Association between asthma and rhinitis according to atopic sensitization in a population-based study☆

Leynaert, Bénédicte; Neukirch, Catherine; Kony, Sabine; Guénégou, Armelle; Bousquet, Jean; Aubier, Michel; Neukirch, Françoise

doi:10.1016/j.jaci.2003.10.010

Cited by 300 publications

(253 citation statements)

References 41 publications

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“…Nasal symptoms are associated with more severe asthma in nonatopic patients [18]. Rhinitis may even be a stronger risk factor for asthma in the nonatopic compared with the atopic population [18,19], although this was not observed in all studies [20].…”

Section: Prevalence Of Rhinitis In Asthmatic Patientsmentioning

confidence: 87%

Asthma-related comorbidities

Boulet¹,

Boulay²

2011

Expert Review of Respiratory Medicine

221

147

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Section: Prevalence Of Rhinitis In Asthmatic Patientsmentioning

confidence: 87%

Asthma-related comorbidities

Boulet¹,

Boulay²

2011

Expert Review of Respiratory Medicine

221

147

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“…This is supported by a recent population-based study, which showed that the strong association between asthma and rhinitis was not fully explained by atopy. 33 A hypothesis already proposed at a physio-pathologic level is that asthma and rhinitis are different expressions of the same disease, thus the factor located on 1p31 may be involved in the different manifestations of the disease. Another proposed hypothesis is that asthma associated with AR corresponds to a severe form of the same disease; detection of linkage to 1p31 would correspond to a genetic factor involved in this severe form.…”

Section: Discussionmentioning

confidence: 99%

Genome screen in the French EGEA study: detection of linked regions shared or not shared by allergic rhinitis and asthma

et al. 2005

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In the sample of 295 French EGEA families with at least one asthmatic subject, a genome screen was conducted to identify potential linkage regions specific either to allergic rhinitis (AR) or to asthma as well as those shared by the two diseases. Two binary rhinitis phenotypes based on (1) diagnosis (AR bin1 ) and (2) symptoms (AR bin2 ) and a categorical ordered trait (AR cat ) were considered. Asthma phenotype was based on answers to a standardized questionnaire plus the presence of bronchial hyper-responsiveness. Linkage analyses were conducted using the maximum likelihood binomial (MLB) method. These analyses provided potential evidence for linkage to three regions in the whole sample: 1p31 for the phenotype defined by AR bin2 plus asthma (P ¼ 0.00016), 2q32 for AR bin2 (P ¼ 0.00016) and 3p24-p14 for AR cat (P ¼ 0.001). Two other regions were detected in the subset of 185 families with at most one asthmatic sib: 9p22 and 9q22-q34 for AR bin1 (P ¼ 0.001 and 0.0007, respectively). No region showed evidence for linkage to asthma without being also linked to AR. While 1p31 may contain a genetic determinant common to asthma and AR, 2q32, 3p24-p14, 9p22 and 9q22-q34 are more likely to harbor genetic factors specific to AR. Genes and Immunity (2005) 6, 95-102.

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“…[5][6][7] In fact, up to 40% of allergic rhinitis (AR) patients report asthma symptoms and up to 80% of asthmatics have symptomatic AR. 8 Chronic rhinosinusitis (CRS) and asthma severity also co-associate. 9 Sinus disease is evident in up to 88% of mildmoderate asthmatics and in up to 100% in severe steroid-dependent asthma on sinonasal imaging.…”

Section: Introductionmentioning

confidence: 99%

Upper and lower airway remodelling mechanisms in asthma, allergic rhinitis and chronic rhinosinusitis: The one airway concept revisited

Samitas

Carter

Kariyawasam

et al. 2017

Allergy

199

156

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Allergic rhinitis (AR), chronic rhinosinusitis (CRS) and asthma often co-exist. The one airway model proposes that disease mechanisms occurring in the upper airway may mirror lower airway events. Airway remodelling is the term used to describe tissue structural changes that occur in a disease setting and reflect the dynamic process of tissue restructuring during wound repair. Remodelling has been long identified in the lower airways in asthma and is characterized by epithelial shedding, goblet cell hyperplasia, basement membrane thickening, subepithelial fibrosis, airway smooth muscle hyperplasia and increased angiogenesis. The concept of upper airway remodelling has only recently been introduced, and data so far are limited and often conflicting, an indication that more detailed studies are needed. Whilst remodelling changes in AR are limited, CRS phenotypes demonstrate epithelial hyperplasia, increased matrix deposition and degradation along with accumulation of plasma proteins. Despite extensive research over the past years, the precise cellular and molecular mechanisms involved in airway remodelling remain incompletely defined. This review describes our current rather limited understanding of airway remodelling processes in AR, CRS and asthma and presents mechanisms both shared and distinct between the upper and lower airways. Delineation of shared and disease-specific pathogenic mechanisms of remodelling between the sinonasal system and the lung may guide the rational design of more effective therapeutic strategies targeting upper and lower airways concomitantly and improving the health of individuals with inflammatory airway diseases.

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Association between asthma and rhinitis according to atopic sensitization in a population-based study☆

Cited by 300 publications

References 41 publications

Asthma-related comorbidities

Asthma-related comorbidities

Genome screen in the French EGEA study: detection of linked regions shared or not shared by allergic rhinitis and asthma

Upper and lower airway remodelling mechanisms in asthma, allergic rhinitis and chronic rhinosinusitis: The one airway concept revisited

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