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Allergic Rhinitis: Proper Management Benefits Concomitant Diseases

Posted on: Tuesday, 11 January 2005, 03:00 CST

Allergic rhinitis (AR) may be a local manifestation of a systemic allergic disorder, as evidenced by elevated levels of inflammatory cells and mediators in the peripheral blood and physiologic interactions between the upper and lower airways. Consequently, treatment with systemic medication may benefit both AR and concomitant diseases such as sinusitis and asthma. The recent Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines for diagnosis and treatment of AR support the use of antihistamines and intranasal corticosteroids (INC), and also introduce a new class of drugs, the leukotriene modifiers, which may assist clinicians to help AR patients lead a normal life.

AR affects approximately 40 million individuals and is the most common allergic disorder in the United States. Approximately 40% of children and 30% of adults have symptoms of AR. Allergic rhinitis is one of the top 10 reasons for primary care office visits, but the reported prevalence underestimates the true prevalence because many individuals with AR do not consult a clinician about their symptoms. Although AR is generally not considered a severe disorder, it often significantly reduces quality of life and produces substantial socioeconomic costs ($5.5 to $7.7 billion in lost revenue each year in the U.S. alone).12

Long thought to be a disease of the nose only, AR now appears to be more complex, with inflammation spreading well beyond the nose. This article will examine the systemic aspects of AR and its impact on upper and lower airways. Through better understanding of its pathophysiology and its increased prevalence in recent years, the diagnosis and treatment of AR have become the focus of recent guidelines.1,3 These guidelines examine the standard therapies (e.g., antihistamines, intranasal corticosteroids [INS]) and also introduce leukotriene receptor antagonists (LTRAs). Until early 2003, LTRAs were approved only for asthma. This review will apply the ARIA guidelines for the diagnosis and management of AR and show how LTRAs, the newest Food and Drug Administration (FDA) -approved therapy, may help control this disease.

* AR: A Systemic Disorder

Allergic rhinitis represents a local manifestation of what could be called a systemic inflammatory reaction. Consequently, individuals with AR frequently have associated comorbidities, including asthma, sinusitis, and otitis media with effusion (see Figure: "Associated Comorbidities of AR"), all of which can be exacerbated by an allergic crisis.1,4-7 In addition, AR has been associated with a wide variety of other inflammatory and noninflammatory disorders, ineluding allergic conjunctivitis, nasal polyposis, obstructive sleep apnea, dental malocclusion, speech impairment, lower respiratory tract infections, and eczema.1,4

The development of AR is a three-step process: (1) Sensitization occurs in a predisposed individual with the initial allergen exposure leading to the production of antigen-specific immunoglobulin E (IgE). (2) Allergen reexposure initiates the second step, or the early-phase response, which occurs within minutes of exposure with the release, essentially by mast cells and basophils, of preformed (histamine) and newly synthesized (prostaglandins, cysteinyl leukotrienes fCysLTs]) mediators. These mediators produce the early symptoms of AR: sneezing, itching, rhinorrhea, and to a lesser extent, congestion. (3) The late phase, which begins 2 to 4 hours after exposure, represents a shift from an acute to a chronic inflammatory response characterized more by nasal congestion than by sneezing and rhinorrhea. Mediators released during the early phase promote the production of cytokines, chemokines, and adhesion molecules, as well as the infiltration of inflammatory cells (e.g., eosinophils) into nasal tissues. These cells become activated and release more inflammatory mediators, maintaining and enhancing the inflammatory response.

The systemic nature of allergic disease is suggested by some studies of the physiologic interactions between the upper and lower airways. For example, in nonasthmatic individuals with seasonal AR, nasal allergen challenge caused an influx of eosinophils in both nasal and bronchial epithelium and lamina propria, demonstrating that nasal allergens produced a generalized airway inflammation that extended well beyond the nose.8 The reverse was also true. In nonasthmatic patients with AR, segmental bronchial provocation produced eosinophil infiltration into both bronchial and nasal mucosae.9 A similar interaction was seen between the nasal and sinus mucosae. Insufflated ragweed particles do not enter sinus cavities, but experimental and natural ragweed exposure caused sinus hyperemia and increased metabolic activity in susceptible individuals.10,11 Isolated allergen challenge to a single nasal cavity significantly increased eosinophil levels bilaterally in the maxillary sinuses, with no significant differences detected between the two sinuses.12

