Rhinosinusitis.

Abstract: History, physical examination, and allergy testing may distinguish the syndromes of rhinitis, classified as allergic, infectious, perennial, nonallergic, and miscellaneous. All may be associated with sinusitis, probably on the basis of obstruction of the osteomeatal complex. Although topical nasal steroids are useful in the treatment of all forms of rhinitis, diagnosis of the offending type in a given patient is necessary for optimal management.

Key Words: nasal steroids, rhinitis, sinusitis

**********

Rhinitis is a clinical syndrome characterized by annoying nasal discharge, itching, sneezing, congestion, and pressure. The syndrome may be diagnosed and classified according to the clinical patterns recognized.

Allergic Rhinitis

Patients with allergic rhinitis have paroxysms of sneezing, rhinorrhea, nasal obstruction, and itching of the eyes, nose, and palate. Postnasal drip, cough, irritability, and fatigue may occur. (1-5) Allergic rhinitis is classified as seasonal if symptoms occur at a particular time of the year or as perennial if symptoms occur throughout the year.

Symptoms occur in individuals who have produced immunoglobulin (Ig) E specific to individual allergens (ie, sensitization) and release mediators of immediate hypersensitivity when reexposed to these allergens (ie, an allergic reaction). Allergen-specific IgE antibodies bind to IgE receptors on mast cells in the respiratory mucosa. When these antibodies are bridged on the cell surface by allergen, mast cells release preformed (ie, histamine) and granule-associated chemical mediators, causing symptoms immediately after exposure. They also generate other mediators and cytokines that lead to nasal inflammation (ie, leukotrienes) and, with continued allergen exposure, chronic symptoms (Fig. 1). Common allergens causing seasonal allergic rhinitis are wind-borne pollens (ie, tree, grass, weed) and fungi. Indoor allergens such as dust mites, cockroaches, animal proteins, and fungi are frequently associated with perennial rhinitis.

Sinusitis frequently occurs in association with allergic rhinitis. A likely explanation of the coexistence of these syndromes is that mucosal inflammation associated with allergic rhinitis may cause obstruction of the sinus osteomeatal complex, predisposing individuals to bacterial infection of the sinuses (Fig. 2). However, available information suggests that inflammation associated with allergic rhinitis is present throughout the respiratory tract (sinuses, nose, and bronchi), even when symptoms are localized to the nose. This local inflammation within the sinuses may be adequate to induce symptoms of sinusitis independent of osteomeatal complex obstruction. Thus, many cases of sinusitis that seem to be bacterial in origin may reflect noninfectious inflammation alone. Symptoms statistically associated with culture-proven bacterial sinusitis include nasal congestion, purulent rhinorrhea or postnasal drip, facial or dental pain, and cough. Purulent rhinorrhea, purulent postnasal drip, or pain in a maxillary tooth and persistent cough in children are the most useful predictors of bacterial sinusitis. However, no single symptom has a high degree of sensitivity or specificity in discriminating bacterial sinusitis from allergic or viral rhinitis.

Allergic rhinitis must be distinguished from the other forms of rhinitis to choose appropriate therapy. Information about aeroallergens present in the patient's geographic location and the allergens in the patient's home and work areas is therefore helpful.

Episodic exposure to inhaled allergens such as cat salivary proteins, pollen, or house dust mite feces may provoke acute allergic symptoms that are easily diagnosed as episodic allergic rhinitis. If symptoms are seasonal, for example, in the spring (eg, "rose fever" from tree and grass pollen) or in the autumn (eg, ragweed "hay fever"), and the symptoms are predictable and reproducible, seasonal allergic rhinitis may be diagnosed on the basis of the history alone. By comparison, perennial allergic rhinitis is associated with nasal symptoms that occur for more than 2 h/d and for more than 9 mo/yr. Perennial allergic rhinitis usually reflects exposure to indoor allergens such as dust mites, cockroaches, or animal dander, although aeroallergens may cause perennial rhinitis in warm climates.

