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Treatment options for the management of perennial allergic rhinitis, with a focus on intranasal corticosteroids.

Abstract: Perennial allergic rhinitis (PAR) can have a significant impact on a patient's quality of life. While allergen avoidance is the first line of management for PAR, complete avoidance is difficult. Therapeutic options available for PAR include intranasal corticosteroids (INS), [H.sub.1]-antihistamines, decongestants and local chromones, as well as immunotherapy. For mild symptoms, INS and antihistamines are the standard of care, whereas for moderate-to-severe PAR, INS are the preferred therapy due to their proven efficacy. Patient quality of life and therapy preference play a role in maintaining adherence to treatment.

Key Words: perennial allergic rhinitis, avoidance, intranasal corticosteroids, antihistamines


Allergic rhinitis (AR) is the most prevalent chronic allergic disease. It is thought that up to 10% of adults and 40% of children in the US are affected by AR. (1) As such, AR is one of the most common reasons for visits to primary care practitioners, (2) who play a key role in the management of the disease.

The economic burden associated with AR is substantial. In 1996, the estimated total cost of AR in the US was $6 billion. (3) While the symptoms caused by AR are not life threatening, they can significantly impact on patient quality of life (4); the disease reduces productivity at work, (5) impairs concentration (6) and reduces learning ability in children. (7) AR is often associated with a number of comorbidities, including sinusitis, asthma and otitis media. (8-12) Poorly controlled AR can exacerbate these conditions, adding greatly to the morbidity and economic burden of the disease. (2)

Effective management can prevent the adverse events of perennial AR (PAR), restore patient quality of life, avoid exacerbation of comorbid pathologies and reduce economic burden. This article reviews the current recommendations for the diagnosis and management of PAR, providing a practical overview for the primary care practitioner.

Classification and Diagnosis of Perennial Allergic Rhinitis

AR has traditionally been divided into AR that occurs seasonally due to outdoor allergens such as pollen, and AR that occurs perennially due to indoor allergens such as dust mites and pet dander. (13) However, these definitions are a poor reflection of real life, (14) with some pollens occurring perennially (15) and some symptoms of perennial allergies not being present continuously. Therefore, the Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines reclassify AR into intermittent and persistent AR, based on symptom timing and frequency (Table). (11) Both intermittent and persistent AR can be subdivided based on the severity of patient symptoms into mild or moderate-to-severe. The traditional nomenclatures of seasonal and perennial AR are retained herein to allow a direct discussion of published data.

AR clinically presents as some or all of the following symptoms: rhinorrhea, sneezing, nasal congestion, itching of the nose and palate, and ocular symptoms (itchy, watery eyes). Seasonal allergic rhinitis can be easy to diagnose due to the rapid onset of symptoms when the patient is exposed to pollen. (16) For example, the ragweed pollen season occurs during the fall in the northern latitudes of the US; AR symptoms occurring during this period may be caused by ragweed pollen. Conversely, diagnosing PAR can be difficult, as diagnostic criteria can overlap with those of some non-AR diseases such as sinusitis and vasomotor rhinitis. (16) Furthermore, occupational rhinitis can result from both allergic and nonallergic causes. (17) For example, animal dander found in laboratory environments may result in AR, whereas irritants such as wood dust, detergents, dyes and other industrial chemicals can cause non-AR. (18) Diagnosis should focus on symptoms, triggers, seasonal variation, allergies, medical history and current treatments. (17) Accurate diagnosis is paramount, as effective therapies for AR may not be so effective at treating nonallergic rhinitis. (19)

The causative allergens of PAR commonly include house-dust mites, indoor molds, cockroaches and animal dander. (11) The prevalence of the trigger allergen dictates the incidence of a patient's symptoms; the identification of the trigger allergen is an important aspect in the diagnosis of PAR. A thorough clinical history will provide clues as to the probable trigger. Patients should be carefully questioned regarding possible allergens present at home, work or school. Typically, the causative allergens of PAR are ubiquitous and present all year round.

Percutaneous or intradermal skin testing and immunoglobulin E (IgE) testing (assessed by radioallergosorbent testing [CAP-RAST]) are commonly used by qualified personnel to confirm sensitivity to a particular allergen. Skin testing introduces the allergen into the skin and results in a wheal and flare reaction after 15 minutes, (20) whereas CAP-RAST testing is an in vitro test that involves the binding of a specific allergen to specific IgE in serum. Antibodies are used to quantify the amount of specific IgE bound to the allergens. (21,22) The significance of a positive result during these tests must be considered in conjunction with a suggestive clinical history. (23)

Mechanisms of Perennial Allergic Rhinitis

The pathology of AR can be divided into early and late-phase reactions. Early-phase symptoms occur within minutes of allergen exposure and are characterized by rhinorrhea, nasal obstruction, sneezing and pruritus. (24) Immunoglobulin E-mediated activation of mast cells and basophils release mediators, such as histamine and leukotriene, which activate their respective receptors and induce the symptoms of AR. Histamine is probably the major mediator of the early-phase reaction. (25) Both mast cells and T cells also release cytokines such as interleukins, that induce IgE synthesis. (26)

