Allergic rhinitis is the most prevalent of the atopic disorders, affecting 25% to 35% of persons, depending on the population studied. Atopy is an inherited disposition manifested by any, or all, of allergic rhinitis, asthma, or atopic eczema. It is closely, if not invariably, linked to the generation of greater than normal amounts of specific allergic antibody, IgE.

The atopic diseases have become more prevalent over the past century, although the exact reason for this increase is not clear. Considered by nonsufferers to be a trivial disease, allergic rhinitis delivers a significant personal impact on quality of life.

It is responsible for an enormous economic burden because of the direct medical costs for physician visits and medication, and the indirect costs of missed work and school and lost productivity. This cost in the United States has recently been estimated at more than 2 billion dollars annually and is now presumably even greater.

IgE is a mucosal antibody, being produced by plasma cells beneath the mucosal surfaces of the eyes, the upper and lower airways, and the gut, similar to the distribution of IgA. IgE binds to specific, high-affinity receptors on basophils and mast cells, designated FceRI.

Bridging by allergen of two specific IgE molecules on the cell surface is sufficient to cause activation of these cells. The release of vasoactive mediators such as histamine, tryptase, leukotrienes, and prostaglandins, and several chemokines and cytokines, follows.

Symptoms of the immediate allergic (early-phase) reaction, including sneezing, itching, rhinorrhea, and nasal congestion, are due to the former mediators. Chemotactic factors result in the recruitment of inflammatory cells such as basophils, eosinophils, and polymorphonuclear leukocytes.

The influx of these cells is accompanied by a fresh release of vasoactive substances, culminating in the delayed (late-phase) reaction with a recrudescence of symptoms. With a single allergen exposure, the early and late phases are easily discernible, the latter occurring 4 to 6 hours after the initial reaction.

With persistent exposure, such as with indoor allergens like dust mite or animal dander, the late-phase inflammatory process is ongoing, resulting in chronic symptoms.

Well described with outdoor allergens such as pollens is the ‘‘priming effect,’’ the persistence of inflammation from prior exposure resulting in greater sensitivity to further exposures, with lesser pollen amounts resulting in greater symptoms.

Increased IgE production is related to a shift of helper T cell cytokine release to a Th2 profile. Three central cytokines to this allergic phenotype are IL-4, IL-13, and IL-5. The first two cytokines cause isotype switch in B-cells to IgE production. IL-5 is crucial for eosinophil activation and persistence.

Once this shift to a Th2 profile occurs, it tends toward self-perpetuation. Atopic persons may be genetically predisposed to the Th2 phenotype. Allergic rhinitis sensitization is almost always due to airborne, inhalant factors.

These aeroallergens may emanate from indoor or outdoor sources and may be perennial, relatively constant, or have seasonal peaks. Outdoor sources are almost invariably of plant or fungal origin, usually pollen grains or mold spores. With frequently seen seasonal peaks, timing often aids in diagnosing the airborne culprit.

Tree pollens pollinate in the winter into the early spring, although some trees shed pollen in the fall. Grasses generally pollinate from May into July, but have longer seasons in the southern states, and pollination is year-round in tropical or subtropical areas such as Hawaii and southern Florida.

Some weeds overlap with the grasses, whereas most pollinate from July into the fall. Indoor aeroallergens are more likely of animal origin: dust mite or cockroach emanations, or animal dander. Less likely, but possible, are symptoms due to mold spores, especially with water damage or high humidity.

Although exposures are perennial in nature, these also have seasonal peaks: dust mite in late summer to early fall, cat and dog dander in late winter, and cockroach in summer. A recent study has demonstrated that the allergens from dog and cat dander can be found in the dust of essentially all homes, whether pets are present or not.

Vasomotor rhinitis, better referred to as irritant rhinitis, is as frequent as allergic rhinitis, with nasal symptoms driven by perturbations in the environment. The cause of the increased susceptibility to irritants is not fully understood, although the resultant release of mediators is similar to that seen with allergic rhinitis.

A variation of irritant rhinitis is ‘‘gustatory rhinitis,’’ where the eating act triggers rhinorrhea. Viral infection (upper respiratory infection) is perhaps the most common cause of nasal symptoms; other infectious agents are distinctly less common.

Hormonal factors such as hypothyroidism and pregnancy may lead to worsened nasal congestion. Medication-induced nasal congestion was commonly seen with older antihypertensive agents, such as reserpine, and is certainly seen with topical alpha-adrenergic agonist overuse.

Intolerance to aspirin and nonsteroidal anti-inflammatory drugs may manifest as either asthma or chronic sinusitis, or both. Vasculitides such as Wegener’s granulomatosis can present with chronic sinusitis.

A World Health Organization expert panel published a position statement on allergic rhinitis and its impact on asthma (ARIA). Its scope is worldwide and it discusses resources with a global perspective. One of the major points is the frequent concordance of allergic rhinitis and asthma.

It is crucial to suspect rhinitis and inflammation of the upper airway as an aggravator of asthma, and likewise, the lower airway should be evaluated in patients who have rhinitis.

In keeping with the phraseology recommended by National Asthma Education and Prevention Program and Global Initiative for Asthma guidelines for the management of asthma, the position statement also suggested that ‘‘seasonal’’ and ‘‘perennial’’ be replaced by ‘‘intermittent’’ and ‘‘persistent.’’

The evaluation of rhinitis is greatly advanced by a careful directed history: presence of itching and sneezing, severity, seasonality, progression of symptoms, identifiable triggers, occupational exposures, alleviating factors, and medication usage. Family history of atopic disease is helpful.

Also important is the impact of disease and medication on daily activity. The presence of comorbid conditions is suggested by a history of headache, loss of smell and taste, purulent discharge, cough, chest tightness or wheezing, snoring, and sleep disturbance.

Physical examination of the head may reveal characteristic findings. Dark discoloration under the eyes, or ‘‘allergic shiners,’’ is due to venous engorgement, and Dennie’s signs are folds under the eyes due to edema. The transverse crease across the bridge of the nose is seen in children who chronically push their palms upward under their noses in response to itching or rhinorrhea.

The turbinates appearing edematous with a bluish mother-of-pearl hue was felt to be pathognomonic but may be seen in nonallergic rhinitis also. Likewise, turbinates may be engorged and erythematous. Cobble-stoning from lymphoid hyperplasia may be seen on the posterior pharynx.

Chronic mouth breathing from nasal obstruction can cause the ‘‘allergic facies’’ in the developing facial features of children: open mouth with receding chin and overbite, elongation of the face, and arching of the hard palate.

Diagnosis, frequently determined by the appropriate history and findings, is supported by the finding of specific IgE antibodies against airborne agents.

Percutaneous (prick or puncture) skin testing remains the most specific and cost-effective diagnostic modality, although improved cap-radioallergosorbent test (Cap-RAST) testing is approaching similar sensitivity.

Intradermal skin testing is more sensitive but introduces a higher false-positive rate and is not felt to add any diagnostic value to prick testing of potent pollen extracts. Intradermal testing with less potent extracts may, however, have a role.