[FIGURE 1 OMITTED]

Allergic rhinitis seems to be exceedingly common. In the United States, for example, 9 to 40% of the population may have some form of allergic rhinitis. If it is assumed that 20% of the population is affected, then approximately 60 million people may have the disorder. The prevalence of allergic rhinitis is lowest in children younger than 5 years old, has a bimodal peak in the early school and early adult years, and declines thereafter. By the age of 40 years, approximately 45% of individuals will have experienced allergic rhinitis. The prevalence in the industrialized world is increasing, particularly in urban areas. As an example, allergic sensitization as measured by allergy skin testing increased by 11% in an 8-year period in Tucson, AZ. Allergic rhinitis accounts for at least 2.5% of all physician visits, 2 million lost school days per year, 6 million lost workdays, and expenditure of $2.4 billion on prescription medications, with a total indirect and direct cost of $7 billion per year.

Other Syndromes of Rhinitis

Syndromes of rhinitis may be divided into the following categories: allergic, perennial, nonallergic, infectious, and miscellaneous, which includes combinations of the above (Table 1).

Vasomotor Rhinitis

Patients with vasomotor rhinitis complain of chronic nasal congestion intensified by rapid changes in temperature and relative humidity, odors, or alcohol. This may occur with or without persistent rhinorrhea and seems to result from autonomic dysfunction. There is little nasal itching or sneezing, but headaches, anosmia, and sinusitis are common. A family history of allergy or allergic symptom triggers is uncommon. The nasal turbinates are erythematous and boggy in appearance versus the pale bluish hue or pallor that is found along with turbinate edema in allergic rhinitis. Nasal eosinophilia is unusual.

[FIGURE 2 OMITTED]

Although the history and findings on physical examination are suggestive of the condition, negative allergy skin tests are essentially diagnostic for a nonallergic rhinitis syndrome, of which vasomotor rhinitis is the most common. This condition responds best to topical nasal steroid therapy, as discussed later in this article. Ipratropium or azelastine nasal sprays, also discussed later in this article, may be useful.

Atrophic Rhinitis

Atrophic rhinitis is a syndrome of progressive atrophy of the nasal mucosa in elderly patients. Patients report chronic nasal congestion and constantly perceive a bad odor. This condition is associated with mucosal colonization with Klebsiella ozaenae. It is distinguished from allergic rhinitis because it is uncommon, occurs in elderly patients who are in a debilitated condition, is not associated with sneezing, responds poorly to antiallergic medications, and is associated with persistent complaints of foul odor. Patients with this condition respond best to daily nasal irrigation with warm saline using, for example, a Water-Pik apparatus (Water Pik Technologies, Inc., Newport Beach, CA) with a Grossan nasal adaptor (HydroMed, Inc., Sherman Oaks, CA).

Rhinitis Medicamentosa

Rhinitis medicamentosa is a complication of chronic use of vasoconstrictor nasal sprays or intranasal cocaine abuse. Chronic nasal obstruction and nasal inflammation develop and are manifested as beefy red nasal membranes on physical examination. Diagnosis depends on the history and physical examination and a positive response to treatment with topical nasal steroids, which is usually required to withdraw successfully from the culprit medication.

Nonallergic Rhinitis with Nasal Eosinophilia Syndrome

Nonallergic rhinitis with nasal eosinophilia syndrome occurs in as many as 15% of patients with rhinitis. It is characterized by perennial symptoms, an older average age than in patients with allergic rhinitis (39 versus 25 yr), and milder symptoms of nasal itching and sneezing. Nasal secretions contain more than 25% eosinophils. Patients with nonallergic rhinitis with nasal eosinophilia syndrome frequently have sinusitis, nasal polyps, and asthma. IgE to inhalant allergens is usually absent. Symptoms respond to topical nasal steroids. Leukotriene modifiers may potentially be helpful if polyps are present.

