therapy was introduced during the first 3 weeks of life of high- risk infants (Lowe at al., 2018). However, in a larger clinical study, Chalmers and colleagues (2020) found no difference in atopic dermatitis or food allergy sensitization in high-risk infants. There is some evidence that probiotic supplementation in pregnancy or infancy may be protective against the development of atopic dermatitis, but no protection against food allergy or other allergic disorders has been proven (Tham & Leung, 2019). Many interventions have been investigated to try to stop the progression of atopy to the development of asthma. Many clinical trials to date have been effective only for subjects with certain characteristics, possibly related to asthma being a heterogenous condition, with a variety of triggers and clinical phenotypes. Thus far, a universally effective prevention strategy has not been found (Maciag & Phipatanakul, 2019). Vitamin D supplementation during pregnancy has been found to reduce the risk of asthma in the children of the treated mothers at 0 to 3 years (Wolsk et al., 2017). It is believed that low levels of vitamin D are implicated in allergic disorders (Douros et al., 2017). Bolcas and colleagues (2019) report that vitamin D confers protection against asthma development from exposure to traffic-related air pollution. Maintenance of normal vitamin D
levels in childhood significantly lessened the development of AHR in allergic asthma that was worsened by diesel exhaust. Sublingual immunotherapy has been considered for asthma and atopy prevention. Marogna and colleagues (2017) found that patients sensitized to house dust mites who were treated with sublingual immunotherapy demonstrated a protective effect on pulmonary function when compared to a control group of sensitized individuals who did not receive immunotherapy. Additionally, a meta-analysis conducted by Kristiansen and colleagues (2017) demonstrated that low levels of vitamin D may lead to impairment of the immune functions involved in asthma. They evaluated allergen immunotherapy in those with allergic rhinitis and found a significant reduction in the development of asthma in the 2 years following completion of immunotherapy. Omalizumab may limit the allergic inflammation implicated in asthma pathogenesis, aiding in the prevention of asthma. Omalizumab binds to free IgE, which lowers free IgE levels (Kaplan et al., 2017). Blocking IgE may inhibit the allergic sensitization that mediates asthma pathogenesis. Given the noted benefit in asthma and its underlying mechanism of blocking IgE, omalizumab is under consideration as a therapy for asthma prevention and disease modification (Maciag & Phipatanakul, 2019).
COMORBID CONDITIONS AND EXACERBATING CONDITIONS
Gastroesophageal reflux disease GERD is a common coexisting condition of asthma and part of asthma’s differential diagnosis. It is estimated that 80% of people with asthma have GERD (Newsom, 2021). People with asthma are twice as likely to have GERD as those who do not have asthma. People with severe persistent asthma that is resistant to treatment are most likely to also have GERD (Cleveland Clinic, 2019). GERD symptoms include frequent episodes of nocturnal asthma, heartburn, nighttime awakening with an acid taste in the mouth, and dyspepsia after meals. Some people with GERD may have no complaints at all. Persons with frequent nocturnal symptoms despite optimal asthma therapy (and no other complaints) should be evaluated for GERD. The diagnosis of GERD in patients with asthma is often a clinical diagnosis, based on the presence of classic symptoms of GE reflux. There is no esophageal or respiratory diagnostic test that identifies GE reflux treatment-responsive asthma. A referral to a gastroenterologist would be indicated for patients with symptoms that are suspicious for GERD but are atypical (Harding, 2019). GERD and asthma impact each other, creating a vicious cycle (Asthma and Allergy Foundation of America [AAFA], 2021). The refluxed gastric acid irritates the nerve endings in the esophagus, resulting in mucus production in the airways Chronic rhinosinusitis Chronic rhinosinusitis (CRS) is a chronic inflammatory disorder affecting the nasal passages and paranasal sinus cavities, which persists for at least 12 weeks despite treatment. At least two of the following symptoms must be present for this diagnosis to be considered: nasal congestion; mucus discharge from the nose or mucus that drips down the back of the throat; facial pain, pressure, or a sense of fullness; or a decreased sense of smell. Three categories of CRS have been identified: with nasal polyps, without nasal polyps, and with fungal allergy (Hamilos & Holbrook, 2020). CRS affects about 10.9% to 13.4% of the general population, with polyps present in 18% to 20% of all cases (Laidlaw et al., 2020). Persons with CRS with nasal polyps often have severe and recurrent disease. This category of CRS is usually seen in people with asthma. CRS with nasal polyps with comorbid asthma is associated with more severe sinonasal symptoms and worse quality of life, and is more difficult to treat. Asthma in this case is also more difficult to control, more prone to exacerbations, and more likely to cause increased airway obstruction and more extensive eosinophilic inflammation. These findings suggest that CRS with nasal polyps with asthma may be a risk factor for asthma severity (Laidlaw et al., 2020).
and constriction of the small airways, thus producing asthma symptoms. The refluxed stomach contents can also be aspirated into the lungs, irritating the airways and resulting in wheezing, coughing, chest tightness, and other symptoms of asthma. Asthma also may trigger GERD when breathing difficulties or certain asthma medications cause the esophageal sphincter muscle to relax and allow stomach contents to reflux. GERD must be managed to control asthma symptoms. Proton- pump inhibitors and histamine blockers are the recommended treatment options (Clarrett & Hachem, 2018). When treating asthma in people with GERD, beta agonists and theophylline should be avoided because they relax the lower esophageal sphincter and increase reflux symptoms (GINA, 2021). Although not all persons respond to therapy, standard medical treatment for reflux should be prescribed in addition to dietary and behavioral modifications. The person should be taught to eat smaller, more frequent meals and to avoid eating within 3 hr of bedtime. The head of the bed should be elevated. Avoidance of smoking, heavy alcohol consumption, large evening meals, nighttime snacks, and high dietary fat intake should be encouraged (Clarrett & Hachem, 2018; Sandhu & Fass, 2018). CRS with nasal polyps tends to be associated with adult early- onset asthma (onset 18 to 39 years of age) or adult late-onset asthma (onset after 40 years of age) and is not usually linked with childhood asthma. Conversely, CRS without nasal polyps has been linked to childhood-onset asthma (onset before 16 years of age) and to adult early-onset asthma (onset before 40 years of age) in adults. The prevalence of CRS with nasal polyps and concomitant asthma increases with age, implying that disease burden is likely to increase in an aging population (Laidlaw et al., 2020). Initial treatment of CRS with polyps consists of systemic and/or topical glucocorticosteroids, saline irrigations, and occasionally antibiotics. If conservative measures fail, surgery is performed with medical therapy resuming afterward (Avdeeva & Fokkens, 2018). The systemic inflammatory link between CRS with nasal polyps and asthma provides a compelling rationale for systemic treatment directed at the underlying inflammatory processes for patients with both conditions through the use of biologic therapies. Dupilumab has shown broad efficacy for both upper and lower airway disease, with decrease in polyp size, improved nasal congestion, improved FEV1, and improved score on the Asthma Control Questionnaire (Bachert et al., 2019; Laidlaw et al., 2019). This approach allows for common therapeutic management in patients with persistent CRS with nasal polyps and comorbid asthma.
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