Allergic Rhinitis

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Chapter 137 Allergic Rhinitis

Henry Milgrom, Donald Y.M. Leung

Allergic rhinitis (AR) is an inflammatory disorder of the nasal mucosa characterized by nasal congestion, rhinorrhea, and itching, often accompanied by sneezing and conjunctival irritation. Its categorization as a major chronic respiratory disease of children is predicated on its high prevalence, detrimental effects on quality of life and school performance, and co-morbidities. Children with AR often have related sinusitis, conjunctivitis, otitis media, serous otitis, hypertrophic tonsils and adenoids, and eczema. Childhood allergic rhinitis is associated with at least twofold increase in risk for asthma at an older age. Over the past 40 yr an upsurge in AR has taken place throughout the world, sparing rural and underdeveloped regions. In prosperous societies, 20-40% of children suffer from AR. Its symptoms may appear in infancy, with the diagnosis generally established by the time the child reaches age 6 yr. The prevalence peaks late in childhood. Risk factors include family history of atopy and serum immunoglobulin (Ig) E higher than 100 IU/mL before age 6 yr. The risk increases in children introduced to foods or formula early in infancy, those whose mothers smoke heavily, especially before the children are 1 yr old, and those with heavy exposure to indoor allergens. A critical period appears to exist early in infancy when the genetically susceptible individual is at greatest risk of sensitization. Breast-feeding of high-risk infants and exposure to dogs, cats, and endotoxin early in childhood protect against atopy and early wheezing. Delivery by cesarean section is associated with allergic rhinitis and atopy among children with a parental history of asthma or allergies. This association may be explained by the lack of exposure to maternal vaginal/fecal flora during delivery. Children between 2 and 3 yr old who have elevated anti-cockroach and anti-mouse IgE are at increased risk of wheezing, rhinitis, and atopic dermatitis. The occurrence of 3 or more episodes of rhinorrhea in the first year of life is associated with allergic rhinitis at age 7 yr. Early life exposures or their absence have a profound influence on the development of the allergic phenotype.

Etiology

Two factors necessary for expression of AR are sensitivity to an allergen and the presence of an allergen in the environment. AR is currently classified as seasonal (SAR) or perennial (PAR), although these terms may soon be replaced by intermittent allergic rhinitis (IAR) and persistent rhinitis (PER). The 2 sets of terms are based on different premises, but inhalant allergens are the main cause of all forms of rhinitis irrespective of the terminology. SAR follows a well-defined course of cyclical exacerbation, whereas PAR causes year-round symptoms. Approximately 20% of cases are strictly seasonal, 40% perennial, and 40% mixed (perennial with seasonal exacerbations). In temperate climates, airborne pollens responsible for SAR appear in distinct phases: trees pollinate in the spring, grasses in the early summer, and weeds in the late summer. In temperate climates, mold spores persist outdoors only in the summer, and in warm climates, mold spores persist throughout the year. Symptoms of seasonal allergies cease with the appearance of frost. Knowledge of the occurrence of seasonal symptoms, of the regional patterns of pollination and mold sporulation, and of the patient’s specific IgE is necessary to recognition of the cause of SAR. PAR is most often associated with the indoor allergens: house dust mites, animal danders, mice, and cockroaches. Cat and dog allergies are of major importance in the United States. The allergens from the saliva and sebaceous secretions may remain airborne for a prolonged time. The ubiquitous major cat allergen, Fel d 1, may be carried on cat owners’ clothing into such “cat-free” settings as schools and hospitals.