Approximately 30 to 40% of patients develop a late-phase reaction occurring 4 to 5 hours after the initial allergen exposure (25) characterized by nasal obstruction. (25) Cytokines and chemokines, such as interleukin (IL)-8, as well as the mediators released by the early-phase reaction, help recruit and activate inflammatory cells, such as eosinophils, (27) which themselves release mediators. Symptoms are therefore perpetuated, with persistent AR sufferers existing in a continual state of eosinophilia and increased mediator release. (28)

Management of Perennial Allergic Rhinitis

A review of MEDLINE was performed to assess pharmacologic treatment options using the terms 'perennial allergic rhinitis', 'allergen avoidance', 'intranasal corticosteroids', 'antihistamines', 'decongestants' and 'chromones', as well as individual drug names.

Allergen Avoidance

Allergen avoidance is the first line of management for PAR. Reducing the allergens in a patient's immediate environment can have a significant impact on symptom frequency and severity. (29) A range of measures can be employed, depending on the allergen involved. Aggressive cleaning of the home, effective filtering of the air, hot washing of bedding, replacement of carpets with hard flooring and regular wet-wiping of surfaces are general measures that eradicate most allergens. Despite rigorous cleaning, many allergens persist for extended periods of time and are easily transferred between environments. The total exclusion of an allergen from the environment is difficult. If the causative allergen is occupational, allergen avoidance may be unrealistic. Therefore, treatment to control the symptoms of PAR is frequently required.

Mites. Several specific mite-avoidance measures have been investigated in clinical studies, with varying outcomes. For example, tightly woven mattress coverings have been shown to effectively exclude both cat and house-dust mite allergens. (30) In addition, randomized, controlled studies have shown that the use of dust-mite impermeable mattress covers and other specific environmental controls can result in children being less likely to develop sensitization to dust mites (31) and in reductions in nasal symptoms. (32) Another study indicated that impermeable bedding covers significantly reduced the level of exposure to mite allergens, although corresponding improvements in the clinical symptoms of AR were not noted. (33)

Animals. For animal allergy, removing the animal from the home is the first option though this may cause distress to the patient and their family. High-efficiency particulate air (HEPA)-filtered vacuum cleaners have been shown to reduce the concentration and particle size of airborne cat allergens. (34) The effect allergen reduction had on symptoms was not assessed in this study. A further study indicated that despite the combination of a HEPA room air cleaner, the use of mattress and pillow covers and cat exclusion from the bedroom, no effect on disease activity was noted. (35) Therefore, while allergen avoidance can be useful, some avoidance measures may not always be enough as a single approach, and multiple avoidance measures may be needed.

Pharmacologic Options

For PAR, a number of treatment options can be considered. For patients with mild symptoms, [H.sub.1]-receptor antagonists in oral and nasal formulations, INS, local chromones and oral and intranasal decongestants are recommended. Intranasal anticholinergic agents are also recommended for cases where rhinorrhea is the main symptom. (11) Antileukotrienes, such as montelukast, have recently been approved for the treatment of nasal congestion due to AR. (36) In moderate-to-severe PAR, INS are first-line therapy. (11,37-39) Agents can be used individually or in combination to provide optimal symptom relief depending on symptoms.

Intranasal Corticosteroids

Six aqueous INS formulations are currently licensed for the treatment of adult and pediatric PAR in the US: beclomethasone dipropionate (BDP), budesonide, flunisolide, fluticasone propionate (FP), mometasone furoate (MF) and triamcinolone acetonide (TAA).

Mechanism of Action

While the precise mechanism of action of corticosteroids has yet to be fully elucidated, they are known to have a profound impact on the inflammatory response, suppressing many elements of the allergic inflammatory cascade. By binding to the glucocorticoid receptor of nasal epithelial cells, corticosteroids modulate the expression of a number of genes that play a pivotal role in the inflammatory response. (40) Among other functions, corticosteroids have been shown to reduce eosinophil infiltration and survival (41,42) and to suppress the expression of the cytokines IL-3, IL-4, IL-5 and IL-13, (43) dramatically reducing the infiltration of inflammatory cells into the nasal mucosa. Corticosteroids also reduce the release of several chemical mediators of inflammation, including histamine, (44) tryptase (45) and leukotrienes, (46) although these effects may be due to a reduction in the overall number of inflammatory cells in the epithelium.

Safety of Intranasal Corticosteroids

The adverse events arising from the long-term use of systemic corticosteroids, such as skin-thinning, osteoporosis and Cushing syndrome, are well known. (11) However, INS and systemic corticosteroids should not be classified together as they exhibit differing adverse-event profiles. Local application of corticosteroids allows the use of lower doses that are associated with lower risks of adverse events. In addition, the improved pharmacokinetic profile and, hence, reduced bioavailability of the newer INS agents, further reduces the risk of systemic effects.