This systemic nature of AR is further supported by the increased levels of inflammatory cells and mediators, not only in the nasal mucosa or nasal secretions, but also in the peripheral blood. Some of these mediators, including CysLTs and histamine, are released early after allergen exposure and help recruit inflammatory cells to the nose. The increase of eosinophils reflects the presence of newly synthesized eosinophils derived from the bone marrow, as well as the activation and recruitment of these cells to the nasal mucosa. Furthermore, this increase correlates with the symptoms of AR, especially congestion.13 Eosinophils release a wide variety of proinflammatory mediators, including CysLTs and eosinophil cationic protein, which recruit more inflammatory cells. These increases of inflammatory cells and mediators also occur in asthma; eosinophils and CysLTs are elevated and correlate with the severity of the disease.14

The systemic nature of AR suggests that treating AR will benefit not only the nose but also the upper and lower airways, especially in patients with concomitant disease such as sinusitis or asthma. For example, in patients with both asthma and AR, the use of INS significantly reduced asthma symptoms during pollen season.15 Therefore, it is important to correctly diagnose AR and initiate appropriate therapy.

Associated Comorbidities of AR

Venn diagrams demonstrating the interrelationships between AR and asthma, AR and sinusitis, and AR and otitis media with effusion (OME). Areas of each section represent the proportion of individuals in each category. Up to 58% of individuals with AR have asthma, and 75% to 80% of individuals with asthma have AR.14 Sinusitis was detected in 53% of individuals with AR,S and 58% of individuals with sinusitis had AR.47 Otitis media with effusion, a common childhood disorder, may be increased in atopic individuals. Of kindergarten and elementary school children with AR, 21% had OME, and 50% of children with OME had AR.6

* Diagnosis of AR

The recent ARIA guidelines1 and The Allergy Report3 provide valuable assistance in diagnosing and assessing the severity of AR. These guidelines recommend establishing the patient's family history to evaluate risk for atopic disorders, as well as individual history to establish the frequency, severity (impact of symptoms on quality of life, including any performance impairments), duration, and seasonality of symptoms. In addition, the correct determination of trigger factors can provide valuable information. Patients are sometimes aware that they are allergic to pollen or pets, especially when exposure to the allergen is intermittent. In contrast, they are usually less aware of sensitivity to perennial allergens such as dust mites, cockroaches, and mold.1

A thorough examination of the nose should be performed with anterior rhinoscopy to examine the nasal turbinates, color of the mucosa, and the amount and quality of mucus. Nasal endoscopy can be used when needed to find nasal and sinus pathology, which might be missed by routine speculum and nasopharyngeal examination.1 Other components of examination in AR are eyes, oropharynx, ears, skin, and chest.

Selective diagnostic tests should be used to confirm the results of the history and physical examination. Skin tests are widely recommended and used, since they correlate well with symptoms. Because of potential risks in performing these tests and the complexities of interpreting the results, trained professionals should perform them. They are not appropriate, however, in patients who cannot be removed from medications that suppress the histamine response (antihistamines, tricyclic antidepressants) or whose skin is not testable due to widespread lesions or dermographism (urticaria). In these patients, measuring antigen-specific serum IgE levels with a radioallergosorbent test is a useful alternative that closely correlates with the results of skin tests.1

Once diagnosed, AR should be classified to duration and severity. Although the terms seasonal and perennial are still widely used, the ARIA guidelines propose the words intermittent and persistent to define the duration of symptoms (see Table: "Classification of Allergic Rhinitis"). Allergic rhinitis symptoms occurring more than 4 days per week \for more than 4 weeks are considered persistent, otherwise they are intermittent. Similarly, if at least one of the following symptoms appears, AR is considered moderate-severe: sleep disturbance, impairment of daily activities (leisure or sport), impairment of school or work performance, and troublesome symptoms. If none of these symptoms is present, AR is considered mild.1 These classifications, which have recently been validated,16 provide valuable reference points for initiating and determining the most appropriate therapy.