Pathogenesis

The exposure of an atopic host to an allergen leads to specific IgE production. The clinical reactions on re-exposure to the allergen have been designated as early-phase and late-phase allergic responses (EPRs and LPRs). Bridging of the IgE molecules on the surface of mast cells by allergen initiates EPR, characterized by degranulation of mast cells and release of preformed and newly generated inflammatory mediators including histamine, prostaglandin 2, and the cysteinyl leukotrienes. LPR arises 4 to 8 hr following allergen exposure. Inflammatory cells, including basophils, eosinophils, neutrophils, mast cells, and mononuclear cells, infiltrate the nasal mucosa. Eosinophils release proinflammatory mediators, including cysteinyl leukotrienes, cationic proteins, eosinophil peroxidase, and major basic protein, and serve as a source of interleukin-3 (IL-3), IL-5, granulocyte-macrophage colony-stimulating factor (GM-CSF), and IL-13. Repeated intranasal introduction of allergens causes “priming”—a brisk response to reduced provocation. Over the course of an allergy season a multifold increase in epithelial and submucosal mast cells takes place. These cells were once thought to have a role exclusively in the EPR but now appear to have an important function in sustaining chronic allergic disease. Allergens, autoantigens, and components of superimposed infectious agents activate the immune system. Immune regulation in the lymphatic organs and in the tissue has an important role in the control and suppression of allergic disease in all stages of the inflammatory process, such as inflammatory cell migration to tissues, inflammatory cell–mediated destruction in tissues, and inflammatory cell interaction with resident tissue cells to enhance inflammation.

Clinical Manifestations

Symptoms of AR are often ignored or are mistakenly attributed to a respiratory infection. Older children blow their noses, but younger children tend to sniff and snort. Nasal itching brings on grimacing, twitching, and picking of the nose that may result in epistaxis. Children with AR often perform the allergic salute, an upward rubbing of the nose with an open palm or extended index finger. This maneuver relieves itching and briefly unblocks the airway. It also gives rise to the nasal crease, a horizontal skin fold over the bridge of the nose. The diagnosis of AR is based on symptoms in the absence of an upper respiratory tract infection and structural abnormalities. Typical complaints include intermittent nasal congestion, itching, sneezing, clear rhinorrhea, and conjunctival irritation. Symptoms increase with greater exposure to the responsible allergen. The patients may lose their senses of smell and taste. Some experience headaches, wheezing, and coughing. Nasal congestion is often more severe at night, causing mouth-breathing and snoring, interfering with sleep, and inciting irritability.

Signs on physical exam include abnormalities of facial development, dental malocclusion, and the “allergic gape” or continuous open-mouth breathing, chapped lips, “allergic shiners” (dark circles under the eyes), and the transverse nasal crease. Conjunctival edema, itching, tearing, and hyperemia are frequent findings. A nasal exam performed with a source of light and a speculum may reveal clear nasal secretions; edematous, boggy, and bluish mucus membranes with little or no erythema; and swollen turbinates that may block the nasal airway. It may be necessary to use a topical decongestant to perform an adequate examination. Thick, purulent nasal secretions indicate the presence of infection.

Differential Diagnosis

Evaluation of AR calls for a thorough history, including details of the patient’s environment and diet and family history of allergic conditions such as eczema, asthma, and AR, physical examination, and laboratory evaluation. The history and laboratory findings provide clues to the provoking factors. Symptoms that include sneezing, rhinorrhea, nasal itching, and congestion and the laboratory findings of elevated IgE, specific IgE antibodies, and positive allergy skin test results typify AR. SAR differs from PAR by history and skin test results. Nonallergic rhinitides cause sporadic symptoms and may resemble PAR. Their causes are often unknown. Nonallergic inflammatory rhinitis with eosinophils (NARES) imitates AR in presentation and response to treatment, but without elevated IgE antibodies. Vasomotor rhinitis is characterized by excessive responsiveness of the nasal mucosa to physical stimuli. Other nonallergic conditions, such as infectious rhinitis, structural problems including nasal polyps and septal deviation, rhinitis medicamentosa (due to the overuse of topical vasoconstrictors), hormonal rhinitis associated with pregnancy or hypothyroidism, neoplasms, vasculitides, and granulomatous disorders may mimic AR (Table 137-1).

Table 137-1 CAUSES OF RHINITIS

Allergic rhinitis

Perennial with seasonal exacerbation

Nonallergic rhinitis

Structural/mechanical factors:

Deviated septum/septal wall anomalies

Hypertrophic turbinates

Adenoidal hypertrophy

Choanal atresia

Inflammatory/immunologic:

Wegener granulomatosis

Midline granuloma

Systemic lupus erythematosus

Sjögren syndrome

Nasal polyposis

Ciliary dyskinesia syndrome

Atrophic rhinitis

Hormonally induced:

Oral contraceptives

Menstrual cycle

Rhinitis medicamentosa

Oral contraceptives

Antihypertensive therapy

Nonsteroidal anti-inflammatory drugs

Reflex induced:

Gustatory rhinitis

Chemical or irritant induced

Posture reflexes

Environmental factors:

Weather/barometric pressure

Nonallergic rhinitis with eosinophilia syndrome

Perennial nonallergic rhinitis (vasomotor rhinitis)

Emotional factors

From Leung DYM, Sampson HA, Geha RS, et al: Pediatric allergy principles and practice, St Louis, 2003, Mosby, p 290.

