start allergen immunotherapy for controlled asthma patients


This patient has severe asthma, defined as asthma that remains uncontrolled despite treatment with high-dose inhaled corticosteroid long-acting β-agonist therapy, and would therefore not be a candidate for allergen immunotherapy (AIT) at this time (choice D is correct). The 2020 asthma management guidelines conditionally recommend AIT as a potential adjunct treatment to guideline-directed pharmacotherapy for adults who have mild to moderate persistent asthma with symptoms related to allergen exposure and who have documented allergen sensitivity by skin prick testing or measurement of antigen-specific IgE antibody. AIT, however, is only an option for individuals with controlled asthma at the initiation, buildup, and maintenance phases of immunotherapy because of the potential risk and consequences of bronchospasm. Other contraindications to AIT include pregnancy before the start of AIT and unstable cardiovascular disease. Concurrent treatment with β-blockers is commonly listed as well.

AIT involves the delivery of a clinically relevant allergen extract to produce an immunologic tolerance to that allergen. It can be delivered as subcutaneous immunotherapy (SCIT) or sublingual immunotherapy (SLIT) formulations. SCIT involves gradually increasing quantities of the patient's relevant allergen up to an effective dose. The rate of systemic adverse reactions is relatively low at 0.1% to 0.2%, with fatal reactions occurring rarely. SLIT does not require extensive up-dosing and is considered a safer route of delivery but is only approved in the United States to treat allergic rhinoconjunctivitis. Studies of SLIT in asthmatic patients are ongoing, though the 2020 Expert Panel Report found only a “trivial benefit” for critical asthma outcomes, including exacerbations, asthma control, and quality of life.

Meta-analyses and systematic reviews of AIT have mostly incorporated studies on patients with well-controlled, mild to moderate asthma, maintained on inhaled steroids. AIT in this population has been shown to reduce asthma symptoms (choice A is incorrect). In the same population, SCIT has also been shown to decrease use of rescue inhaler use (low certainty of evidence) and long-term medication use (moderate certainty, regarding reduction in the inhaled corticosteroid dose required to maintain asthma control). Evidence that SCIT significantly reduces asthma exacerbations is insufficient. Skepticism about AIT effectiveness remains among pulmonologists.

Most studies involving the addition of SCIT to traditional asthma regimens have been inconclusive regarding improvement in FEV1 and peak expiratory flow. While allergen-specific bronchial hyperreactivity decreases, the effect of AIT on nonspecific bronchial hyperreactivity appears to be less prominent, and with conflicting reports depending on the provocative agent (choice B is incorrect).

Allergen avoidance is an important part of allergic asthma management, though mitigation measures should include multiple allergen-specific strategies. A combination of avoidance measures, such as allergen-impermeable covers, acaricides, high-efficiency particulate air filtration systems, and maintaining the relative humidity in the home <50% to inhibit mite growth, should be used in place of a single-strategy intervention such as focusing on the bed alone. A systematic review showed that single interventions are not associated with improvement in asthma measures (choice C is incorrect). These strategies, however, are often complicated and expensive, are not regularly adhered to by most patients, and certainly should not be used as a primary strategy in asthma management.

Treatment options in this patient include the addition of tiotropium and/or add-on biologic therapy. In the setting of a high house dust mite–specific IgE antibody level, treatment with the anti-IgE monoclonal antibody, omalizumab, would be a reasonable choice. The elevated blood eosinophil count expands his options to include monoclonal antibodies targeting IL-4, IL-5, and IL-13.1

Footnotes

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