Local adverse events. Local adverse events associated with INS are generally minor and easily managed; the most common adverse events include irritation of the nasal epithelium, minor nosebleeds and headaches. These adverse events can usually be managed, although if they persist, switching to another agent or delivery device often eliminates the problem. (11) Septal perforation is an extremely rare adverse event of INS therapy that may largely be avoided by correct administration. (47) Patients should be advised to direct the spray away from the septum to minimize any risk of septal perforation. (48)

Systemic adverse events. Suppression of the hypothalamic-pituitary-adrenal (HPA) axis is a well-characterized adverse event of systemic corticosteroids. However, a number of clinical studies have shown that TAA, MF and FP have little or no effect on the HPA axis. (49,50) A preliminary study found no evidence of HPA-axis suppression with both FP 200 [micro]g once daily and TAA 220 [micro]g once daily when used in combination with the same agents administered at clinically recommended dosages for inhaled administration (FP 1760 [micro]g daily and TAA 1600 [micro]g daily). (51) It is advisable to use the lowest corticosteroid dose possible to control allergic disease because of a potential additive effect of intranasal and inhaled corticosteroids.

Concerns have also been raised over the effect of long-term INS therapy on linear growth in young children, (52) with one study suggesting that long-term use of BDP reduced growth in children. (53) The weight of evidence from data collected in recent years suggests that INS therapy has no significant long-term effect on normal growth in children. For example, a 1-year trial of MF 100 [micro]g once daily showed no evidence of growth suppression or impaired bone metabolism in children with PAR. (54) Similarly, a study of FP 100 [micro]g administered twice daily for 1 year to children aged 1 to 3 years showed no significant effect on growth. (55) Another 1-year study in children aged 6 to 14 years also demonstrated no significant effect of TAA treatment on growth velocity. (56) Finally, a comparative study of TAA 110 [micro]g and 220 [micro]g once daily and FP 200 [micro]g in children showed no significant statistical difference in mean growth velocity compared with placebo. (57)


Despite marked differences in the pharmacokinetic properties of the currently available INS formulations, all have proven efficacy in controlling the symptoms of PAR. (58) Furthermore, several head-to-head and comparative studies have indicated no clinical differences in efficacy between INS agents. For example, one study compared the efficacy of MF and FP at treating PAR in a 3-month, double-blind, double-dummy, placebo-controlled trial. Both agents were significantly (P < 0.01) superior to placebo at reducing nasal symptoms. There was no statistically significant difference between the two agents. (59) In a similar trial comparing TAA and FP, both agents were found to be equally effective in reducing total nasal symptom score from baseline (3.17 [+ or -] 0.18 and 3.15 [+ or -] 0.19, respectively). (60)

Quality of Life

PAR can have a strong negative impact on patient quality of life. A study of health-related quality of life found that patients with PAR reported more pain, felt less healthy, had poorer mental health and felt less able to function effectively than healthy volunteers. (61) INS agents have been shown to have benefits in patient health-related quality of life. (62) For example, a placebo-controlled, multicenter, randomized, double-blind study in patients with PAR found that TAA 220 [micro]g once daily significantly (P = 0.04) improved health-related quality of life, as assessed using the Rhinoconjunctivitis Quality of Life Questionnaire. Improvement in quality of life directly correlated with reductions in nasal symptoms. (63) A similar trial compared the effects of budesonide and FP on quality of life in patients with AR. (64) Both agents significantly (P < 0.05) improved patient quality of life as measured by the Rhinoconjunctivitis Quality of Life Questionnaire when compared with placebo. Greater improvements in patient quality of life were seen with budesonide than FP. (64) A study concerning nocturnal symptoms only found that TAA 220 [micro]g once daily for 3 weeks significantly improved (P < 0.001) nocturnal symptoms compared with baseline (65) as measured by the Nocturnal Rhinoconjunctivitis Quality of Life Questionnaire and Pittsburgh Sleep Quality Index.

Patient Preference/Adherence

Successful treatment of PAR requires good long-term patient adherence. (66) Patient education and involvement is crucial to maintaining good treatment compliance, and patient preference for certain aspects of INS treatment, including convenience of administration, sensation during and after administration, irritation upon administration, and INS odor and taste, is thought to play a significant role in maintaining adherence to a therapeutic regimen. (67,68) A number of studies have compared patient preference for MF, FP and TAA; however, these have included the old MF formulation, before the current alcohol-free formulation was available. Therefore, the comparisons with the old formulation are no longer relevant.

For example, a multicenter, randomized, double-blind, crossover study comparing patient assessments of the sensory attributes of MF (old formulation), FP and TAA, found that TAA was rated as having little or no odor, a milder, more pleasant taste and a less drying effect on the throat than FP (P [less than or equal to] 0.05). (67) During the same trial, a greater proportion of patients indicated that they would be more compliant with medication if they were prescribed TAA over FP. (67) An earlier study also demonstrated preference for TAA over FP and BDP when rated for odor or taste. (69) Patient preference has also been shown for budesonide over FP (70) and the new MF formulation over FP based on sensory attributes. (71)

