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Espada-Sánchez, M.;  María, R.S.D.S.;  Martín-Astorga, M.D.C.;  Lebrón-Martín, C.;  Delgado, M.J.;  Eguiluz-Gracia, I.;  Rondón, C.;  Mayorga, C.;  Torres, M.J.;  Aranda, C.J.; et al. Diagnosis and Treatment in Allergic Rhinitis. Encyclopedia. Available online: https://encyclopedia.pub/entry/40867 (accessed on 17 July 2025).
Espada-Sánchez M,  María RSDS,  Martín-Astorga MDC,  Lebrón-Martín C,  Delgado MJ,  Eguiluz-Gracia I, et al. Diagnosis and Treatment in Allergic Rhinitis. Encyclopedia. Available at: https://encyclopedia.pub/entry/40867. Accessed July 17, 2025.
Espada-Sánchez, Marta, Rocío Sáenz De Santa María, María Del Carmen Martín-Astorga, Clara Lebrón-Martín, María Jesús Delgado, Ibón Eguiluz-Gracia, Carmen Rondón, Cristobalina Mayorga, María José Torres, Carlos José Aranda, et al. "Diagnosis and Treatment in Allergic Rhinitis" Encyclopedia, https://encyclopedia.pub/entry/40867 (accessed July 17, 2025).
Espada-Sánchez, M.,  María, R.S.D.S.,  Martín-Astorga, M.D.C.,  Lebrón-Martín, C.,  Delgado, M.J.,  Eguiluz-Gracia, I.,  Rondón, C.,  Mayorga, C.,  Torres, M.J.,  Aranda, C.J., & Cañas, J.A. (2023, February 06). Diagnosis and Treatment in Allergic Rhinitis. In Encyclopedia. https://encyclopedia.pub/entry/40867
Espada-Sánchez, Marta, et al. "Diagnosis and Treatment in Allergic Rhinitis." Encyclopedia. Web. 06 February, 2023.
Diagnosis and Treatment in Allergic Rhinitis
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This entry is adapted from the peer-reviewed paper 10.3390/app13031273

Respiratory diseases are pathological conditions that affect airways, hampering breathing and causing high mortality. In particular, asthma and allergic rhinitis (AR) are two of the most common airway diseases that affect millions of people and have a high prevalence in childhood and adulthood. Asthma is a heterogeneous chronic inflammatory disease characterized by wheezing, chest tightness, shortness of breath, and cough. AR occurs with rhinorrhea, nasal congestion, and sneezing. Indeed, these pathologies share common physiopathological mechanisms such as airway hyperresponsiveness and similar immunopathology such as tissue eosinophilia and T-helper type 2 inflammation. Moreover, AR can be an important risk factor for suffering asthma.

asthma allergic rhinitis eosinophils diagnosis treatment

1. Diagnosis of Allergic Rhinitis

Clinical Tools to Diagnose Allergic Rhinitis

The allergological study begins with a detailed clinical history [1] (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 [2]. 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 pathognomonic 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 [3]. Skin prick tests are considered to be more sensitive, fast, and cost-effective than serum IgE tests [4].
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 [5][6].
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 [2] or when it is not possible to determine sIgE (serum and/or skin tests) [7]. In addition, NAC is currently the gold standard for the diagnosis of local allergic rhinitis (LAR), as it is a safe and reproducible technique [8].
The diagnosis is, therefore, clinical; therefore, it is important to differentiate between sensitization and allergy [9]. 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 [10]. Once a diagnosis is reached, the researchers will use methods to assess control: the VAS, considering uncontrolled rhinitis ≥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) [11][12][13][14][15][16][17]. Patients with AR are characterized by a pattern with a cellular infiltrate that induces a nasal production of mediators such as tryptase, eosinophilic cationic protein (ECP) [18][19], and sIgE [20]. In this context, a study performed by Chen 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 [21]. 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 [22]. In this regard, for example, high levels of eotaxin-1 (CCL11) were obtained after NAC in patients with AR in comparison with controls [23].
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 [24][25], and they are functionally like T cells (but lack antigen receptors). Allergic phenotypes of rhinitis are determined by measuring allergen-sIgE in serum and BAT [26]. BAT reproduces in vitro, after allergen exposure, the type I hypersensitivity reaction [27]; an immediate reaction that involves IgE-mediated release of antibodies against the soluble antigen [28]. For LAR diagnosis, BAT exhibits a high specificity (100%), in contrast to its sensibility (ranging from 50% to 66.6%) depending on the allergen evaluated [29][30][31]. In this regard, 37.5% of LAR individuals (all of them with NAC positive to Dermatophagoides pteronyssinus) and 60% of dual allergic rhinitis (DAR) patients showed positive BAT responses with perennial allergens, as opposed to NAR and healthy subjects (negative for all of them) [32].

