1. Rhinitis and asthma: Evidence for respiratory system integration
Alkis Togias, MD 
Journal of Allergy and Clinical Immunology 
Volume 111, Issue 6, Pages (June 2003)
DOI: /mai
Copyright © 2003 Mosby, Inc. Terms and Conditions

2. Fig. 1
Prevalence of rhinitis in individuals with the diagnosis of asthma from a Danish population participating in the Copenhagen Allergy Study. The sample derives from an original population of 7000 individuals who responded to a screening questionnaire and represents those individuals whose evaluation for rhinitis and asthma was done on 2 occasions 8 years apart (1990 and 1998). Attribution of asthma-rhinitis to a particular allergen was based on a question of whether exposure to the relevant material caused respiratory symptoms in conjunction with the presence of specific IgE against that allergen in the subject's serum. Adapted from data presented in tabular form in Linneberg et al.12
Journal of Allergy and Clinical Immunology  , DOI: ( /mai )
Copyright © 2003 Mosby, Inc. Terms and Conditions

3. Fig. 2
Thickness of the reticular basement membrane (lamina reticularis) of the nasal and bronchial mucosa in a group of healthy control subjects and in a group of untreated subjects with perennial allergic rhinitis and asthma. Several observations can be made. First, the thickness of the nasal reticular basement membrane is in correlation with that of the bronchial tissue in both the healthy control and asthmatic groups. Second, in asthmatic patients both the nasal and the bronchial mucosa demonstrate increased thickness compared with that seen among the control subjects. The latter observation supports the notion that nasal and bronchial disease develops in parallel in the chronic allergic respiratory syndrome. Adapted with permission from Chanez et al.18
Journal of Allergy and Clinical Immunology  , DOI: ( /mai )
Copyright © 2003 Mosby, Inc. Terms and Conditions

4. Fig. 3
A model to illustrate the relationships between allergic rhinitis and asthma. The basic premise is that the 2 conditions are manifestations of one syndrome in 2 parts of the respiratory tract. We refer to this syndrome as the chronic allergic respiratory syndrome. The horizontal axis represents the severity of the syndrome, whereas the vertical axis represents the severity of each of the syndrome's components (ie, allergic rhinitis and asthma). The tracings represent the relationship between syndrome severity and the severity of each component. Individuals with only allergic rhinitis are at the low end of the wide severity spectrum of the syndrome. These individuals have no clinically evident lower airways disease, but their large airways show pathologic changes that are not very different from those seen in patients with mild asthma. In individuals with a more severe expression of the syndrome, the rhinitis is worse, and the abnormalities in the lower airways manifest themselves clinically with asthma. From there on, the severity of asthma and rhinitis follows a parallel track in correlation with the overall severity of the chronic allergic respiratory syndrome. The bidirectional arrows represent the interactions between rhinitis and asthma that result from (a) the beneficial functions that the nose provides for the lower airways and (b) the concept that rhinitis and asthma are manifestations of a systemic syndrome that allows for cross-talk between the nasal and the lower airways. Because of its functions, the nose signals to the lower airways more intensely and through a variety of mechanisms compared with the signals that the lower airways send to the nose.
Journal of Allergy and Clinical Immunology  , DOI: ( /mai )
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5. Fig. 4
Mechanisms through which the nasal airways might interact with the lower airways.
Journal of Allergy and Clinical Immunology  , DOI: ( /mai )
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6. Fig. 5
The effect of nasal breathing on exercise-induced bronchospasm in 12 children with mild-to-moderate, nonsteroid-dependent asthma. Three exercise (treadmill walking with a moderate workload achieving 75%-80% of maximal heart rate) tests were performed in random order by using different routes of breathing: oropharyngeal (spontaneous) breathing, oral breathing, and nasal breathing. Minute ventilation and heart rate tracings were not different between the 3 trials. The reduction in FEV1 from baseline at the 7- to 12-minute period was significantly lower with nasal breathing compared with that with either spontaneous or oral breathing. Modified with permission from Shturman-Ellstein et al.131
Journal of Allergy and Clinical Immunology  , DOI: ( /mai )
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7. Fig. 6
Nasal allergen provocation results in increased expression of vascular adhesion molecules in bronchial mucosa. Double immunohistochemistry for adhesion molecules and CD31 (endothelial marker) on bronchial biopsy specimens was performed at baseline and 24 hours after nasal allergen challenge in 9 subjects with allergic rhinitis and in 9 healthy nonallergic control subjects. Bars represent median values, and asterisks indicate statistical significance over baseline. Created from data presented in tabular form in Braunstahl et al.88
Journal of Allergy and Clinical Immunology  , DOI: ( /mai )
Copyright © 2003 Mosby, Inc. Terms and Conditions