Classification and Diagnosis of Allergic Rhinitis
Allergic rhinitis (AR) and perennial nonallergic rhinitis (PNAR) represent conditions affecting millions of individuals across the world. Although the diagnosis of AR might be presumptively based on the types of symptoms and the history of allergen triggers, confirmation requires documentation of specific IgE reactivity. In contrast, PNAR is a condition with similar symptomatology but in which the patient has no identifiable specific allergic sensitivities. This review presents the diverse options of currently available pharmacologic agents for the treatment of AR and PNAR, including intranasal corticosteroids, H1-antihistamines, decongestants, cromolyn sodium, antileukotrienes, anticholinergics, capsaicin, anti-IgE, and intranasal saline. Furthermore, appropriate stepped-up, stepped-down pharmacotherapeutic algorithms are described for the various forms of rhinitis.
Classification and diagnosis of AR
AR, an inflammatory condition of the nasal mucosa mediated by an IgE-associated response to indoor and outdoor environmental allergens, has traditionally been classified as being seasonal or perennial, depending on whether an individual is sensitized to cyclic pollens or year-round allergens, such as dust mites, pets, cockroaches, and molds. This classification scheme has proved to be artificial and often inconsistent because, depending on the locale, allergic sensitization to multiple seasonal allergens can result in year-round disease, and conversely, allergic sensitization to perennial allergens, such as animal dander, can result in symptoms during only a limited period of time.
Although clinical research and regulatory agencies continue to use this nomenclature, recent global guidelines for classification and treatment of AR, as set forth by the Allergic Rhinitis and Its Impact on Asthma workshop, have proposed that allergic nasal disease be defined as being intermittent or persistent and mild or moderate-severe.5 Intermittent rhinitis is defined on the basis of symptoms that are present for less than 4 days per week or less than 4 weeks in duration. If symptoms are present for more than 4 days per week and are present for more than 4 weeks, AR is defined as being persistent. Mild symptoms do not affect sleep, interfere with work or school, or impair daily activities, sports, and leisure and, although present, are not considered troublesome. Conversely, moderate-severe symptoms can result in impairment or disturbances of any or all of these activities or aspects of life. Although the duration categories of intermittent and persistent appear to be a practical system, further refinement of the severity categories would be valuable. In addition, development of a validated method for assessing rhinitis control would be useful to monitor the often variable course of a patient’s disease.
The diagnosis of AR can be made presumptively based on the types of symptoms and the history of allergen triggers. Confirmation requires documentation of specific IgE reactivity through determination of allergen sensitivity by using skin prick testing or in vitro specific IgE determination. These procedures can help detect specific allergic sensitivities and provide information for directing environmental control interventions.
Classification and diagnosis of PNAR
PNAR is a condition in which the patient has no identifiable specific allergic sensitivities. Although it is controversial how to best subdivide PNAR, one previous approach has been to do so based on the presence or absence of nasal eosinophilia. Individuals with nasal eosinophilia and with no IgE sensitivity have traditionally been classified as having nonallergic rhinitis with eosinophilia syndrome (NARES). Although the reported number of eosinophils required to make a diagnosis of NARES varies, it is generally accepted that nasal scrapings from the nasal turbinate demonstrating 5 to 25 eosinophils per high-power field are compatible with such a diagnosis.
Individuals with PNAR who lack nasal eosinophilia can be classified as having vasomotor rhinitis (VMR), which some clinicians have termed idiopathic rhinitis. VMR is characterized by the presence of chronic symptoms for 9 or more months each year.It can be differentiated from AR by the relative later age of onset, frequent lack of atopic comorbidities, nature of triggering factors, and type of symptoms. Precipitants include climate changes and nonspecific olfactory irritants, such as perfumes and tobacco smoke. Nasal obstruction and rhinorrhea are hallmark features of VMR and are more commonly seen than sneezing or itching.A study by Togiasfound that patients with VMR were more likely than patients with AR to report headaches, nasal pressure, and posterior rhinorrhea and less likely to be affected by sneezing, nasal pruritus, and conjunctival symptoms.
The exact pathophysiology of PNAR remains elusive. Some groups have found that affected individuals have infiltrating mast cellsand IgE-positive cells in the nasal mucosa11 similar in quantity to their counterparts with AR. In fact, approximately two thirds of individuals with PNAR might respond to nasal allergen challenges with cat, dog, grass, and dust mite allergens.Thus it has been hypothesized that the underlying pathophysiology of PNAR might involve a local allergic process.Consistent with this possibility has been the finding that B cells residing in the nasal mucosa are able to undergo switching to IgE in the context of a local immune response to allergen, a process that was only thought to occur in lymphoid tissue.
In contrast, other groups have noted a lack of cellular inflammation in the nasal mucosa, as evidenced by the absence of infiltrating eosinophils, mast cells, and T cells in biopsy specimens.Some of the discrepancies between these various findings might be explained by the fact that individuals with inflammatory changes did not have nasal smears done to rule out NARES, which could possibly account for the observed inflammation. Eosinophils, through production and release of their toxic and proinflammatory products, such as superoxide radicals, major basic protein, and eosinophilic cationic protein, could presumably interfere with normal nasal functioning and lead to pathologic rhinitis.
Increasing evidence points toward the importance of nasal neurovascular mechanisms in the pathogenesis of noneosinophilic PNAR. Neurovascular homeostasis is maintained by a balance of sympathetic and parasympathetic tone in the upper airways.The former pathway controls the release of norepinephrine and neuropeptide Y, which favor a state of nasal patency. In contrast, parasympathetic fibers release acetylcholine and, among other neuropeptides, vasoactive intestinal peptide. These are thought to induce nasal congestion and mucus secretion. In VMR there might be a state of relative hyperreactivity of the parasympathetic nervous system and hyporesponsiveness of the sympathetic nervous system, perhaps as a result of being exposed to irritants or noxious stimuli, such as cold dry airor, alternatively, histamine and methacholine
Others groups have hypothesized that the neurogenic imbalance responsible for inducing VMR might be due to overactivity of C-fibers contained in the nasal mucosa. C-fibers define the nonadrenergic noncholinergic system, an abnormally heightened tone of which can promote release of substance P, calcitonin gene-related protein, and neurokinins A and K, which can lead to nasal congestion and overproduction of nasal secretions
- Alexander N. Greiner, Eli O. MeltzerPharmacologic rationale for treating allergic and nonallergic rhinitis. The Journal of Allergy and Clinical Immunology Volume 118, Issue 5, Pages 985-996, November 2006
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