[H.sub.1]-Receptor Antagonists

[H.sub.1]-receptor antagonists are a mainstay treatment for patients with mild-to-moderate PAR, and can be classified into first- and second-generation agents. First-generation antihistamines have been effective treatments for symptoms of AR, but are known to cause adverse events due to their lack of selectivity, resulting in anticholinergic effects such as dry mouth, tachycardia, urinary retention and gastrointestinal disturbances. (72) Further adverse events are caused by the ability of the first-generation agents to cross the blood-brain barrier, resulting in sedation and impairment of psychomotor and cognitive function. (73) Nasal antihistamines such as levocabastine, azelastine and antazoline, however, have almost no associated adverse events, targeting only the organs to which they are administered. (74) Nasal antihistamines are of particular benefit to children whose symptoms are limited to the eyes or the nose. (75)

Second-generation antihistamines, such as cetirizine, loratadine, desloratadine and fexofenadine, are also effective at controlling the main symptoms of mild-to-moderate PAR, (76-79) but are more selective for the [H.sub.1]-receptor than their first-generation predecessors and have a lower tendency to cross the blood-brain barrier. (80) Due to their improved safety profile, a recent consensus report recommended that second-generation antihistamines should be used instead of the first-generation agents in all patients with AR. (80)

Second-generation oral antihistamines generally have a fast onset of action (1-3 h) (81,82) and are convenient to use due to their once-daily formulations. However, compared with INS, oral antihistamines are less effective against nasal congestion. Therefore, in persistent or moderate-to-severe PAR, antihistamines are often used concurrently with an INS or a decongestant.

Oral and Intranasal Decongestants

Decongestants may also be used to relieve nasal congestion. For patients with moderate-to-severe nasal congestion, decongestants are used as add-on therapies to INS. (11) While the intranasal agents are faster than the oral formulations, the duration of treatment is limited to less than 10 days to prevent rhinitis medicamentosa (11); intranasal decongestants are not used as long-term therapy except during severe symptoms. The adverse events associated with oral decongestants are dose-dependent and include irritability, dizziness, headaches, tremor and insomnia. Care should be taken when giving oral decongestants to susceptible patients such as pregnant women and the elderly.

Combinations of oral decongestants with second-generation oral antihistamines are also available. There are limited published studies on the use of such combinations in PAR, but they have been shown to be more effective at treating the whole range of symptoms in patients with seasonal AR, compared with the individual monotherapies. (83-86)

Local Chromones

Intranasal chromones are considered to be less effective than other treatment options, with a short-lasting effect. (11) Although typically associated with the treatment of seasonal AR, chromones can be used for the treatment of mild PAR symptoms, especially in children, due to their excellent safety profile. However, compliance is generally poor due to twice-/three times-daily dosing.


Allergen immunotherapy can be an effective method of treating PAR. (11) Patients whose AR cannot be controlled by avoidance measures and pharmacologic treatments and who need to avoid potential adverse events associated with pharmacologic treatments are good candidates for receiving immunotherapy. (87) Immunotherapy works by gradually increasing doses of allergen administered subcutaneously by an allergy specialist to induce tolerance to the allergen. Immunotherapy has been shown to be effective and has a high safety profile, although treatment is typically required over a number of years (88) and anaphylaxis following injection can be fatal. (89)


Although not yet a United States Food and Drug Administration-approved treatment for PAR, omalizumab has been shown to be an effective treatment for patients with PAR and seasonal AR. (90) Omalizumab is an antibody that binds IgE, preventing IgE from binding to basophils, thereby attenuating mediator release and reducing allergic symptoms. (91) Omalizumab has been shown to be well tolerated. (91)


Perennial AR has a significant negative impact on patient quality of life and may further exacerbate a number of common comorbidities. Allergen avoidance can improve symptoms; however, the allergens most frequently associated with PAR are ubiquitous and complete avoidance is difficult. Many patients affected by PAR require medication to control symptoms.

A number of options exist for the treatment of PAR, including INS, antihistamines, decongestants and chromones. While INS and antihistamines are first-line therapies for mild symptoms, ARIA guidelines have recommended INS therapy as the gold-standard treatment for moderate-to-severe PAR symptoms. The safety profiles of INS agents are associated with few systemic adverse events, with the newer INS agents being associated with little or no HPA-axis suppression and no significant long-term growth reduction in children. The efficacies of the currently available aqueous agents are broadly equivalent. To maximize symptom relief and improve patient quality of life, it is important that patients adhere to an INS treatment regimen. Recent studies have suggested that tailoring treatment to patient preference improves treatment adherence, hence improving long-term clinical outcome.


1. Sibbald B. Epidemiology of allergic rhinitis. In: Burr ML. ed. Epidemiology of Clinical Allergy. Monographs in Allergy. Vol 31. Basel, Karger, 1993, pp 61-79.

2. Meltzer EO. The prevalence and medical and economic impact of allergic rhinitis in the United States. J Allergy Clin Immunol 1997;99(6 Pt 2):S805-S828.

3. Smart B. The costs of asthma and allergy. American Academy of Allergy, Asthma, and Immunology. Available at: Accessed May 19, 2005.

4. Thompson AK, Juniper E, Meltzer EO. Quality of life in patients with allergic rhinitis. Ann Allergy Asthma Immunol 2000;85:338-347.

5. Reilly MC, Tanner A, Meltzer EO. Work, classroom and activity impairment instruments: validation studies in allergic rhinitis. Clin Drug Invest 1996;11:278-288.

