## 3 Results
### Allergic Rhinities
#### 3.2.1 Diagnosis of Allergic Rhinitis  
Clinical Tools to Diagnose Allergic Rhinitis  
The allergological study begins with a detailed clinical history [125] (symptoms, seasonality, relationship with triggers, associated symptoms, need for treatment, and response) as the diagnosis is fundamentally clinical. Complementary tests are necessary to study its etiology and phenotype, as well as a correct physical examination [126]. Physical examination by anterior rhinoscopy or nasal endoscopy provides information (mucosal coloration, turbinate morphology, or the presence of polyps) that may indicate the presence of other associated pathologies, although there are no pathognonic signs. To confirm the presence of allergen-specific IgE, intraepidermal SPT and/or detection of specific IgE in serum against allergens that are considered clinically relevant for the patient can be performed. Skin tests can diagnose two out of three allergic diseases and up to 90% of respiratory allergies [127]. Skin pick tests are considered to be more sensitive, fast, and cost-effective than serum IgE tests [128]. Circulating sIgE against whole allergens or components allows us to differentiate between genuine sensitization or cross-reactivity, which is essential information for the indication of treatments such as immunotherapy [129; 130]. NAC can be performed by acoustic rhinometry, anterior or posterior rhinomanometry, or measurement of nasal peak inspiratory flow (NPIF). Although its use is becoming increasingly widespread, NAC is not routinely performed. NAC can be used to assess the clinical relevance in polysensitized patients [126] or when it is not possible to determine sIgE (serum and/or skin tests) [131]. In addition, NAC is currently the gold standard for the diagnosis of local allergic rhinitis (LAR), as it is a safe and reproducible technique [116]. The diagnosis is, therefore, clinical; therefore, it is important to differentiate between sensitization and allergy [132]. In addition, the infiltration of cells and inflammatory mediators can be studied by the detection of sIgE in nasal secretions, which is common in research, as well as BAT [133]. Once a diagnosis is reached, we will use methods to assess control: the VAS, considering uncontrolled rhinitis \(\geq\)5, and specific validated questionnaires, commonly used in research, such as the Rhinitis Control Assessment Test (RCAT) and Allergic Rhinitis Control Test (ARCT), or the more recently published ARIA-c, with the same parameters used for the staging of severity. Cellular Diagnostic of Allergic Rhinitis  
Similar to asthma, AR is characterized by an inflammation produced by the T2 immune response, which involves: Th2 cells, IgE-producing B cells, basophils, mast cells, eosinophils, and a plethora of Th2 cytokines (IL-4, IL-5, IL-9, IL-13, IL-25, IL-31, IL-33, and TSLP) [134; 135; 136; 137; 138; 139; 140]. Patients with AR are characterized by a pattern with a cellular infiltrate that induces a nasal production of mediators such as tryptrase, eosinophil cationic protein (ECP) [141; 142], and sIgE [143]. In this context, a study performed by [PERSON] and colleagues concluded that the levels of activated and pathogenic eosinophils, which are associated with higher production of ECP, eosinophil peroxidase (EPX), and IL-4 in the peripheral blood were elevated in patients with moderate-severe AR in comparison with mild patients and healthy controls [144]. In addition, several chemokines, such as the eotaxin family, which recruit and activate Th2 lymphocytes, mast cells, and eosinophils, seem important in allergic diseases as well [145]. In this regard,for example, high levels ofotaxin-1 (CCL11) were obtained after NAC in patients with AR in comparison with controls [146]. On the other hand, ILC2 residing at mucosal and barrier surfaces can act as effector immune cells. ILC2 are associated with allergic disorders, including AR [147; 148], and they are functionally like T cells (but lack antigen receptors).