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      Self-Reported Allergic Rhinitis and/or Allergic Conjunctivitis Associate with <b><i>IL13</i></b> rs20541 Polymorphism in Finnish Adult Asthma Patients

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          Abstract

          Our aim was to observe factors associated with IL13 rs20541 polymorphism and other factors with or without allergic comorbidities such as subject-reported allergic rhinitis (AR) and/or allergic conjunctivitis (AC) symptoms in adult asthmatics.

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          Asthma is Different in Women.

          Joe G. Zein, Serpil Erzurum (2015)
          Gender differences in asthma incidence, prevalence and severity have been reported worldwide. After puberty, asthma becomes more prevalent and severe in women, and is highest in women with early menarche or with multiple gestations, suggesting a role for sex hormones in asthma genesis. However, the impact of sex hormones on the pathophysiology of asthma is confounded by and difficult to differentiate from age, obesity, atopy, and other gender associated environmental exposures. There are also gender discrepancies in the perception of asthma symptoms. Understanding gender differences in asthma is important to provide effective education and personalized management plans for asthmatics across the lifecourse.
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            Beyond atopy: multiple patterns of sensitization in relation to asthma in a birth cohort study.

            D Heckerman, Iain Buchan, Stephen Bishop … (2010)
            The pattern of IgE response (over time or to specific allergens) may reflect different atopic vulnerabilities which are related to the presence of asthma in a fundamentally different way from current definition of atopy. To redefine the atopic phenotype by identifying latent structure within a complex dataset, taking into account the timing and type of sensitization to specific allergens, and relating these novel phenotypes to asthma. In a population-based birth cohort in which multiple skin and IgE tests have been taken throughout childhood, we used a machine learning approach to cluster children into multiple atopic classes in an unsupervised way. We then investigated the relation between these classes and asthma (symptoms, hospitalizations, lung function and airway reactivity). A five-class model indicated a complex latent structure, in which children with atopic vulnerability were clustered into four distinct classes (Multiple Early [112/1053, 10.6%]; Multiple Late [171/1053, 16.2%]; Dust Mite [47/1053, 4.5%]; and Non-dust Mite [100/1053, 9.5%]), with a fifth class describing children with No Latent Vulnerability (623/1053, 59.2%). The association with asthma was considerably stronger for Multiple Early compared with other classes and conventionally defined atopy (odds ratio [95% CI]: 29.3 [11.1-77.2] versus 12.4 [4.8-32.2] versus 11.6 [4.8-27.9] for Multiple Early class versus Ever Atopic versus Atopic age 8). Lung function and airway reactivity were significantly poorer among children in Multiple Early class. Cox regression demonstrated a highly significant increase in risk of hospital admissions for wheeze/asthma after age 3 yr only among children in the Multiple Early class (HR 9.2 [3.5-24.0], P < 0.001). IgE antibody responses do not reflect a single phenotype of atopy, but several different atopic vulnerabilities which differ in their relation with asthma presence and severity.
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              Targeting the interleukin pathway in the treatment of asthma.

              Kian Fan Chung (2015)
              Asthma is a common heterogeneous disease with a complex pathophysiology. Current therapies based on inhaled corticosteroids and longacting β2 agonists are effective in controlling asthma in most, but not all patients, with a few patients falling into the severe asthma category. Severe asthma is characterised by poor asthma control, recurrent exacerbations, and chronic airflow obstruction despite adequate and, in many cases, high-dose treatments. There is strong evidence supporting the role for interleukins derived from T-helper-2 (Th2) cells and innate lymphoid cells, such as interleukins 4, 5, and 13, as underlying the eosinophilic and allergic inflammatory processes in nearly half of these patients. An anti-IgE antibody, omalizumab, which binds to circulating IgE, a product of B cells from the actions of interleukin 4 and interleukin 13, is used as treatment for severe allergic asthma. Studies examining cytokine blockers such as anti-interleukin-5, anti-interleukin-4Rα, and anti-interleukin-13 monoclonal antibodies in patients with severe asthma with recurrent exacerbations and high blood eosinophil counts despite use of inhaled corticosteroids have reported improved outcomes in terms of exacerbations, asthma control, and forced expiratory volume in 1 s. The US Food and Drug Administration's recommendation to use an anti-interleukin-5 antibody for the treatment of severe eosinophilic asthma suggests that there will be a therapeutic place for these anti-Th2 agents. Biomarkers should be used to identify the right patients for such targeted approaches. More guidance will be needed as to which patients should receive each of these classes of selective antibody-based treatments. Currently, there is no treatment that targets the cytokines driving asthma associated with non-eosinophilic inflammation and low Th2 expression.
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                Author and article information

                Journal
                Title: International Archives of Allergy and Immunology
                Abbreviated Title: Int Arch Allergy Immunol
                Publisher: S. Karger AG
                ISSN (Print): 1018-2438
                ISSN (Electronic): 1423-0097
                Publication date Created: March 28 2017
                Publication date Created: March 28 2017
                Publication date (Print): 2017
                Publication date (Electronic): March 9 2017
                Volume: 172
                Issue: 2
                Pages: 123-128
                Article
                DOI: 10.1159/000456009
                PubMed ID: 28273659
                SO-VID: dd0e2c04-1dfb-4962-bae3-b1b18c15c423
                Copyright © © 2017
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                https://www.karger.com/Services/SiteLicenses

                https://www.karger.com/Services/SiteLicenses

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