6. Meltzer E, Nathan R, Selner J, et al. Quality of life and rhinitis symptoms: Results of a nationwide survey with the SF-36 and RQLQ questionnaire. J Allergy Clin Immunol 1997;99:S815-S819.

7. Vuurman EF, van Veggel LM, Uiterwijk MM. Seasonal allergic rhinitis and antihistamine effects on children's learning. Ann Allergy 1993;71:121-126.

8. Settipane RA. Complications of allergic rhinitis. Allergy Asthma Proc 1999 20:209-213.

9. Spector S. Overview of comorbid associations of allergic rhinitis. J Allergy Clin Immunol 1997;99:S773-S780.

10. Slavin R. Sinusitis in adults and its relation to allergic rhinitis, asthma, and nasal polyps. J Allergy Clin Immunol 1988;82:950-956.

11. Bousquet J, van Cauwenberge P, Khaltaev N. Allergic rhinitis and its impact on asthma. J Allergy Clin Immunol 2001;108(Suppl 5):S147-S334.

12. Corey JP, Adham RE, Abbass AH, et al. The role of IgE-mediated hypersensitivity in otitis media with effusion. Am J Otolaryngol 1994;15:138-144.

13. International consensus report on the diagnosis and management of rhinitis. International rhinitis management working group. Allergy. 1994;49(19 Suppl):1-34.

14. Ciprandi G, Cirillo I, Vizzaccaro A, et al. Seasonal and perennial allergic rhinitis: is this classification adherent to real life? Allergy 2005;60:882-887.

15. Bucholtz GA, Lockey RF, Wunderlin RP, et al. A three-year aerobiologic pollen survey of the Tampa Bay area, Florida. Ann Allergy 1991;67:534-540.

16. Skoner DP. Allergic rhinitis: definition, epidemiology, pathophysiology, detection, and diagnosis. J Allergy Clin Immunol 2001;108(1 Suppl):S2-S8.

17. Quillen DM, Feller DB. Diagnosing rhinitis: allergic vs. nonallergic. Am Fam Physician 2006;73:1583-1590.

18. Slavin RG. Occupational rhinitis. Ann Allergy Asthma Immunol 1999;83(6 Pt 2):597-601.

19. Agency for Healthcare Research and Quality. Evidence report/technology assessment No. 54. Management of allergic and nonallergic rhinitis. May, 2002.

20. Gendo K. Larson EB. Evidence-based diagnostic strategies for evaluating suspected allergic rhinitis. Ann Intern Med 2004;140:278-289.

21. Hamilton RG, Adkinson NF Jr 23. Clinical laboratory assessment of IgE-dependent hypersensitivity. J Allergy Clin Immunol 2003;111(2 Suppl):S687-S701.

22. Johansson SG. ImmunoCAP Specific IgE test: an objective tool for research and routine allergy diagnosis. Expert Rev Mol Diagn 2004;4:273-279.

23. Sibbald B, Barnes G, Durham SR. Skin prick testing in general practice: a pilot study. J Adv Nurs 1997;26:527-542.

24. Lebel B, Bousquet J, Morel A, et al. Correlation between symptoms and the threshold for release of mediators in nasal secretions during nasal challenge with grass-pollen grains. J Allergy Clin Immunol 1988;82(5 Pt 1):869-877.

25. Naclerio RM, Meier HL, Kagey-Sobotka A, et al. Mediator release after nasal airway challenge with allergen. Am Rev Respir Dis 1983 128:597-602.

26. Pawankar R, Yamagishi S, Yagi T. Revisiting the roles of mast cells in allergic rhinitis and its relation to local IgE synthesis. Am J Rhinol 2000;14:309-317.

27. White M. Mediators of inflammation and the inflammatory process. J Allergy Clin Immunol 1999;103(3 Pt 2):S378-S381.

28. Wang DY, Clement P. Pathogenic mechanisms underlying the clinical symptoms of allergic rhinitis. Am J Rhinol 2000;14:325-333.

29. Carswell F, Oliver J, Weeks J. Do mite avoidance measures affect mite and cat airborne allergens? Clin Exp Allergy 1999;29:193-200.

30. Vaughan JW, McLaughlin TS, Perzanowski MS, et al. Evaluation of materials used for bedding encasement: Effect of pore size in blocking cat and dust mite allergen. J Allergy Clin Immunol 1999;103:227-231.

31. Arshad SH, Bojarskas J, Tsitoura S, et al. Prevention of sensitization to house dust mite by allergen avoidance in school age children: a randomized controlled study. Clin Exp Allergy 2002;32:843-849.

32. Moon JS, Choi SO. Environmental controls in reducing house dust mites and nasal symptoms in patients with allergic rhinitis. Yonsei Med J 1999;40:238-243.

33. Terreehorst I, Hak E, Oosting AJ, et al. Evaluation of impermeable covers for bedding in patients with allergic rhinitis. N Engl J Med 2003;349:237-246.

34. Woodfolk JA, Luczynska CM, de Blay F. The effect of vacuum cleaners on the concentration and particle size distribution of airborne cat allergen. J Allergy Clin Immunol 1993 91:829-837.