Molecular Diagnostic Parameters in Allergic Rhinitis

In the last few decades, several studies have focused on molecular parameters associated with inflammation in AR, such as chemokines associated with Th2 function [33]. In this context, high levels of CCL22 (monocyte-derived chemokine (MDC)), which promote selective migration of Th2 cells, were found in the serum of patients with AR sensitized to birch pollen [34] and ragweed pollen [35], suggesting a possible role in the pathogenesis of AR. Another chemokine that has been associated with AR is CCL13, whose expression is stimulated by IL-4 and was found to be increased in the serum of AR patients after NAC [36].
On the other hand, miRNAs are thought to be involved in the pathogenesis of AR [37][38][39]. MiR-155 levels in serum of children with pollen-induced AR were higher in comparison with healthy controls, and miR-155 in the serum correlated significantly with nasal symptoms in children with AR (r = 0.494, p < 0.001) [40]. Moreover, Luo and colleagues found serum TSLP, expression of miR-375 from whole blood, and frequencies of ILC2 in peripheral blood levels significantly higher in AR children compared with controls [17]. Moreover, another study showed that the level expression of miR-487b was repressed in AR in comparison to control cases [41]. Finally, Teng et al. found that the expression of miR-143 was significantly decreased in nasal mucosal tissues from AR patients compared with tissues from NAR subjects [42].
Additionally, Th1/Th17 were also proposed to be involved in allergic diseases, such as AR [43]. In this context, Erkan et al. [20] showed that serum and nasal IL-17 were higher in AR in comparison with control individuals. Moreover, Lee and collaborators showed that serum levels of IL-8 were significantly higher in patients with allergic asthma in comparison with AR and controls, suggesting that IL-8 is associated with a more severe inflammatory response [44]. However, other studies showed that elevated levels of IL-8 can also be related to pollution and not only allergic sensitization, suggesting that air pollution might induce or aggravate AR through this cytokine [45]. Other studies, such as Yu et al., showed a decreased surface CXC motif chemokine receptor 3 (CXCR3) expression in CD4+ T cells of AR patients [46].
In the case of the innate immune response, a study performed by Kant (which excluded individuals with an active infection), with 205 AR patients and 49 healthy controls, found that the neutrophil/lymphocyte ratio was significantly lower in patients with AR than in healthy controls [47]. In relation to ILC2, several studies showed that these cells in peripheral blood and nasal samples are increased after NAC, and there was also a positive correlation between eosinophils and IL-5 concentrations in patients with AR [48][49]. In this context, several studies showed evidence of increased epithelial proinflammatory cytokines, such as IL-25, IL-33, and TSLP in the nasal lavage from patients with house dust mite (HDM) sensitivity [50][51]. Other studies have shown that patients with AR displayed high levels of IL-33 and TSLP mRNA in the nasal epithelium [52][53][54].