Classification of Allergie Rhinitis

Before initiating any therapy for a particular patient, it is important to recommend allergen avoidance, determine which treatments have already been tried and the effects of those treatments, and discuss any patient concerns that might jeopardize adherence to therapy.1

* Pharmacotherapy for AR

The goal of treating AR is to allow the patient to lead a normal life. This requires getting control of the inflammation associated with AR without producing adverse effects, and reducing nasal symptoms so that the patient sleeps well and has no daytime somnolence or fatigue. Depending on the duration and severity of AR, achieving this goal may require various therapeutic approaches. Because some patients respond to therapies differently, the choice of treatment must be individually determined.1 Treatments may include the standard pharmacotherapies for AR-antihistamines and intranasal steroids-or the most recent entry, LTRAs. The following recommendations are based on the ARIA guidelines, including the potential use of an LTRA.

Antihistamines

Antihistamines and competitive H1 histamine receptor antagonists are the oldest drugs used to treat allergic diseases. Histamine is released within minutes of allergen exposure, mostly by mast cells, and mediates the early symptoms of AR: sneezing, itching, rhinorrhea, and to a lesser extent, congestion (see Table: "Mediators of the Early- and LatePhase Reactions in Allergic Rhinitis").

Mediators of the Early- and Late-Phase Reactions in Allergic Rhinitis

First-generation antihistamines (e.g., brompheniramine, chlorpheniramine, diphenhydramine, promethazine, triprolidine) have poor selectivity, as well as sedative and anticholinergic effects, and are no longer recommended for the treatment of AR. Newer, second- generation antihistamines (e.g., cetirizine [Zyrtec], desloratadine [Clarinex], fexofenadine [Allegra], and loratadine [Claritin]) have comparable potency, a longer duration of action, and produce minimal sedative and anticholinergic effects. Administered either systemically or topically, they effectively reduce itching, sneezing, and rhinorrhea, but only minimally reduce nasal obstruction.1 The vasoconstrictor pseudoephedrine may be added to reduce congestion. However, the alpha-adrenergic effects of this family of drugs have significant adverse effects (e.g., insomnia) and should be used cautiously.

In a few recent trials, second-generation antihistamines had beneficial effects on some comorbid conditions associated with AR. They increased small-airway caliber and reduced airway hyperresponsiveness in patients with atopic asthma,17 and significantly reduced exercise-induced asthma in children.18 Some efficacy in preventing allergeninduced pulmonary inflammation and subsequent reduced airway function have been reported,19 as well as possible anti-inflammatory effects.20'21 In general, however, antihistamines are not considered anti-inflammatory drugs and are not currently approved or recommended for the treatment of asthma.

Several studies reported antihistamines to be only slightly better than placebo for treating AR and22"24 they are often used in combination with other drugs to control AR inflammation and its associated congestion.

Intranasal Corticosteroids (INCs)

Intranasal corticosteroids are recommended to treat all symptoms of AR. They are particularly effective on the late-phase response and chronic inflammation resulting from prolonged exposure to allergen. Intranasal corticosteroids decrease the influx of inflammatory cells and reduce the release of preformed and newly generated mediators.1

Since corticosteroids are the most potent antiinflammatory medication available, the development of INC is one of the best examples of how the therapeutic index of a drug can be significantly improved by going from systemic delivery to topical delivery. Intranasal corticosteroids have low oral bioavailability and minimal systemic effects at usual dosage. Consequently, they have become first-line therapy for moderate-severe AR. Patients with severe or persistent AR usually have significant nasal congestion and are well managed with an INC. When used regularly, INCs effectively reduce nasal congestion as well as itching, sneezing, and rhinorrhea.1 Intranasal corticosteroids may also confer protection against asthma exacerbations. The relative risk (RR) of an emergency department visit for an asthma exacerbation was reduced by INC (RR: 0.70; 95% confidence interval [CI]: 0.59-0.94) but not by prescription antihistamines (RR: 0.90; 95% CI: 0.78-1.11).25

The low systemic bioavailability of INCs makes them preferable to oral corticosteroids. However, some patients are reluctant to use nasal sprays. Although rare when patients are taught correct spray technique, nasal irritation and epistasis are potential adverse effects. In such cases, alternative treatment is a good choice, especially in patients with mild or intermittent symptoms.