35. Wood RA, Johnson EF, Van Natta ML, et al. A placebo-controlled trial of a HEPA air cleaner in the treatment of cat allergy. Am J Respir Crit Care Med 1998;158:115-120.

36. Davies MJ, Fisher LH, Chegini S, et al. A practical approach to allergic rhinitis and sleep disturbance management. Allergy Asthma Proc 2006;27:224 230.

37. Van Cauwenberge P, Bachert C, Passalacqua G, et al. Consensus statement on the treatment of allergic rhinitis. Allergy 2000;55:116-134.

38. International consensus report on the diagnosis and managnment of rhinitis. International rhinitis managment working group. Allergy 1994;49:1-34.

39. Dykewicz MS, Fineman S, Skoner DP, et al. Diagnosis and management of rhinitis: complete guidelines of the Joint Task Force on Practice Parameters in Allergy, Asthma and Immunology. American Academy of Allergy, Asthma, and Immunology. Ann Allergy Asthma Immunol 1998;81(5 Pt 2):478-518.

40. Pujols L, Mullol J, Torrego A, et al. Glucocorticoid receptors in human airways. Allergy 2004;59:1042-1052.

41. Mullol J, Xaubet A, Lopez E, et al. Comparative study of the effects of different glucocorticosteroids on eosinophil survival primed by cultured epithelial cell supernatants obtained from nasal mucosa and nasal polyps. Thorax 1995;50:270-274.

42. Mullol J, Lopez E, Roca-Ferrer J, et al. Effects of topical anti-inflammatory drugs on eosinophil survival primed by epithelial cells. Additive effect of glucocorticoids and nedocromil sodium. Clin Exp Allergy 1997;27:1432-1441.

43. Sim TC, Reece LM, Hilsmeier KA, et al. Secretion of chemokines and other cytokines in allergen-induced nasal responses: inhibition by topical steroid treatment. Am J Respir Crit Care Med 1995;152:927-933.

44. Pipkorn U, Proud D, Lichtenstein LM, et al. Inhibition of mediator release in allergic rhinitis by pretreatment with topical glucocorticosteroids. N Engl J Med 1987;316:1506-1510.

45. Scadding GK, Darby YC, Austin CE. Effect of short-term treatment with fluticasone propionate nasal spray on the response to nasal allergen challenge. Br J Clin Pharmacol 1994;38:447-451.

46. Wang D, Smitz J, De Waele M, et al. Effect of topical applications of budesonide and azelastine on nasal symptoms, eosinophil count and mediator release in atopic patients after nasal allergen challenge during the pollen season. Int Arch Allergy Immunol 1997;114:185-192.

47. Cervin A, Andersson M. Intranasal steroids and septum perforation-an overlooked complication? A description of the course of events and a discussion of the causes. Rhinology 1998;36:128-132.

48. Holm AF, Fokkens WJ, Godthelp T, et al. A 1-year placebo-controlled study of intranasal fluticasone propionate aqueous nasal spray in patients with perennial allergic rhinitis: a safety and biopsy study. Clin Otolaryngol 1998;23:69-73.

49. Wilson AM, McFarlane LC, Lipworth BJ. Effects of repeated once daily dosing of three intranasal corticosteroids on basal and dynamic measures of hypothalamic-pituitary-adrenal-axis activity. J Allergy Clin Immunol 1998;101(4 Pt 1):470-474.

50. Wilson AM, Sims EJ, McFarlane LC, et al. Effects of intranasal corticosteroids on adrenal, bone, and blood markers of systemic activity in allergic rhinitis. J Allergy Clin Immunol 1998;102(4 Pt 1):598-604.

51. Wilson AM, Lipworth BJ. 24 hour and fractionated profiles of adrenocortical activity in asthmatic patients receiving inhaled and intranasal corticosteroids. Thorax 1999;54:20-26.

52. Cave A, Arlett P, Lee E. Inhaled and nasal corticosteroids: factors affecting the risks of systemic adverse effects. Pharmacol Ther 1999;83:153-179.

53. Skoner DP, Rachelefsky GS, Meltzer EO, et al. Detection of growth suppression in children during treatment with intranasal beclomethasone dipropionate. Pediatrics 2000;105:E23.

54. Schenkel EJ, Skoner DP, Bronsky EA, et al. Absence of growth retardation in children with perennial allergic rhinitis after one year of treatment with mometasone furoate aqueous nasal spray. Pediatrics 2000;105:E22.

55. Bisgaard H, Allen D, Milanowski J, et al. Twelve-month safety and efficacy of inhaled fluticasone propionate in children aged 1 to 3 years with recurrent wheezing. Pediatrics 2004;113:e87-94.

56. Ober S, Gentile D, Kairis E, et al. Growth velocity and HPA axis function during 1-year treatment with triamcinolone acetonide aqueous (TAA) nasal spray in children with allergic rhinitis. J Allergy Clin Immunol 2005;115:1064.-

57. Skoner DP, Gentile D, Angelini B, et al. The effects of intranasal triamcinolone acetonide and intranasal fluticasone propionate on short-term bone growth and HPA axis in children with allergic rhinitis. Ann Allergy Asthma Immunol 2003;90:56-62.