Rhinitis in Association with Hormone Changes and Certain Drugs

Rhinitis of pregnancy and rhinitis associated with birth control pills or hypothyroidism reflect nasal obstruction that occurs on a hormonal basis. Topical nasal steroids frequently relieve symptoms.

Rhinitis with Immunologic Disorders

A number of systemic autoimmune disorders present with nasal symptoms or can affect nasal mucosa. These are diagnosed by biopsy and include sarcoidosis, Wegener's granulomatosis, and relapsing polychondritis. They respond to appropriate therapy for the respective disease.

Management of Allergic Rhinosinusitis

Avoidance Measures

The treatment of allergic rhinitis centers on decreasing nasal inflammation and maintaining patency of the osteomeatal complex. If there is concurrent active bacterial sinusitis, the infection must first be treated with appropriate antibiotics and anti-inflammatory agents. Subsequently, therapy of allergic rhinitis is directed at allergen identification and avoidance (where possible), appropriate medications and immunotherapy (when indicated), and surgery (if necessary).

The treatment of patients with allergic rhinitis begins with the identification of possible allergen triggers. Once identified, the avoidance of such triggers may markedly decrease symptoms. A careful home and work environmental history frequently identifies involvement of one or more of the four major allergen categories that trigger allergic rhinitis: pollens, molds, house dust mites, and insects (eg, fleas, cockroaches) or animal allergens (eg, cat, dog).

Identifying allergens by history may be difficult in perennial rhinitis. In this setting, carefully performed immediate hypersensitivity skin testing (skin prick tests) is a quick, inexpensive, and safe way to identify the presence of allergen-specific IgE. In sensitive patients, testing with selected diagnostic vaccines of tree, grass, or weed pollen; mold; house dust mite; and/or animal allergens results in a wheal-and-flare reaction at the skin test site within 20 minutes.

The most common indoor allergens among patients with allergic rhinitis or asthma appear to be dust mites and dog and cat dander. In one study of 3,371 consecutive patients with allergic rhinitis, asthma, or both, the prevalence of sensitization from skin prick test results to common airborne indoor and outdoor allergens was 66, 63, and 54% for cat hair epithelium, dog hair dander, and house dust mite antigens, respectively. (4)

Simple measures to avoid allergens include maintaining the relative humidity at 50% or less to limit house dust mite and mold growth and avoiding exposure to irritants such as cigarette smoke. Appropriately maintained air conditioners decrease concentrations of pollen, mold, and dust mite allergens in indoor air. Avoiding exposure to feces of the house dust mite, the most common cause of perennial allergic rhinitis, is facilitated by removing carpets and furry pets; covering mattresses, box springs, and pillows with plastic (or with tightly woven materials that do not permit mite fecal particles to pass through); and washing bedding in water hotter than 130[degrees]F once weekly. Also, high-efficiency particulate air filters may be useful and may help reduce animal allergens, but animal removal is optimal.

Pharmacologic Treatment

If avoiding allergens does not result in relief of symptoms, drug therapy is a reasonable next step. In such patients, it is also important to reassess the probability of underlying sinus infection. Limited computed tomographic scanning of the sinuses is prudent if symptoms of infection such as purulent postnasal drip are present, if resolution of symptoms that are troubling to the patient do not resolve within several weeks, or if symptoms recur.

Nasal decongestant sprays are not used regularly in the treatment of allergic rhinitis. Tachyphylaxis develops after 3 to 7 days, rebound nasal congestion results, and continued use causes rhinitis medicamentosa. Nevertheless, they may occasionally be helpful for periods of a week or less when used just before the administration of topical nasal steroids for patients with severe nasal obstruction (see "Intranasal Corticosteroids" below).

