Clinical and nasal biopsy response to treatment of perennial rhinitis

Spector, Sheldon L.; English, Gerald M.; Jones, Lowell

doi:10.1016/0091-6749(80)90060-3

Cited by 37 publications

(11 citation statements)

References 14 publications

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“…Spector et al [7] and Pipkorn et al [8] did not find a reduction of nasal mast cells after treatment of patients with allergic rhinitis with local corticosteroids; however these investigators examined mast cells only in the deeper layers ofthe nasal mucosa, from the lamina propria to the submucosa. It is likely that mast cells in the superficial layers are more susceptible to corticosteroid.…”

Section: Discussionmentioning

confidence: 98%

Effect of beclomethasone dipropionate on nasal metachromatic cell sub‐populations

Otsuka

Denburg

Befus

et al. 1986

Clin Experimental Allergy

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Abstract. The effect has been investigated of local administration of beclomethasone dipropionate (BDP) on cell numbers of nasal epithelial metachromatic cell (NMC) sub‐populations. Twenty‐one patients with perennial allergic rhinitis were studied in four groups according to the duration of treatment or after treatment with BDP. Nasal scrapings were taken after 1 week (Group 1) or 2 weeks (Group 2) of BDP treatment, or after discontinuing BDP for 1 week (Group 3) or 2 weeks (Group 4). Cells were fixed with Mota's lead acetate or 10% buffered formalin followed by toluidine blue staining to count the number of NMC and to classify these according to morphological subtypes (basophils or mast cells). Formalin‐sensitive mast cells and basophils in nasal scrapings were reduced more than formalin‐resistant mast cells with BDP treatment. Formalin‐sensitive mast cells were also more prompt to recover from BDP than formalin‐resistant mast cells. The results suggest that the formalin‐sensitive NMC is a sub‐population of cells which responds to BDP treatment in allergic rhinitis.

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Section: Discussionmentioning

confidence: 98%

Effect of beclomethasone dipropionate on nasal metachromatic cell sub‐populations

Otsuka

Denburg

Befus

et al. 1986

Clin Experimental Allergy

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“…The inclusion of nasal eosinophilia in the descriptions of these syndromes has, in general, arisen following assessment of nasal secretions and lavage [13][14][15]. Spector et al [56] performed a biopsy series on a group of 'perennial non-AR' patients and demonstrated a wide range of eosinophil numbers with considerable overlap with non-rhinitic controls, even though there was a significant difference between the groups when summary statistics were used. From a diagnostic point of view, non-AR can be difficult to distinguish from AR on history alone, but can be identified by tests for the presence of relevant IgE such as skin tests and radioallergosorbent test.…”

Section: Non-allergic Rhinitismentioning

confidence: 99%

Eosinophils and rhinitis

Howarth

2005

Clin Exp All Rev

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Summary Allergic rhinitis (AR) is typified by the nasal mucosal and luminal recruitment of eosinophils. These changes are evident in both seasonal and perennial disease, although the magnitude of these cellular changes is often greater with the more transient intense stimulation associated with seasonal allergen exposure than with the chronic persistent stimulation linked to perennial disease. Measures of eosinophil activation markers in nasal lavage such as eosinophil cationic protein and eosinophil protein X parallel the eosinophilic cellular changes and have been used serially to monitor allergic inflammation in association with intranasal allergen challenge and in therapeutic intervention studies. In both naturally occurring disease and laboratory allergen challenge, there is considerable inter‐subject variability in the magnitude of eosinophil airway recruitment and activation. Studies evaluating the mechanisms involved in nasal eosinophil recruitment identify systemic involvement of bone marrow stimulation and tissue recruitment of circulating progenitor cells. Interleukin‐5 (IL‐5) is a key cytokine involved in this process, acting on both marrow and circulating progenitors, with chemokines such as stromal cell derived factor‐1, RANTES (regulated on activation, normal T cell expressed and secreted) and eotaxin potentially being involved in tissue uptake and localization within the nasal airways. Inflammatory mediators such as leukotrienes acting through the cys‐LT1 receptor, in conjunction with IL‐5, and prostaglandin D2 acting through eosinophil‐expressed DP and CRTH2 cell surface receptors also contribute in animal models of allergic inflammation. The function of nasal eosinophils in AR can be debated. Genetic and nasal challenge models, with chemokines that promote eosinophil influx, support the relevance of eosinophils to symptom expression in rhinitis while the timing of the eosinophil recruitment following intranasal allergen challenge, the relationship between eosinophils and plasma protein exudation as well as the appreciation that clinical disease expression can arise in the apparent absence of nasal eosinophilia favour a restorative function for this cell. In the absence of specific eosinophil‐targeted intervention in rhinitis, it is not possible to conclusively apportion the relative involvement of eosinophils in these inductive and restorative processes but it has to be appreciated that the close association between eosinophils and clinical disease expression in rhinitis is not necessarily causal.

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“…Moreover, in allergic patients, there is an increase in Langerhan-like cells (CD1 + ) during the season (790). In patients with indoor allergy, nasal eosinophilia is not a permanent feature (78,199,(791)(792)(793). Mast cells are not always increased in the mucosa.…”

Section: Allergic Inflammationmentioning

confidence: 99%