LTRAs

Like INCs, LTRAs have anti-inflammatory properties. They block the effects of CysLTs in both the early- and late-phase responses. Cysteinyl leukotrienes are major mediators of the allergic inflammatory response. Cysteinyl leukotriene levels are elevated in nasal fluid after nasal allergen challenge or natural exposure.26'27 When inhaled, CysLTs produce several of the symptoms of AR, including both sneezing and rhinorrhea. They also mediate nasal congestion28 (increased nasal airway resistance and nasal obstruction).29 More importantly, CysLTs play a key role in eosinophilic airway inflammation because they attract eosinophils by promoting adhesion, infiltration, and migration of eosinophils into the nasal mucosa. Finally, they maintain elevated eosinophil levels by increasing eosinophil survival.

Although only montelukast is approved for AR in the United States, other LTRAs have proven efficacious in AR. For example, in a crossover evaluation comparing pranlukast (available in Japan) to an antihistamine in patients with persistent AR, both drugs significantly reduced rhinorrhea, but only pranlukast significantly reduced nasal congestion (P < 0.01).30 Similarly, in patients with intermittent AR exposed to pollen for 2 days at the peak of ragweed season, zafirlukast significantly reduced sneezing and rhinorrhea (P ≤ 0.05) and nasal congestion (P < 0.01) compared with placebo.31 In several trials, montelukast significantly reduced symptoms, improved quality of life, and decreased peripheral blood eosinophil counts in patients with intermittent AR.32-34 These improvements in AR symptoms were similar to those found with loratadine.35 Several studies that showed improvement of AR symptoms with zafirlukast or montelukast showed significantly greater improvement of symptoms with an INC.36-38

LTRAs may be preferred to antihistamines or INCs in select cases. For example, in patients with moderate-severe or persistent AR who do not like and/or will not use an INC, oral LTRAs may provide anti- inflammatory effects. They are a proven asthma therapy in both children and adults and may be considered in patients with both asthma and AR. Moreover, the efficacy of LTRAs can be assessed in a relatively short period of time since some of their actions, as demonstrated in asthma studies, begin within hours.39

* Combination Therapy: The Old with the New

Combination therapy may be necessary to achieve treatment goals. In one evaluation, 48% of patients with intermittent AR who started on an INC and 87% who started on an antihistamine required a second drug to adequately control their symptoms.40 In general, antihistamine-INC combinations are no more effective than INC monotherapy.41 An LTRA combined with an antihistamine may be as effective as an INC. In a crossover study of patients with intermittent AR, treatment responses were equivalent with either oral montelukast plus cetirizine or intranasal mometasone.42 Similarly, either montelukast plus cetirizine or the combination of intranasal and inhaled budesonide had similar clinical effects in patients with both AR and asthma.43,44 However, in a comparative study of intranasal fluticasone versus montelukast plus loratadine, intranasal fiuticasone was significantly more effective.37

Immunotherapy

In patients with AR, specific allergen immunotherapy decreases symptoms and medication requirements, improves quality of life, and mayprevent the development of asthma. Thus, it should be considered in patients who cannot avoid offending allergens or whose symptoms are incompletely controlled by or who have a constant need for pharmacotherapy. Because of the risk, although very low, of systemic reactions, including severe asthma and anaphylaxis, only trained specialists should initiate and manage this type of therapy, which involves subcutaneous injection once or twice a month at maintenance. In addition, because allergic sensitization often starts early in life (first decade) and because immunotherapy is less effective in older patients than in children, this therapy should be started as early as possible in the disease process.1

Nonspecific immunotherapy (anti-IgE) has been developed for patients with multiple sensitivities who may not benefit from specific immunotherapy. This therapy is based on the principle that AR is an IgE-mediated reaction. After initial allergen exposure, there is a production of antigen-specific Ig\E that binds to high- affinity receptors present on both mast cells and basophils. Upon reexposure, allergen binds to IgE located on mast cells and basophils, causing the release within minutes of preformed and newly synthesized mediators (e.g., histamine, CysLTs, cytokines). Nonspecific immunotherapy uses an antibody against circulating IgE that blocks the action of IgE by binding to it. The only such FDA- approved antibody, omalizumab, has proven beneficial in the treatment of moderate-to-severe asthma.45 It may be mildly effective in the treatment of AR,46 but lacks FDA approval for this use and is significantly more costly than previously available treatments.