Intranasal Corticosteroids

Topical intranasal steroid therapy is presently the most effective single maintenance therapy for allergic rhinitis and causes few side effects at the recommended doses (Table 2). In our opinion, nasal corticosteroids are the first-line treatment for allergic rhinitis and all other therapies should be considered as possible alternative strategies. Glucocorticosteroids inhibit allergic inflammation in the nose at many levels. On experimental nasal allergen challenge, they decrease the amount of histamine release by 75% in the early nasal response to allergen and increase the threshold dose for a positive response to allergen. Intranasal steroids administered 7 days before nasal allergen challenge inhibit both immediate and late-phase mediator release.

Topical nasal steroids are more effective than cromolyn and second-generation antihistamines in treating allergic rhinitis and in improving the symptoms of seasonal asthma in patients with concomitant seasonal allergic rhinitis and seasonal allergic asthma. Topical nasal corticosteroids are also more effective than antihistamines in reducing nasal blockage because of their anti-inflammatory effects. Some of these are approved for use in young children.

Topical nasal steroids are available in both aqueous and Freon-propelled preparations. The aqueous preparations may be particularly useful in patients in whom Freon preparations cause mucosal drying, crusting, or epistaxis. Rarely, nasal steroids are associated with nasal septal perforation, probably secondary to nasal septal wall damage from inappropriate use of the pressurized aerosol.

Treatment failures occur if mucus or other debris is not cleaned from the nose before application. Saline nasal sprays or washes can facilitate this cleaning. Because newer topical nasal steroids act rapidly, as-needed use appears to be almost as effective as daily use and seems appropriate in patients with episodic symptoms. To optimize compliance, we prefer the preparations requiring once-daily dosing. These include triamcinolone acetonide, budesonide, fluticasone propionate, and mometasone furoate. Intranasal corticosteroids are not as effective in reducing concomitant symptoms of allergic conjunctivitis, and additional agents may be necessary.

Antihistamines

Any of the present antihistamines are clearly less effective than topical nasal steroids for relieving symptoms of allergic rhinitis. Antihistamines help control sneezing, rhinorrhea, and itching associated with the early nasal reactions but may provide inadequate relief from nasal obstruction associated with the late-phase reaction. The reaction reflects a second spontaneous wave of mediator release from mast cells and symptoms 6 to 12 hours after allergic exposure. Azelastine, available in a topical nasal spray, also appears to have some anti-inflammatory effect.

First-generation antihistamines produce sedation and other central nervous system symptoms in 20% or more of patients and may cause drying of the mouth and urinary hesitancy. Adverse effects on intellectual and motor function, including driving, also occur. These include performance defects on tests of divided attention, working memory, vigilance, and speed. We also do not regularly recommend first-generation antihistamines. We avoid them altogether in young children, who may have paradoxical agitation, and in the elderly, who may experience confusion and dysequilibrium.

These effects occur uncommonly with second-generation antihistamines other than cetirizine and azelastine. The second-generation antihistamines are equal to or more efficacious than the first-generation antihistamines; they also appear to be equally efficacious to each other.

Oral antihistamine combinations that contain the decongestant pseudoephedrine provide better symptom relief than that associated with antihistamine alone. However, decongestants should be used cautiously because they may cause a variety of side effects and are contraindicated in patients receiving monoamine oxidase therapy.

Some authors classify metabolites of second-generation antihistamines, such as the metabolite of fexofenadine (Allegra; Aventis Pharmaceuticals, Kansas City, MO) and desloratadine (Clarinex; Schering-Plough, Kenilworth, NJ) as "third-generation antihistamines." Available second- and third-generation antihistamines (cetirizine, fexofenadine, desloratadine, and loratadine) have not been associated with QT prolongation.

Second-generation antihistamines for acute symptoms and combination second-generation antihistamine-decongestants (eg, loratadine-pseudoephedrine [Claritin D; Schering-Plough] or fexofenadine-pseudoephedrine [Allegra D; Aventis]) for chronic symptoms may be useful in patients with mild symptoms or those preferring pills to nasal sprays, especially if allergic conjunctivitis is also present.