Complications

AR is frequently associated with complications and co-morbid conditions. Children with AR experience frustration over their appearance. Chronic sinusitis is a common complication of AR, sometimes associated with purulent infection, but in the majority of patients, marked mucosal thickening, sinus opacification, and nasal polyposis with inflammation but negative culture results develop. The inflammatory process is characterized by marked eosinophilia. Allergens, possibly fungal, may be the inciting agents. The sinusitis of triad asthma (asthma, sinusitis with nasal polyposis, and aspirin sensitivity) often responds poorly to therapy. Patients who undergo repeated endoscopic surgery derive diminishing benefit with each successive procedure.

Rhinitis that coexists with asthma may be taken too lightly or completely overlooked. Up to 78% of patients with asthma have AR, and 38% of patients with AR have asthma. Aggravation of AR coincides with exacerbation of asthma, and treatment of nasal inflammation reduces bronchospasm, asthma-related emergency department visits, and hospitalizations. Postnasal drip associated with AR commonly causes persistent or recurrent cough. Eustachian tube obstruction and middle ear effusion are frequent complications. Chronic allergic inflammation causes hypertrophy of adenoids and tonsils that may be associated with eustachian tube obstruction, serous effusion, otitis media, and obstructive sleep apnea. AR is strongly associated with snoring in children. The association between rhinitis and sleep abnormalities and subsequent daytime fatigue is well documented, but the mechanisms remain poorly understood.

Quality of life indices have been developed to explore the effects of the disease and of therapeutic interventions. The Pediatric Rhinoconjunctivitis Quality of Life Questionnaire (PRQLQ) is suitable for children from 6 to 12 yr old, and the Adolescent RQLQ is appropriate for patients between 12 and 17. Studies using the PRQLQ in children with rhinitis have documented anxiety and physical, social, and emotional issues that affect learning and the ability to integrate with peers. The disorder contributes to headaches and fatigue, limits daily activities, and interferes with sleep. There is evidence of impaired cognitive functioning and learning that may be further threatened by the adverse effects of sedating medications. Rhinitis is an important cause of lost school attendance, resulting in more than 2 million absent days in the United States annually. A classification based on severity is shown in Figure 137-1.

Figure 137-1 Allergic Rhinitis and Its Impact on Asthma (ARIA) classification of allergic rhinitis.

(From Adkinson NF Jr, Bochner BS, Busse WW, et al, editors: Middleton’s allergy principles and practice, ed 7, Philadelphia, 2009, Mosby/Saunders, p 977.)

Laboratory Findings

Epicutaneous skin tests provide the best method for detection of allergen-specific IgE (positive predictive value of 48.7% for the epidemiologic diagnosis of allergic rhinitis). They are inexpensive and sensitive, and the risks and discomfort are minimal. Responses to seasonal respiratory allergens are rare before two seasons of exposure, and children younger than 1 yr rarely display positive skin test responses to these allergens. To avoid false-negative results, montelukast should be withheld for 1 day, most sedating antihistamine preparations for 3-4 days, and nonsedating antihistamines for 5-7 days. Serum immunoassays for IgE to allergens provide a suitable alternative (positive predictive value 43.5%) for patients with dermatographism or extensive dermatitis, patients taking medications that interfere with mast cell degranulation, others at high risk for anaphylaxis, and some who cannot cooperate with the procedure. Presence of eosinophils in nasal smear supports the diagnosis of AR, and that of neutrophils, of infectious rhinitis. Eosinophilia and measurements of total serum IgE concentrations have relatively low sensitivity. Improved methods for objective evaluation are still needed to assess the effects of treatment and to guide future developments.

Treatment

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