Allergen Avoidance

AU the therapies mentioned above presuppose that patients try to maximally reduce allergen exposure. Total allergen avoidance is an effective means of eliminating AR. However, the magnitude of allergen reduction necessary is unclear, and creating this degree of reduction may be difficult. In addition, patients are frequently sensitive to multiple allergens, further reducing the possibility of total avoidance.1 Thus, pharmacotherapy, combined with allergen avoidance, and possibly immunotherapy is most likely necessary to control symptoms.

* Constraints in Treating AR

Treatment efficacy may be limited by poor environmental controls and/or by nonadherence to the therapeutic regimen. For example, INCs can effectively reduce nasal congestion when used appropriately. In a study of patients with asthma and AR, those who reported using, not merely having, a prescription for INC reduced their emergency department visits more than patients taking antihistamines.25

Insurance companies also significantly influence therapy. Frequently, failure of an over-the-counter antihistamine must be documented before insurance approval for a prescription medication. Even then, coverage may be influenced by the patient's comorbidities. For example, montelukast may require a third-tier copayment for the patient with only AR, but a second-tier copayment when prescribed to a patient with both AR and asthma. Even so, some pharmaceutical companies have copayment rebate coupons to reduce the cost and encourage adherence.

* Conclusions

The clinician has several goals when treating patients with AR. The first is to help patients understand and appreciate all ramifications of AR. The clinician must also understand the patient's sensitivity, exposure, and preferred treatments and adherence behaviors, as well as prescribe therapy appropriately. Allergic rhinitis can be a systemic inflammatory disorder; when selecting a specific therapy, the clinician should consider the possibility of systemic effects-as well as the availability of therapy. When there is associated comorbidity, serious consideration should be given to how medications effectively treat more than one organ system (i.e., nose and lungs). Best practice is based on the recommendations of the ARIA guidelines and The Allergy Report. Because antihistamines and INC may not provide optimal control, immunotherapy or systemically administered anti-inflammatory medications, such as LTRAs, may play a role in the treatment of patients with AR and its comorbidities.

CE Test

Allergic Rhinitis: Proper Management Benefits Concomitant Diseases

Instructions:

* Read the article beginning on page 26.

* Take the test, recording your answers in the test answers section (section B) of the CE enrollment form. Each question has only one correct answer.

* Complete registration information (section A) and course evaluation (section C).

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Allergic Rhinitis: Proper Management Benefits Concomitant Diseases

General Purpose: To examine the systemic aspects of allergic rhinitis and its impact on both upper and lower airways, as well as its diagnosis and management. Learning Objectives: After reading the preceding article and taking the following test, you will be able to: 1. Discuss the etiology, prevalence, and pathophysiology of allergic rhinitis. 2.Outline the diagnostic approach and the standard therapy for managing allergic rhinitis. 3. Explain the indications and effects of some of the newer, specific therapies for managing allergic rhinitis.

In patients with moderate-severe or persistent AR who do not like and/or will not use an INC, oral LTRAs may provide anti- inflammatory effects.

Registration Deadline: December 31, 2006

REFERENCES

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3. AAAAI: The allergy report. American Academy of Allergy Asthma & Immunology, Inc. (19 September 2003).

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11. Boris MR, Slavin RG, Samuels LD, et al.: Further studies in allergic sinusitis utilizing single photon emission computerized tomography (SPECT). J Allergy Clin Immunol 1989;83(1):302 (abstract).

12. Baroody FM, Saengpanich S, de Tineo M, et al.: Nasal allergen challenge leads to bilateral maxillary sinus eosinophil influx. I Allergy Clin Immunol 2002;109(1 part 2):S84 (abstract).

