose is to filter, humidify, and regulate the temperature of inspired air. This is accomplished on a large surface area spread over 3 turbinates in each nostril. A triad of physical elements (ie, a thin layer of mucus, cilia, and vibrissae [hairs] that trap particles in the air) accomplishes temperature regulation. The amount of blood flow to each nostril regulates the size of the turbinates and affects airflow resistance. The nature of the filtered particles can affect the nose. Irritants (eg, cigarette smoke, cold air) cause short-term rhinitis; however, allergens cause a cascade of events that can lead to more significant inflammatory reactions.

In short, rhinitis results from a local defense mechanism in the nasal airways that attempts to prevent irritants and allergens from entering the lungs.

Allergic reactions require exposure and then sensitization to allergens. To be sensitized, the patient must be exposed to allergens for a period of time. Sensitization to highly allergenic indoor allergens can occur in children younger than 2 years. Sensitization to outdoor allergens usually occurs when a child is older than 3-5 years, and the average age at presentation is 9-10 years. The allergic reaction begins with the cross-linking of the allergen to 2 adjacent IgE molecules that are bound to high-affinity Fcε receptors on the surface of a mast cell. This cross-linking causes mast cells to degranulate, releasing various mediators. The best-known mediators are histamine, prostaglandin D₂, tryptase, heparin, and platelet-activating factor, as well as leukotrienes and other cytokines.

These substances produce 2 types of reactions: immediate and late-phase. The immediate reactions in the nasal mucosa induce acute allergy symptoms (eg, nasal itch, clear nasal discharge, sneezing, congestion). The late-phase reaction occurs hours later, secondary to the recruitment of inflammatory cells into the tissue by the action of mediators (termed chemokines) released by the mast cell. Recruited cells are predominated by eosinophils and basophils, which, in turn, release their inflammatory mediators, leading to continuation of the cascade. In very sensitive individuals, this allergen-induced nasal inflammation causes priming of the nasal mucosa. Primed nasal mucosa becomes hyperresponsive, at which point even nonspecific triggers or small amounts of the antigen can cause significant symptoms.

Frequency

United States

Prevalence in the United States is 10-20%.^[4] One survey demonstrated rates as high as 38.2% when patients were asked if they experienced fewer than 7 days of symptoms. When allergic rhinitis was defined as symptoms lasting more than 31 days, prevalence dropped to 17%.

International

In temperate areas of Europe and Asia, frequency is similar to that in the United States.

Mortality/Morbidity

Mortality is not associated with allergic rhinitis, but significant morbidity occurs. Morbidity is manifested in several ways. Annually, an estimated 824,000 school days are missed, and an estimated 4,230,000 days of reduced quality-of-life functions are reported.^[5] Comorbidity of other atopic diseases (asthma, atopic dermatitis) or upper airway inflammation (sinusitis, otitis media) is significant in allergic rhinitis. Individuals with allergic rhinitis have a higher frequency of these conditions than individuals without allergic rhinitis.

Quality-of-life surveys have revealed that patients with significant allergic rhinitis found symptoms to be just as debilitating as symptoms in patients with moderate-to-severe asthma. Patients with allergic rhinitis felt they were equally impaired and unable to participate in the activities of normal living similar to those with the moderate-to-severe asthma. They felt that chronic congestion, sneezing, the need to wipe the nose, and a decrease in restful sleep compromised levels of their daily activity.

The financial cost of allergic rhinitis is difficult to estimate. Self-treating patients are estimated to spend an average of 56 dollars per year. The direct cost of prescription medication exceeds 6 billion dollars per year worldwide, and lost productivity is estimated at 1.5 billion dollars per year.

Race

Allergic rhinitis has no race predilection; however, individuals from nonwhite backgrounds seek out medical attention less often than whites.

Sex

Allergic rhinitis has no sex predilection.

Age

Allergic rhinitis usually presents in early childhood. Allergic rhinitis caused by sensitization to outdoor allergens can occur in children older than 2 years; however, sensitization in children aged 4-6 years is more common. Clinically significant sensitization to indoor allergens may occur in children younger than 2 years. This is typically associated with significant exposures to indoor allergens (eg, molds, furry animals, cockroaches, dust mites). Some children may be sensitized to outdoor allergens at this young age if they have significant exposure. Incidence continues to increase until the fourth decade of life, when symptoms begin to fade; however, individuals can develop symptoms at any age.

Allergic rhinitis–like symptoms (runny nose, blocked nose, or sneezing apart from a cold) may begin as early as age 18 months. In a report from the Pollution and Asthma Risk: an Infant Study (PARIS), 9.1% of the 1859 toddlers in the study cohort reported allergic rhinitis–like symptoms at age 18 months.^[6]