58. Lumry WR. A review of the preclinical and clinical data of newer intranasal steroids used in the treatment of allergic rhinitis. J Allergy Clin Immunol 1999;104(4 Pt 1):S150-S158.

59. Mandl M, Nolop K, Lutsky BN. Comparison of once daily mometasone furoate (Nasonex) and fluticasone propionate aqueous nasal sprays for the treatment of perennial rhinitis. The 194-079 Study Group. Ann Allergy Asthma Immunol 1997;79:237-245.

60. Berger WE, Kaiser H, Gawchik SM, et al. Triamcinolone acetonide aqueous nasal spray and fluticasone propionate are equally effective for relief of nasal symptoms in patients with seasonal allergic rhinitis. Otolaryngol Head Neck Surg 2003;129:16-23.

61. Bousquet J, Bullinger M, Fayol C, et al. Assessment of quality of life in patients with perennial allergic rhinitis with the French version of the SF-36 Health Status Questionnaire. J Allergy Clin Immunol 1994;94(2 Pt 1):182-188.

62. Tripathi A, Patterson R. Impact of allergic rhinitis treatment on quality of life. Pharmacoeconomics 2001;19:891-899.

63. Potter PC, Van Niekerk CH, Schoeman HS. Effects of triamcinolone on quality of life in patients with persistent allergic rhinitis. Ann Allergy Asthma Immunol 2003;91:368-374.

64. Ciprandi G, Canonica WG, Grosclaude M, et al. Effects of budesonide and fluticasone propionate in a placebo-controlled study on symptoms and quality of life in seasonal allergic rhinitis. Allergy 2002;57:586-591.

65. Mintz M, Garcia J, Diener P, et al. Triamcinolone acetonide aqueous nasal spray improves nocturnal rhinitis-related quality of life in patients treated in a primary care setting: the Quality of Sleep in Allergic Rhinitis study. Ann Allergy Asthma Immunol 2004;92:255-261.

66. Loh CY, Chao SS, Chan YH, et al. A clinical survey on compliance in the treatment of rhinitis using nasal steroids. Allergy 2004;59:1168-1172.

67. Bachert C, El-Akkad T. Patient preferences and sensory comparisons of three intranasal corticosteroids for the treatment of allergic rhinitis. Ann Allergy Asthma Immunol 2002;89:292-297.

68. Shah S, Mahadevia PJ, Lelbman C, et al. Patient preferences and willingness to adhere to intranasal corticosteroids: a conjoint analysis in allergic rhinitis. Ann Allergy Asthma Immunol 2005;94:192 (P240).

69. Gerson I, Green L, Fishken D. Patient preference and sensory comparisons of nasal spray allergy medications. J Sens Stud 1999;14:491-496.

70. Shah SR, Miller C, Pethick N, et al. Two multicenter, randomized, single-blind, single-dose, crossover studies of specific sensory attributes of budesonide aqueous nasal spray and fluticasone propionate nasal spray. Clin Ther 2003;25:2198-2214.

71. Meltzer EO, Bardelas J, Goldsobel A, et al. A preference evaluation study comparing the sensory attributes of mometasone furoate and fluticasone propionate nasal sprays by patients with allergic rhinitis. Treat Respir Med 2005;4:289-296.

72. Babe KS, Serafin WE. Histamine, bradykinin, and their antagonists. In: Hardman JG, Limbird LE, Molinoff PB, et al eds. Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed. New York, McGraw-Hill, 1996, pp581-600.

73. Shamsi Z, Hindmarch I. Sedation and antihistamines: a review of inter-drug differences using proportional impairment ratios. Hum Psychopharmacol 2000;15:S3-S30.

74. Ratner PH, Findlay SR, Hampel F Jr, et al. A double-blind, controlled trial to assess the safety and efficacy of azelastine nasal spray in seasonal allergic rhinitis. J Allergy Clin Immunol 1994;94:818-825.

75. Schata M, Jorde W, Richarz-Barthauer U. Levocabastine nasal spray better than sodium cromoglycate and placebo in the topical treatment of seasonal allergic rhinitis. J Allergy Clin Immunol 1991;87:873-878.

76. Bruttmann G, Charpin D, Germouty J, et al. Evaluation of the efficacy and safety of loratadine in perennial allergic rhinitis. J Allergy Clin Immunol 1989;83(2 Pt 1):411-416.

77. Mansmann HC Jr, Altman RA, Berman BA, et al. Efficacy and safety of cetirizine therapy in perennial allergic rhinitis. Ann Allergy 1992;68:348-353.

78. Simons FE, Prenner BM, Finn A Jr. Efficacy and safety of desloratadine in the treatment of perennial allergic rhinitis. J Allergy Clin Immunol 2003;111:617-622.

79. Lee DK, Gray RD, Robb FM, et al. A placebo-controlled evaluation of butterbur and fexofenadine on objective and subjective outcomes in perennial allergic rhinitis. Clin Exp Allergy 2004;34:646-649.