Cromolyn

Cromolyn decreases allergic inflammation by inhibiting the intermediate-conductance chloride channel pathways of mast cells, eosinophils, epithelial and endothelial cells, fibroblasts, and sensory neurons. It inhibits mast cell mediator release. Cromolyn is more effective than placebo in the treatment of seasonal allergic rhinitis. However, most studies show it to be less effective than topical nasal steroids. Cromolyn is particularly useful for individuals who experience episodic symptoms to allergens, such as a cat, where it may be used 30 minutes before exposure. It has no serious side effects and is available over the counter.

Ipratropium

This agent, which is a congener of atropine in a 0.03% nasal solution, reduces rhinorrhea when used intranasally. It does not block sneezing, pruritus, or nasal obstruction and is thus of greater use in nonallergic rhinitis with predominant rhinorrhea. Nevertheless, ipratropium reportedly controls rhinorrhea, nasal congestion, and sneezing in children with perennial allergic rhinitis.

Leukotriene Modifiers

Although sneezing and nasal itching correlate best with histamine levels in experimental allergic rhinitis, nasal congestion correlates with leukotriene C4 levels. Clinical trials of montelukast (a leukotriene receptor antagonist) in various combinations with placebo controls suggested that montelukast performed as well as loratadine alone and provided additive benefits in combination. Because of the efficacy of topical nasal steroids, we consider these agents as second-line therapy for allergic rhinitis. We consider them, for example, in patients that experience epistaxis with nasal sprays.

Allergen Immunotherapy

Allergen immunotherapy involves the SC administration of increasing doses of therapeutic vaccines of allergens to which a patient is known to be allergic until reaching an arbitrary "maintenance" dose. In the United States, a number of allergenic vaccines have been standardized and are available in bioequivalent allergy units. These include cats; the two predominant mite species; short ragweed; and Bermuda, red top, June, rye, orchard, timothy, and sweet vernal grasses. The standardized vaccines allow for more consistent potency than former vaccines, thereby decreasing the probability of anaphylaxis. They have been used in the most recent clinical studies.

A large number of controlled studies have demonstrated that allergen immunotherapy to tree, grass, and ragweed pollens; Alternaria mold; and the house dust mite are efficacious in allergic rhinitis. A meta-analysis published in 2000 evaluated 16 studies published between 1966 and 1996 that assessed the efficacy of immunotherapy in the treatment of allergic rhinitis. In the combined analysis of 759 patients (consisting of 546 adults, 53 children, and 160 patients of all ages), immunotherapy was associated with significant clinical improvement. Immunotherapy should be considered in patients in whom pharmacotherapy and avoidance of allergens have failed to resolve symptoms or in whom pharmacotherapy has produced unacceptable side effects or is not cost-effective.

Regulation of IgE Function

Recombinant human monoclonal antibody to IgE, omalizumab (Xolair; Genetech, Inc., South San Francisco, CA; Novartis Pharmaceuticals, East Hanover, NJ), binds circulating IgE and prevents the interaction of IgE with surface receptors on mast cells. Anti-IgE therapy has been shown to decrease IgE levels and modulate early and late-phase reactions in atopic asthma. It is presently in clinical trials for other clinical applications.

Key Points

* Topical nasal steroids are effective in all types of rhinitis.

* Topical nasal steroids are more effective than antihistamines in allergic rhinitis.

* Treatment of chronic rhinitis frequently resolves chronic sinusitis.

