## 3 Results
### Asthma
#### 3.1.1 Asthma Diagnosis  
Clinical Diagnosis of Asthma  
Over many years, the diagnosis of asthmatic pathology has been made by assessing the evaluating airflow limitation, bronchodilator responses, and by bronchial provocation challenges [13]. Additionally, the use of several biomarkers, such as fractional exhaled nitric oxide (FeNO), forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), and peripheral blood eosinophils, are of great utility (Figure 2). However, due to the heterogeneity in the pubHomechanisms involved in this disease, currently, there are many challenges related to the development of more personalized and precise diagnostic tools [14].  
The development in recent years of drawing up guidelines updated by societies and working groups has led to an improved approach and clinical management of asthma [15]. An anamnesis should always be carried out to search for possible triggers and a complete allergological study should also be performed: with skin pick tests (SPT), detection of total and specific IgE (sIgE), and an allergen-specific nasal or bronchial challenge test to indicate an atopic state (Figure 2) [16]. Although there is no _gold standard_ test, spirometry is essential, despite it maybe not being sufficient to confirm the diagnosis. Then, the spirometry parameters include FEV1 and FVC, which are variable according to age, height, weight,  
Figure 2: Diagnostic tools in asthma and AR. Different diagnostic methods can be used in asthma diagnosis, from classical methods (lung function, medical history, skin pick test) to cellular (eosinophil counts, basophil activation test) and molecular (measurements of cytokines and chemokines, and other biomarkers such as miRNAs) novel methods.  
sex, and ethnic group. The main alterations in asthma are airflow obstruction, reversibility, variability, and bronchial hyperresponsiveness, so a reversible obstruction that improves after short-acting beta-agonists (SABA) administration confirms the diagnosis, although a normal result does not exclude it. Variations in peak expiratory flow (PEF) and FEV1 between exacerbations and stable periods in the same patient are also common. Spirometry with bronchodilator test and PEF measurement should be performed prior to the initiation of treatment, since as lung function improves, variability decreases. In cases where spirometry values comprised the normal range (FEV1/FVC > 0.7, FEV1 increase < 12%), it is possible to confirm the diagnosis by bronchial challenge with direct (methacholine) [17], indirect (mannitol, physical exercise) [18] or allergen-specific (decreasing FEV1 \(\geq\) 20%) bronchoconstrtor agents, measurement of nitric oxide in exhaled air (FeNO > 40 ppb) [19], diurnal variability of peak expiratory flow (PEF \(\geq\) 20%) [20], or analysis of induced sputum (levels of sputum eosinophils, elevated values of eosinophil cationic proteins and Creola bodies) [21]. In addition, when a diagnosis cannot be reached, normalization of the pattern after treatment with oral glucocorticoids (GCs) for 14-21 days confirms it [22].  
In any case, a correct differential diagnosis should be always reached, especially in treatment-refractory cases and if the evolution is not favorable. Imaging tests such as thorax radiography can rule out other respiratory diseases (signs of air trapping, atelectasis, or bronchial thickening) [15]. Establishing the phenotype (total and specific IgE determination, peripheral eosinophil, FeNO measurement, and induced sputum), mainly in patients with severe asthma, allows for improvement in the clinical management of these patients and to offer them the most appropriate treatment.