80. Casale TB, Blaiss MS, Gelfand E, et al. First do no harm: managing antihistamine impairment in patients with allergic rhinitis. J Allergy Clin Immunol 2003;111:S835-S842.

81. Day J, Briscoe M, Welsh A. et al. Onset of action, efficacy and safety of a new antihistamine (fexfenadine HCI) using controlled antigen exposure in an environmental exposure unit (EEU). Clinical Investigations in Medicine 1996;19:S4 (Abs 9).

82. Day JH, Briscoe M, Rafeiro E, et al. Comparative onset of action and symptom relief with cetirizine, loratadine, or placebo in an environmental exposure unit in subjects with seasonal allergic rhinitis: confirmation of a test system. Ann Allergy Asthma Immunol 2001;87:474-481.

83. Sussman G, Mason J, Compton D, et al. The efficacy and safety of fexofenadine HCI and pseudoephedrine, alone and in combination, in seasonal allergic rhinitis. J Allergy Clin Immunol 1999;104:100-106.

84. Grosclaude M, Mees K, Pinelli ME, et al. Cetirizine and pseudoephedrine retard, given alone or in combination, in patients with seasonal allergic rhinitis. Rhinology 1997;35:67-73.

85. Bronsky E, Boggs P, Findlay S, et al. Comparative efficacy and safety of a once-daily loratadine-pseudoephedrine combination versus its components alone and placebo in the management of seasonal allergic rhinitis. J Allergy Clin Immunol 1995;96:139-147.

86. Pleskow W, Grubbe R, Weiss S, et al. Efficacy and safety of an extended-release formulation of desloratadine and pseudoephedrine vs the individual components in the treatment of seasonal allergic rhinitis. Ann Allergy Asthma Immunol 2005;94:348-354.

87. Allergen immunotherapy: a practice parameter. American Academy of Allergy, Asthma and Immunology. American College of Allergy, Asthma and Immunology. Ann Allergy Asthma Immunol 2003;90(1 Suppl):1-40.

88. Mailing HJ. Immunotherapy as an effective tool in allergy treatment. Allergy 1998;53:461-472.

89. Borchers AT, Keen CL, Gershwin ME. Fatalities following allergen immunotherapy. Clin Rev Allergy Immunol 2004;27:147-158.

90. Berger WE. Treatment of allergic rhinitis and other immunoglobulin E-mediated diseases with anti-immunoglobulin E antibody. Allergy Asthma Proc 2006;27(2 Suppl 1):S29-32.

91. Belliveau PP. Omalizumab: a monoclonal anti-IgE antibody. MedGenMed 2005;7:27.

Stephen A. Brunton, MD, and Leonard M. Fromer, MD

From the Cabarrus Family Medicine Residency Program, Charlotte, NC, and the Department of Family Medicine, UCLA School of Medicine, CA.

Reprint requests to Dr. Stephen Brunton, Cabarrus Family Medicine Residency Program, 7011 Summerhill Ridge Drive, Charlotte, North Carolina 28226. Email:

Stephen A. Brunton, MD, is a consultant to Sanofi-Aventis, Schering Plough and GlaxoSmithKline; Leonard M. Fromer, MD, has been a participant in CME events and advisory boards funded by unrestricted educational grants from Sanofi-Aventis.

Accepted January 4, 2007.


* Several classes of pharmacologic agents are available for the treatment of perennial allergic rhinitis (PAR), including intranasal corticosteroids (INS), [H.sub.1]- antihistamines, local chromones and decongestants.

* Intranasal corticosteroids are the first-line option in moderate-to-severe PAR and can also be used in mild PAR, due to their proven efficacy.

* Second-generation oral antihistamines are effective at controlling mild-to-moderate PAR, have a fast onset of action and good safety profiles.

* Oral decongestants, usually in combination with oral antihistamines, are recommended for mild nasal congestion and as add-on therapy to INS for moderate-to-severe nasal congestion. Intranasal decongestants can also be used in severe cases of blockage.

* Local chromones are available as intranasal formulations for reducing the nasal symptoms of PAR, particularly in children.

* Successful treatment of PAR requires long-term treatment and patient adherence. Therefore, patient quality of life and patient preference for an agent should be considered when choosing a therapeutic option.
Table. ARIA classification of allergic rhinitis

Symptoms are present:
* Less than 4 days a week
* OR, for less than 4 weeks

Symptoms are present:
* More than 4 days a week
* AND, for more than 4 weeks

None of the following are present:
* Sleep disturbance
* Impairment of daily activities, leisure and/or sport
* Impairment of school or work
* Troublesome symptoms

One or more of the following are present:
* Sleep disturbance
* Impairment of daily activities, leisure and/or sport
* Impairment of school or work
* Troublesome symptoms

Reprinted with permission from Bousquet J, et al. Allergic rhinitis and
its impact on asthma. J Allergy Clin Immunol 2001;108(Suppl 5):S147-
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Title Annotation:Review Article
Author:Brunton, Stephen A.; Fromer, Leonard M.
Publication:Southern Medical Journal
Article Type:Disease/Disorder overview
Geographic Code:1USA
Date:Jul 1, 2007
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