Allergic Asthma with Monoclonal Anti-IgE Antibody
January 30, 2000
Clinical Briefs
Allergic Asthma with Monoclonal Anti-IgE Antibody
Allergic mechanisms, dominantly mediated through IgE activation, are responsible for a significant burden of symptomatic asthma. After infusion of a binding antibody specifically directed against IgE (anti-E), serum-free IgE levels are dramatically lowered. This study evaluated the effect of 13 intravenous doses of anti-E over 20 weeks on asthma. Effect was measured on asthma symptoms, pulmonary function tests, use of inhaled beta agonists, and use of steroids.
The late phase reaction of asthma, beginning 2-8 hours after antigen exposure, has been linked to asthmatic inflammation and the long-term consequences of bronchial hyperreactivity, which correlate with asthma severity. Interruption of IgE affinity for target cells, or decreases in levels of activated IgE should reduce the late phase reaction intensity and its consequences.
Asthma symptom scores were significantly decreased by anti-E, as well as use of inhaled beta-agonist among recipients of high-dose IgE. Steroid use (inhaled and systemic) was able to be successfully reduced in patients who received anti-E. Peak expiratory flow rates were significantly improved at 20 weeks. Modulation of IgE activity through use of specific antibody may prove to be a useful therapeutic tool.
Milgrom H, et al. N Engl J Med 1999; 341:1966-1973.
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