13. Juliusson S, Pipkorn U, Karlsson G, et al.: Mast cells and eosinophils in the allergic mucosal response to allergen challenge: changes in distribution and signs of activation in relation to symptoms. J Allergy Clin Immunol 1992;90(6 Pt 1):898-909.

14. Louis R, Lau LC, Bron AO, et al.: The relationship between airways inflammation and asthma severity. Am J Respir Crit Care Med 2000;161(1):9-16.

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16. Demoly P, Allaert FA, Lecasble M, et al.: Validation of the classification of ARIA (allergic rhinitis and its impact on asthma). Allergy 2003;58(7):672-5.

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18. Baki A, Orhan F: The effect of loratadine in exercise- induced asthma. Arch Dis Child 2002;86(l):38-9.

19. Gelfand EW, Cui ZH, Takeda K, et al.: Fexofenadine modulates T-cell function, preventing allergen-induced airway inflammation and hyperresponsiveness. J Allergy Clin Immunol 2002;110(1):85-95.

20. Abdelaziz MM, Devalia JL, Khair OA, et al.: Effect of fexofenadine on eosinophil-induced changes in epithelial permeability and cytokine release from nasal epithelial cells of patients with seasonal allergic rhinitis. J Allergy Clin Immunol 1998;101(3):410-20.

21. Murris-Espin M,Melac M, Charpentier JC, et al.: Comparison of efficacy and safety of cetirizine and ebastine in patients with perennial allergic rhinitis. Ann Allergy Asthma Immunol 1998;80(5):399-403.

22. Bensch GW, Nelson HS, Borish LC: Evaluation of cytokines in nasal secretions after nasal antigen challenge: lack of influence of antihistamines. Ann Allergy Asthma Immunol 2002;88(5):457-62.

23. Bernstein DI, Schoenwetter WF, Nathan RA, et al.: Efficacy and safety of fexofenadine hydrochloride for treatment of seasonal allergic rhinitis. Ann Allergy Asthma Immunol 1997;79(5):443-8.

24. Golden S, Teets SJ, Lehman EB, et al.: Effect of topical nasal azelastine on the symptoms of rhinitis, sleep, and daytime somnolence in perennial allergic rhinitis. Ann Allergy Asthma Immunol 2000;85(1):53-7.

25. Adams RJ, Fuhlbrigge AL, Finkelstein JA, et al.: Intranasal steroids and the risk of emergency department visits for asthma. J Allergy Clin Immunol 2002;109(4):636-42.

26. Creticos PS, Peters SP, Adkinson NF Jr, et al.: Peptide leukotriene release after antigen challenge in patients sensitive to ragweed. N Engl J Med 1984;310(25):1626-30.

27. Wang D, Clement P, Smitz J, et al.: Correlations between complaints, inflammatory cells and mediator concentrations in nasal secretions after nasal allergen challenge and during natural allergen exposure. Int Arch Allergy Imimmol 1995;106(3):278-85.

28. Bisgaard H, Olsson P, Bende M: Effect of leukotriene D4 on nasal mucosal blood flow, nasal airway resistance and nasal secretion in humans. Clin Allergy 1986;16(4):289-97.

29. Miadonna A, Tedeschi A, Leggieri E, et al.: Behavior and clinical relevance of histamine and leukotrienes C4 and B4 in grass pollen-induced rhinitis. Am Rev Respir Dis 1987;136(2):357-62.

30. Numata T, Konno A1 Yamakoshi T, et al.: Comparative role of peptide leukotrienes and histamine in the development of nasal mucosal swelling in nasal allergy. Ann Otol Rhinol Laryngol 1999;108(5):467-73.

31. Donnelly AL, Glass M, Minkwitz MC, et al.: The leukotriene D^sub 4^-receptor antagonist, ICI 204,219, relieves symptoms of acute seasonal allergic rhinitis. Am J Respir Grit Care Med 1995;151(6):1734-9.

32. Philip G, Malmstrom K, Hampel FC, et al.: Montelukast for treating seasonal allergic rhinitis: a randomized, double-blind, placebo-controlled trial performed in the spring. Clin Exp Allergy 2002;32(7): 1020-8.

