Once daily intranasal fluticasone propionate (200 μg) reduces nasal symptoms and inflammation but also attenuates the increase in bronchial responsiveness during the pollen season in allergic rhinitis

Foresi, Antonio; Pelucchi, Andrea; Gherson, G; Mastropasqua, Berardino; Chiapparino, Anita; Testi, Rossana

doi:10.1016/s0091-6749(96)70150-1

Cited by 166 publications

(91 citation statements)

References 28 publications

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“…Epidemiologic (1), pathophysiologic (2,3), and clinical studies (4,5) strongly suggest a link between rhinitis and asthma. Asthma and rhinitis, which are considered to be manifestations of the atopic syndrome, often coexist and share a common genetic background.…”

mentioning

confidence: 99%

Segmental Bronchial Provocation Induces Nasal Inflammation in Allergic Rhinitis Patients

Braunstahl

KleinJan

Overbeek

et al. 2000

Am J Respir Crit Care Med

355

211

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Allergic rhinitis and asthma often coexist and share a genetic background. Pathophysiologic connections between the nose and lungs are still not entirely understood. This study was undertaken to compare allergic inflammation and clinical findings in the upper and lower airways after segmental bronchial provocation (SBP) in nonasthmatic allergic rhinitis patients. Eight nonasthmatic, grass pollen-sensitive patients with allergic rhinitis and eight healthy controls were included. Bronchial biopsies and blood samples were taken before (T 0 ) and 24 h (T 24 ) after SBP. Nasal biopsies were obtained at T 0 , 1 h after SBP (T 1 ), and T 24 . Immunohistochemical staining was performed for eosinophils (BMK13), interleukin (IL)-5, and eotaxin. The number of eosinophils increased in the challenged and unchallenged bronchial mucosa (p Ͻ 0.05) and in the blood (p ϭ 0.03) of atopic subjects at T 24 . We detected an increase of BMK13-positive and eotaxin-positive cells in the nasal lamina propria and enhanced expression of IL-5 in the nasal epithelium of atopic subjects only at T 24 (p Ͻ 0.05). SBP induced nasal and bronchial symptoms as well as reductions in pulmonary and nasal function in the allergic group. No significant changes could be observed in healthy controls. The study shows that SBP in nonasthmatic allergic rhinitis patients results in peripheral blood eosinophilia, and that SBP can induce allergic inflammation in the nose.Epidemiologic (1), pathophysiologic (2, 3), and clinical studies (4, 5) strongly suggest a link between rhinitis and asthma. Asthma and rhinitis, which are considered to be manifestations of the atopic syndrome, often coexist and share a common genetic background. Although several studies have shown that asthma and rhinitis are characterized by a similar inflammatory process (6-9), pathophysiologic interactions between upper and lower airways are not entirely understood. It is clear that the condition of the upper airways definitely influences the lower airways. In allergic rhinitis patients without bronchial hyperreactivity (BHR), signs of allergic inflammation of the lower airways have been found in induced sputum, bronchoalveolar lavage fluid (BALF), and bronchial biopsy specimens (10-13). The nasal-bronchial reflex, an altered breathing pattern, pulmonary aspiration of nasal contents, and increased levels of inflammatory factors in the blood are possible mechanisms for lower airway dysfunction among patients with rhinitis (14). To shed more light on the role of systemic induction in the allergic inflammatory response, we designed a study in which blood samples and nasal and bronchial mucosal biopsy specimens were taken from a group of nonasthmatic allergic rhinitis patients with an isolated grass pollen allergy after segmental bronchial provocation (SBP) at a time other than the grass pollen season. The aim of the study was to compare allergic mucosal inflammation and clinical findings in the upper and lower airways. Eosinophils, major effector cells in allergic inflammation, interleukin (I...

