2024
DOI: 10.3390/jcm13030754
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Eosinophilic Patterns in Patients with Seasonal Allergy Affected by Bronchial Asthma and Rhinitis/Rhinosinusitis: Efficacy of Benralizumab in Patients with the Persistent Pattern

Valentina D’Aiuto,
Ilaria Mormile,
Francescopaolo Granata
et al.

Abstract: Background: Eosinophilia can be influenced by multiple factors. This study aims to set a protocol for monitoring blood absolute eosinophil count (AEC) in patients with seasonal allergy affected by bronchial asthma (BA), allergic rhinitis (AR), or chronic rhinosinusitis with or without nasal polyposis (CRSw/sNP). Methods: We planned a total of four annual blood samples to measure AEC in- and out-seasonal pollen exposure (i.e., one measurement every three months for one year). Results: We identified two distinct… Show more

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Cited by 2 publications
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“…During the elicitation phase, when a new encounter with an allergen causes cross-linking of the IgE-FcεRI complexes, sensitized basophils and mast cells are activated and subsequently release mediators responsible for the classical symptoms of the immediate phase (type 1 hypersensitivity) [ 66 ] such as histamine, prostaglandins, leukotrienes, tryptase, and platelet-activating factor [ 58 ]. A late-phase reaction follows, due to the accumulation of inflammatory mediators produced by mast cells and basophils and to the activation of allergen-specific Th2 cells, which produce interleukins, promote eosinophilia, maintain allergen-specific IgE levels, and recruit additional inflammation cells causing tissue damage and perpetuation of inflammation [ 67 , 68 ].…”
Section: Pathogenesismentioning
confidence: 99%
“…During the elicitation phase, when a new encounter with an allergen causes cross-linking of the IgE-FcεRI complexes, sensitized basophils and mast cells are activated and subsequently release mediators responsible for the classical symptoms of the immediate phase (type 1 hypersensitivity) [ 66 ] such as histamine, prostaglandins, leukotrienes, tryptase, and platelet-activating factor [ 58 ]. A late-phase reaction follows, due to the accumulation of inflammatory mediators produced by mast cells and basophils and to the activation of allergen-specific Th2 cells, which produce interleukins, promote eosinophilia, maintain allergen-specific IgE levels, and recruit additional inflammation cells causing tissue damage and perpetuation of inflammation [ 67 , 68 ].…”
Section: Pathogenesismentioning
confidence: 99%