33. van Adelsberg J, Philip G, LaForce CF, et al.: Randomized controlled trial evaluating the clinical benefit of montelukast for treating spring seasonal allergic rhinitis. Ann Allergy Asthma Immunol 2003;90(2):214-22.

34. NayakAS, Philip G, LuS, et al.: Efficacy and tolerability of montelukast alone or in combination with loratadine in seasonal allergic rhinitis: a multicenter, randomized, double-blind, placebo- controlled trial performed in the fall. Ann Allergy Asthma Immunol 2002;88(6):592-600.

35. Meltzer EO, Malmstrom K, Lu S, et al.: Concomitant montelukast and loratadine as treatment for seasonal allergic rhinitis: a randomized, placebocontrolled clinical trial. J Allergy Clin Immunol 2000;105{5):917-22.

36. Pullerits T, Praks L, Skoogh BE, et al.: Randomized placebo- controlled study comparing a leukotriene receptor antagonist and a nasal glucocorticoid in seasonal allergic rhinitis. Am I Respir Crit Care Med 1999;159(6):1814-8.

37. Pullerits T, Praks L, Ristioja V, et al.: Comparison of a nasal glucocorticoid, antileukotriene, and a combination of antileukotriene and antihistamine in the treatment of seasonal allergic rhinitis. J Allergy Clin Immunol 2002;109(6):949-55.

38. Nathan RA: Pharmacotherapy for allergic rhinitis: a critical review of leukotriene receptor antagonists compared with other treatments. Ann Allergy Asthma Immunol 2003;90(2):182-91.

39. Dockhorn RJ, Baumgartner RA, Leff JA, et al.: Comparison of the effects of intravenous and oral montelukast on airway function: a double blind, placebo controlled, three period, crossover study in asthmatic patients. Thorax 2000;55(4):260-5.

40. Juniper EF, Guyatt GH, Ferrie PJ, et al.: First-line treatment of seasonal (ragweed) rhinoconjunctivitis. A randomized management trial comparing a nasal steroid spray and a nonsedating antihistamine. Can Med Assoc J 1997;156(8):1123-31.

41. Nielsen LP, Mygind N, Dahl R: Intranasal corticosteroids for allergic rhinitis: superior relief? Drugs 2001;61(11):1563-79.

42. Wilson AM, Orr LC, Sims EJ, et al.: Effects of monotherapy with intra-nasal corticosteroid or combined oral histamine and leukotriene receptor antagonists in seasonal allergic rhinitis. CHn Exp Allergy 2001;31(1):61-8.

43. Wilson AM, Orr LC, Sims EJ, et al.: Antiasthmatic effects of mediator blockade versus topical corticosteroids in allergic rhinitis and asthma. Am J Respir Crit Care Med 2000;162(4 Pt 1}:1297- 301.

44. Wilson AM, Sims EJ, Orr LC, et al.: Effects of topical corticosteroid and combined mediator blockade on domiciliary and laboratory measurements of nasal function in seasonal allergic rhinitis. Ann Allergy Asthma Immunol 2001;87(4):344-9.

45. Milgrom H, Pick RB Jr, Su JQ, et al.: Treatment of allergic asthma with monoclonal anti-IgE antibody. rhuMAb- E25 Study Group. N Engl J Med 1999;341(26):1966-73.

46. Adelroth E, Rak S, Haahtela T, et al.: Recombinant humanized mAb-E25, an anti-IgE MAb, in birch pollen-induced seasonal allergic rhinitis. J Allergy Clin Immunol 2000;106:253-9.

47. Harlin SL, Ansel DG, Lane SR, et al.: A clinical and pathologic study of chronic sinusitis: the role of the eosinophil. J Allergy Clin Immunol 1988;81(5 Pt 1):867-75.

DISCLOSURE

The author has disclosed that she has no significant relationship or financial interest in any commercial companies that pertain to this education activity.

Mary Lou Hayden RN, MS, CFNP

ABOUT THE AUTHOR

Mary Lou Hayden is a Clinical Assistant Professor of Nursing at the University of Virginia, Charlottesville.

Copyright Springhouse Corporation Dec 2004

Source: Nurse Practitioner

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