PT  - JOURNAL ARTICLE
AU  - AJ Frew
TI  - Effects of anti-IgE in asthmatic subjects
AID  - 10.1136/thx.53.2008.S52
DP  - 1998 Aug 01
TA  - Thorax
PG  - S52--S57
VI  - 53
IP  - suppl 2
4099  - http://thorax.bmj.com/content/53/suppl_2/S52.short
4100  - http://thorax.bmj.com/content/53/suppl_2/S52.full
SO  - Thorax1998 Aug 01; 53
AB  - A humanized murine monoclonal antibody directed to the Fc epsilon R1- binding domain of human IgE (rhuMAb-E25) has been shown to inhibit the binding of IgE to mast cells without provoking mast cell activation. To examine the effects of neutralizing IgE on allergic airway responses, we assessed the effects of 9 wk of treatment with rhuMAb-E25 in a parallel group, randomized, double-blind, placebo-controlled study of 19 allergic asthmatic subjects. We found that treatment with rhuMAb-E25 reduced the serum IgE, increased the dose of allergen needed to provoke an early asthmatic response, reduced the mean maximal fall in FEV1 during the early response (30 +/- 10% at baseline to 18.8 +/- 8%, versus 33 +/- 8% at baseline to 34 +/- 4% after placebo; p = 0.01), and reduced the mean maximal fall in FEV1 during the late response (24 +/- 20% at baseline to 9 +/- 10% versus 20 +/- 17% at baseline to 18 +/- 17% after placebo; p = 0.047). We conclude that an anti-IgE monoclonal antibody, which inhibits binding of IgE to its receptor, suppresses the early- and late-phase responses to inhaled allergen in allergic asthmatic subjects. Targeting IgE with rhuMAb-E25 might be a useful treatment for allergic asthma.