Table 2. Some drugs for allergic rhinitis (a)

Drug                                    Adult dosage

Corticosteroid nasal sprays

  Beclomethasone dipropionate   1 or 2 sprays per nostril, bid
  (Beconase AQ;
  GlaxoSmithKline)

  Budesonide (Rhinocort Aqua;   1 spray per nostril once/d
  AstraZeneca)

  Flunisolide (generic price)   2 spray per nostril, bid

    Nasalide (Ivax)

    Nasarel (Ivax)

  Fluticasone propionate        2 sprays per nostril once/d or
  (Flonase; GlaxoSmithKline)

                                1 spray per nostril, bid

  Mometasone furoate (Nasonex;  2 sprays per nostril once/d
  Schering)

  Triamcinolone acetonide       2 sprays each nostril once/d
  (Nasacort; Aventis)

  Nasacort AQ

Oral [H.sub.1]-receptor
blockers

  Cetirizine (Zyrtec (d);       5 or 10 mg once/d
  Pfizer)

  Desloratadine (Clarinex;      5 mg once/d
  Schering)

  Fexofenadine (Allegra;        60 mg bid or 180 mg once/d
  Aventis)

  Loratadine (e) (Claritin      10 mg once/d
  (d); Schering)

    Claritin Reditabs (f)

    Alavert (f) (Wyeth)

Leukotriene modifier

  Montelukast (Singulair;       10 mg once/d
  Merck)

Drug                                    Pediatric dosage

Corticosteroid nasal sprays

  Beclomethasone dipropionate   6-11 yr: 1 spray per nostril, bid
  (Beconase AQ;

   GlaxoSmithKline)

  Budesonide (Rhinocort Aqua;   6-11 yr: 1 spray per nostril, once/d
  AstraZeneca)

  Flunisolide (generic price)   6-14 yr: 1 spray per nostril, tid, or 2
                                  sprays per nostril, bid

    Nasalide (Ivax)

    Nasarel (Ivax)

  Fluticasone propionate        4-11 yr: 1 spray per nostril, once/d
  (Flonase; GlaxoSmithKline)

  Mometasone furoate (Nasonex;  3-11 yr: 1 spray per nostril, once/d
  Schering)

  Triamcinolone acetonide       6-11 yr: 2 sprays per nostril once/d
  (Nasacort; Aventis)

  Nasacort AQ                   6-11 yr: 1 spray per nostril once/d

Oral [H.sub.1]-receptor
blockers

  Cetirizine (Zyrtec (d);       6-11 yr: 5 or 10 mg once/d
  Pfizer)

                                2-5 yr: 2.5 or 5 mg once/d or 2.5 mg bid

  Desloratadine (Clarinex;
  Schering)

  Fexofenadine (Allegra;        6-11 yr: 30 mg bid
  Aventis)

  Loratadine (e) (Claritin      6-11 yr: 10 mg once/d
  (d); Schering)

    Claritin Reditabs (f)       2-5 yr: 5 mg once/d

    Alavert (f) (Wyeth)

Leukotriene modifier

  Montelukast (Singulair;       6-14 yr: 5 mg once/d
  Merck)

                                2-5 yr: 4 mg once/d

Drug                            Cost (b)

Corticosteroid nasal sprays

  Beclomethasone dipropionate   $36.90
  (Beconase AQ;

   GlaxoSmithKline)

  Budesonide (Rhinocort Aqua;   $33.65
  AstraZeneca)

  Flunisolide (generic price)   $45.59 (c)

    Nasalide (Ivax)             $62.69

    Nasarel (Ivax)              $62.27

  Fluticasone propionate        $62.41
  (Flonase; GlaxoSmithKline)

  Mometasone furoate (Nasonex;  $65.98
  Schering)

  Triamcinolone acetonide       $71.82
  (Nasacort; Aventis)

  Nasacort AQ                   $66.21

Oral [H.sub.1]-receptor
blockers

  Cetirizine (Zyrtec (d);       $63.29
  Pfizer)

  Desloratadine (Clarinex;      $65.75
  Schering)

  Fexofenadine (Allegra;        $84.62
  Aventis)

  Loratadine (e) (Claritin      $27.87 (c)
  (d); Schering)

    Claritin Reditabs (f)       $38.97 (e)

