Evidence-based practice! Novelli and colleagues (2018) assessed the effect of different comorbidities on clinical, functional, and biologic features of severe asthma. They examined data on 72 patients, including smoking status, asthma history, and assessment of comorbidities. Pulmonary function, inflammatory biomarkers, upper airway disease evaluation, asthma control, and quality of life were assessed. Their findings revealed the comorbidities with the highest prevalence were CRS with or without nasal polyps, obesity, and gastroesophageal reflux, with some overlapping among them. Individuals with asthma who had CRS with nasal polyps had lower lung function and higher sputum eosinophilia; individuals with asthma who were also obese had worse asthma control and quality of life and tended to have lower sputum eosinophils; individuals with asthma who also had gastroesophageal reflux showed worse quality of life. Lower lung function was associated with the male sex and longer duration of asthma (Novelli et al., 2018).
Healthcare Professional Consideration: The exact relationship between asthma and obesity is unclear. Obesity and asthma are diseases of high prevalence, with significant increases occurring in the last 2 decades. Adipose tissue in individuals who are obese leads to a systemic proinflammatory state, which lends itself to airway inflammation and hyperresponsiveness. Obesity makes the diagnosis, treatment, and course of asthma more difficult. The treatment of individuals with asthma who are obese must include a weight- control program. Because sedentary lifestyles and avoidance of physical activity are common, all individuals with asthma should be taught the importance of regular exercise for improved disease outcomes. Additional research is needed to more fully understand the link between obesity and asthma and to establish guidelines for growth and development indices, physical activity levels, and healthy eating lifestyles for individuals with asthma. Several commonly used medications may worsen asthma. These include aspirin (acetylsalicylic acid [ASA]), NSAIDs, other medications used for pain relief, and medications used to control high blood pressure. The presence of aspirin-exacerbated Nonsteroidal anti-inflammatory drugs AERD, which is also called NSAID-exacerbated respiratory disease, refers to the combination of asthma, CRS with nasal polyps, and acute upper and lower respiratory tract reactions to ingestion of aspirin and other cyclooxygenase-1 (COX-1)- inhibiting NSAIDs. Reactions to aspirin and NSAIDs include nasal congestion and bronchoconstriction, typically beginning 20 min to 3 hr after ingestion (Laidlaw & Israel, 2019). The prevalence of AERD is approximately 7% of persons with asthma. For persons with severe asthma, the prevalence is twice as high, approximately 14%. Persons with nasal polyposis or CRS have prevalence rates of about 10% and 9%, respectively. NSAID sensitivity is particularly prevalent in persons with both CRS and nasal polyposis. It is estimated that up to 20% of patients with AERD go undiagnosed. The management of AERD involves guideline-based treatment of the patient’s asthma and CRS, in addition to suppression of the consequences of abnormal leukotriene metabolism. Patients must avoid all NSAIDs or, in selected cases, undergo aspirin desensitization followed by daily NSAID therapy (Laidlaw & Israel, 2019; Samter’s Society, n.d.). ASA triad, also known as Samter’s triad or asthma triad, is characterized by three conditions: nasal polyps, asthma, and aspirin intolerance. The only environmental factors that have been linked to the development of Samter’s triad are related to smoking and secondhand smoke. Persons with this condition develop a specific rash and/or asthmatic reaction, which can be life-threatening, when they take aspirin or NSAIDs. Symptoms include wheezing, tightness in the chest, a stuffed or blocked nose, thick nasal mucus, loss of smell and taste, facial pain, pain in the upper teeth and behind the eyes, and headaches. Urticaria (hives) and gastrointestinal upset are less common but frequently reported. These problems will be chronic and progressive even if aspirin and other NSAIDs are avoided. Ingestion of aspirin or NSAIDs results in an acute reaction, but the underlying disease is not dependent on them or caused by them. Because of this type of reaction, some patients with nasal polyps and asthma are often advised to avoid aspirin, even if they have never had a reaction to aspirin. Optimal treatment includes sinus
ADVERSE MEDICATION EFFECTS AND ASTHMA
respiratory disease (AERD) or NSAID in association with asthma and nasal polyps is referred to as ASA triad, asthma triad, and/or Samter’s triad.
surgery and medical management. Most patients with ASA triad require systemic and topical (nasal) corticosteroids. Good asthma treatment is critical as well. Some centers employ aspirin desensitization, a specific technique to create aspirin tolerance, which seems to improve both the asthma and the rhinosinusitis (Samter’s Society, n.d.). If a patient presents with a history of more than one episode of reaction to aspirin or other NSAIDS, then a diagnosis of AERD can be made with some degree of certainty. However, if they have no history of aspirin or NSAID use or it is ambiguous, then proper diagnosis of AERD would require a physician-observed aspirin challenge, where responses are measured by clinical presentation and pulmonary function tests. Aspirin challenge testing starts with a low dose of aspirin, and gradually increasing dosages are given until a positive response is achieved. Most symptoms occur within 30 to 60 min of ingesting doses of between 45 and 100mg. Doses increase incrementally with 3 hr or less between each dose. Once a respiratory reaction is observed, the diagnosis of AERD can then be confirmed. Pulmonary function tests are used to document the respiratory response. FEV1 is measured every 30min up to 120min after the final dosage is given. A positive reaction is defined as a decrease in FEV-1 greater than 20%. If no response is achieved regardless of the dose, then the patient does not have aspirin sensitivity (Dominas et al., 2020). Acetaminophen is usually well tolerated in patients with aspirin- induced asthma at doses less than 1,000 mg. However, at higher doses, acetaminophen can induce mild asthmatic reactions in 28% to 34% of patients with AERD. Meloxicam and nimesulide are preferred COX-2 inhibitors, and are usually well tolerated by patients with AERD when given at low doses. However, they can elicit mild respiratory reactions at higher therapeutic doses. The COX-2 selective inhibitors, like valdecoxib and celecoxib, are generally well tolerated by patients with AERD when given at therapeutic doses. These do not cross-react with ASA or other NSAIDs in patients with AERD (Rodríguez-Jiménez et al., 2018). beta-2 blockers (e.g., propranolol) are more likely to cause bronchoconstriction in susceptible individuals. In contrast, selective beta-1 blockers (e.g., atenolol, metoprolol) have a 20-fold greater affinity for beta-1 adrenergic receptors than beta-2 adrenergic receptors and, therefore, are less likely to induce bronchoconstriction (Morales et al., 2017; Weinberger, 2020). Angiotensin-converting enzyme (ACE) inhibitors, used for hypertension or heart disease, include lisinopril and enalapril. Although they usually do not cause asthma, a small percentage
Beta Blockers and Angiotensin-Converting Enzyme Inhibitors Other medications should be avoided or be taken with caution for the person with asthma. Beta blockers, commonly used for hypertension, heart failure, and coronary artery disease, as well as ocular beta blockers for glaucoma, can exacerbate asthma by worsening bronchospasm and decreasing the bronchodilator effect of quick-relief medication. These medications act on beta-2 receptors, which can cause bronchoconstriction. Because beta-adrenergic receptors of large and small airway smooth muscle are primarily the beta-2 subtype, nonselective beta-1/
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