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mentioning

confidence: 99%

Segmental Bronchial Provocation Induces Nasal Inflammation in Allergic Rhinitis Patients

Braunstahl

KleinJan

Overbeek

et al. 2000

Am J Respir Crit Care Med

355

211

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“…Untreated rhinitis can result in increased lower respiratory tract inflammation (2) due to a variety of possible mechanisms (3). There is good evidence to show that treating the upper airway inflammation in seasonal allergic rhinitis with intranasal corticosteroids alone has beneficial effect on lower airway inflammation in terms of an improvement in bronchial hyperreactivity (4).…”

mentioning

confidence: 99%

Antiasthmatic Effects of Mediator Blockade versus Topical Corticosteroids in Allergic Rhinitis and Asthma

Wilson

Orr

Sims

et al. 2000

Am J Respir Crit Care Med

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To compare the antiasthmatic efficacy of inflammatory mediator blockade versus topical corticosteroid therapy in patients with seasonal allergic rhinitis (SAR) and asthma, 14 patients were enrolled into a single-blind, double-dummy, placebo-controlled crossover study comparing 2 wk therapy of ( 1 ) 400 g orally inhaled budesonide plus 200 g intranasal budesonide (BUD) or ( 2 ) 10 mg oral montelukast plus 10 mg oral cetirizine (ML ϩ CZ). Before each treatment period, patients received 7 to 10 d placebo washout. All treatments were given once daily in the morning. Throughout the study, patients recorded the following domiciliary measures: peak expiratory flow (PEF), rescue inhaler requirement, asthma symptoms, and daily activity score. Laboratory measurements were made at trough of adenosine monophosphate (AMP) bronchial challenge and exhaled nitric oxide (NO). Compared with pooled placebo (PL), there were significant (p Ͻ 0.05) improvements in all domiciliary measures with both treatments (mean PEF [L/min] PL: 463; BUD: 478; ML ϩ CZ: 483). For geometric mean AMP PC 20 (mg/ml), there was an improvement (p Ͻ 0.05), compared with PL (47), for ML ϩ CZ (133) but not for BUD (51); whereas for NO (ppb) there was significant suppression with BUD (7.6) but not ML ϩ CZ (11.5) compared with PL (13.6). In conclusion, both combined mediator blockade and combined topical corticosteroids are equally effective antiasthma therapy in patients with asthma and SAR.Asthma and allergic rhinitis are common conditions, occurring with increasing prevalence, and frequently coexisting (1). Both conditions occur in patients with underlying atopy and have a common etiology and pathophysiology. Untreated rhinitis can result in increased lower respiratory tract inflammation (2) due to a variety of possible mechanisms (3). There is good evidence to show that treating the upper airway inflammation in seasonal allergic rhinitis with intranasal corticosteroids alone has beneficial effect on lower airway inflammation in terms of an improvement in bronchial hyperreactivity (4).Topically delivered inhaled and intranasal corticosteroids are widely recognized as effective anti-inflammatory treatment for both conditions (5, 6). They work by altering gene transcription to increase or decrease a plethora of cytokines, inflammatory mediators and enzymes, and adhesion molecules (7). Histamine and cysteinyl leukotrienes are important inflammatory mediators in the pathogenesis of asthma and allergic rhinitis. With the introduction of leukotriene receptor antagonists it is now possible to selectively block the effects of both of these mediators. This may have a theoretical advantage over corticosteroid therapy as a result of a better adverse effect profile as well as the preference for taking tablets rather than inhalers and nasal sprays.The anti-inflammatory properties of leukotriene receptor antagonists have been shown to exhibit beneficial effects on asthma disease control (8). Antihistamines have been considered to be effective in the management of asthma ...

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“…This beneficial effect of intranasal corticosteroids on bronchial hyperresponsiveness was confirmed by another study in asthmatic patients with allergic rhinitis. The subjects who used intranasal fluticasone propionate during the allergy season exhibited less nasal symptoms and the expected increase in bronchial hyper-responsiveness was attenuated [Foresi, 1996]. Treatment of AR in asthmatic patients has also been shown to decrease asthma-related emergency room visits and hospitalizations.…”

Section: Therapeutic Links Between Rhinitis and Asthmamentioning

confidence: 99%

Allergic Rhinitis and Its Impact on Bronchial Asthma

Samara¹,

Velegrakis²,

Karatzanis³

2012

Allergic Rhinitis

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Once daily intranasal fluticasone propionate (200 μg) reduces nasal symptoms and inflammation but also attenuates the increase in bronchial responsiveness during the pollen season in allergic rhinitis

Cited by 166 publications

References 28 publications

Segmental Bronchial Provocation Induces Nasal Inflammation in Allergic Rhinitis Patients

Segmental Bronchial Provocation Induces Nasal Inflammation in Allergic Rhinitis Patients

Antiasthmatic Effects of Mediator Blockade versus Topical Corticosteroids in Allergic Rhinitis and Asthma

Allergic Rhinitis and Its Impact on Bronchial Asthma

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