    Alavert (f) (Wyeth)         $29.95 (c)

Leukotriene modifier

  Montelukast (Singulair;       $83.93
  Merck)

(a) From, Montelukast (Singulair) for allergic rhinitis. Med Lett Drugs
Ther 2003 Mar 17;45(1152):21.
(b) Cost for 30 days' treatment at the lowest initial dosage for adults,
according to AWP listings in Drug Topics Red Book 2002 and March 2003
Update.
(c) Cost for 30 days' treatment according to listings on drugstore.com,
March 10, 2003.
(d) Also available in a syrup formulation: 1 mg/ml.
(e) Available without a prescription.
(f) Disintegrating tablets.

From the Department of Medicine, University of Mississippi Medical Center, Jackson, MS.

Reprint requests to Richard D. deShazo, MD, Department of Medicine, University of Mississippi Medical Center, 2500 N. State Street, Jackson, MS 39216. Email: [e-mail]

Accepted August 19, 2003.

Copyright [c] 2003 by The Southern Medical Association

0038-4348/03/9611-1055

References

1. Ng ML, Warlow RS, Chrishanthan N, et al. Preliminary criteria for the definition of allergic rhinitis: A systematic evaluation of clinical parameters in a disease cohort (I). Clin Exp Allergy 2000;30:1314-1331.

2. Ng ML, Warlow RS, Chrishanthan N, et al. Preliminary criteria for the definition of allergic rhinitis: A systematic evaluation of clinical parameters in a disease cohort (II). Clin Exp Allergy 2000;30:1417-1422.

3. Dykewicz MS, Fineman S, Skoner DP, et al; American Academy of Allergy, Asthma, and Immunology. Diagnosis and management of rhinitis: Complete guidelines of the Joint Task Force on Practice Parameters in Allergy, Asthma and Immunology. Ann Allergy Asthma Immunol 1998;81:478-518.

4. Boulet LP, Turcotte H, Laprise C, et al. Comparative degree and type of sensitization to common indoor and outdoor allergens in subjects with allergic rhinitis and/or asthma. Clin Exp Allergy 1997;27:52-59.

5. Craig TJ, Teets S, Lehman EB, et al. Nasal congestion secondary to allergic rhinitis as a cause of sleep disturbance and daytime fatigue and the response to topical nasal corticosteroids. J Allergy Clin Immunol 1998;101:633-637.

6. Adcock I. Role of mediators in late-phase allergic symptoms including congestion. Clin Exp All Rev 2002;2:85-87.

7. Montelukast (singulair) for allergic rhinitis. Med Lett Drugs Ther 2003 Mar 17;45:21-22.

8. Lieberman PL, Blaiss MS. Atlas of Allergic Diseases. Philadelphia, Lippincott Williams & Wilkins, 2002.

RELATED ARTICLE: Table 1. Classification of rhinitis

Allergic rhinitis

Acute

Seasonal

Perennial

Occupational

Infectious rhinitis

Acute: Viral, bacterial

Chronic

Specific: Bacterial, fungal

Nonspecific: Associated with immune deficiency (antibody deficiency, cystic fibrosis, ciliary abnormalities)

Perennial nonallergic rhinitis

Idiopathic (vasomotor rhinitis)

Nonallergic rhinitis with eosinophilia

Miscellaneous forms

Hormonal: Pregnancy, hypothyroidism

Drug-induced: Associated with aspirin sensitivity, rhinitis medicamentosa (vasoconstrictor nasal sprays), antihypertensives

Food-associated: Gustatory, IgE mediated, preservative induced

Atrophic rhinitis (Klebsiella ozaenae)

Mechanical: Hypertrophied turbinates, deviated nasal septum, foreign body, nasal polyps

Granulomatous: Wegener's granulomatosis, sarcoidosis, midline granuloma

Richard D. deShazo, MD, and Stephen F. Kemp, MD