2. Treatment of Allergic Rhinitis

AR management includes patient education, allergen avoidance, pharmacotherapy, immunotherapy, and biologics. It is essential to explain to the patient about their disease and how to take their treatments. The first step is to avoid exposure to the allergen. However, if the symptoms persist, the first line of treatment is drug therapy. Immunotherapy is recommended when the disease is not controlled with the usual drugs. In addition, in recent years, biologics have emerged as a novel therapeutic option with promising results [55][56][57][58] (Figure 1).
Figure 1. Therapeutic tools in asthma and AR. Traditionally, asthma and AR have been treated with classical drugs, such as bronchodilators, antihistamines, and corticosteroids. The form of administration of glucocorticoids is inhaled in asthmatic patients, while in patients with AR it is intranasal. However, in the last decades, the development of novel and more specific therapeutic tools such as biologicals and immunotherapy have permitted a more personalized medicine for asthma and AR.
Typical AR drugs include AHs, GCs, and leukotriene receptor antagonists. Second-generation oral antihistamines are the first line of pharmacological treatment, as well as intranasal corticosteroids (INCs), which have demonstrated even greater efficacy than AHs. [59]. Intranasal combination therapies with AHs and GCs, such as azelastine hydrochloride/fluticasone propionate (AZE/FP), are also recommended [60].
Antihistamines bind to the histamine H1 receptor and block its action. First-generation of oral antihistamines (OAHs), such as diphenhydramine or chlorpheniramine, have been widely used in the clinic. However, due to their adverse effects, they are no longer supported for AR [61]. Their main secondary effect is sedation as they cross the blood-brain barrier causing drowsiness and fatigue, among other symptoms [62]. Therefore, the use of new-generation AHs (such as desloratadine, loratadine, cetirizine, levocetirizine and rupatadine, fexofenadine, and bilastine) is strongly recommended. These have been shown to be safer than the previous ones, maintaining the same efficacy without the sedative effect [61][63].
Intranasal antihistamines (INAHs) improve the effect of oral antihistamines at the nasal mucosa [64][65]. Moreover, they are more effective in controlling local symptoms, such as nasal congestion [66][67]. In addition, they act faster than OAHs and reduce potentially systemic effects [67]. They are recommended as first-line treatment for seasonal AR (SAR) [68]. The two INAHs approved for the management of SAR are azelastine and olopatadine. Both have demonstrated similar efficacy [69]. They differ in that azelastine inhibits both H1 and H2 receptors, while olopatadine only inhibits H1.
INCs (beclomethasone, budesonide, ciclesonide, fluticasone propionate, fluticasone furoate, mometasone furoate, and triamcinolone acetonide) have a local anti-inflammatory effect by preventing the recruitment of immune cells into the nasal mucosa. They are indicated as first-line treatment in patients with moderate or persistent symptoms [60]. In addition, they have the advantage of having no systemic adverse effects [70][71]. INCs have demonstrated efficacy in controlling the main symptoms of AR: nasal congestion, itching, rhinorrhea, and sneezing [72][73]. INCs have been described to be more effective than AHs for nasal congestion [59].
OCs are not used as a routine treatment for rhinitis, because their adverse effects exceed the potential benefits [74]. A short course, only for a few days, with oral corticosteroids, can be indicated in patients with severe symptoms that do not respond to other drugs [75]
A novel formulation combines azelastine hydrochloride (AZE) and fluticasone propionate (FP) in a single nasal spray. This combined therapy has proved to be faster [76] and more effective than both drugs taken individually. [77][78]. One of the advantages is that it increases adherence to treatment by administering both drugs at the same time. In addition, the drugs are more homogeneously distributed in the nasal mucosa than if AZE and FP sprays were used sequentially [79]. It is recommended for the initial treatment of moderate to severe nasal symptoms of SAR [60], as well as for patients with both seasonal and perennial AR who do not respond to monotherapy [68].
LTRAs act by blocking the activity of cysteinyl leukotrienes, an inflammatory mediator associated with the main symptoms of AR, such as nasal congestion and mucus production [80]. The main LTRAs are montelukast and zafirlukast. They should only be used when the patient does not respond to any other drug. This is because they are equally or less effective than INAH, INCs, or OAH, [81][82] and have also been associated with serious neuropsychiatric adverse effects. In fact, in Europe, they are only approved for the treatment of patients with asthma and rhinitis comorbidity [83].

3. Biologicals in Asthma and Allergic Rhinitis

Due to the diversity of adverse effects induced by classical drugs, new approaches for the treatment of asthma have been sought. Among these new therapies for asthma and rhinitis are biologicals (Figure 2). Biologicals are humanized monoclonal antibodies that target several molecules responsible for the T2 response, inhibiting it and ameliorating asthma symptoms. The main targets of biologics for asthma treatment are IgE (omalizumab), IL-5 (mepolizumab and reslizumab), the IL-5 receptor (benralizumab), the IL-4/IL-13 receptor (dupilumab), and TSLP (tezepelumab) [84] (Figure 2), although novel biologicals against other targets are being developed. Although these drugs have been studied and approved for asthma treatment, only the use of omalizumab and dupilumab in rhinitis have also been extensively studied [85][86]; however, to date, none have been approved by drug agencies for the treatment of AR.
Figure 2. Biologicals used in asthma and AR. Mechanisms of action of different biologics are schematized (omalizumab, mepolizumab, reslizumab, benralizumab, tezepelumab, and dupilumab). Biologicals usually target inflammatory molecules, cytokines, or their receptors, blocking downstream inflammatory pathways or triggering-induced cell death. ADCC: antibody-dependent cell-mediated cytotoxicity; mAb: monoclonal antibody.

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Subjects: Allergy
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Marta Espada-Sánchez
,
Rocío Sáenz de Santa María
,
María del Carmen Martín-Astorga
,
Clara Lebrón-Martín
,
María Jesús Delgado
,
Ibón Eguiluz-Gracia
,
Carmen Rondón
,
Cristobalina Mayorga
,
María José Torres
,
Carlos José Aranda
,
José Antonio Cañas
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Update Date: 08 Feb 2023
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