Effect of anti-immunoglobulin E on nasal inflammation in patients with seasonal allergic rhinoconjunctivitis

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Binding of allergens to IgE on mast cells and basophils causes release of inflammatory mediators in nasal secretions.


The combined effect of specific immunotherapy (SIT) and omalizumab, a humanized monoclonal anti-IgE antibody, on release of eosinophilic cationic protein (ECP), tryptase, IL-6, and IL-8 in nasal secretion was evaluated.


Two hundred and twenty five children (aged 6–17 years) with a history of seasonal allergic rhinoconjunctivitis induced by birch and grass pollen were randomized into four groups: either birch- or grass-pollen SIT in combination with either anti-IgE or placebo. Complete sets of nasal secretion samples before treatment Visit 1 (V1), during birch- (V2) and grass (V3)-pollen season and after the pollen season (V4) were collected from 53 patients.


A significant reduction in tryptase only was seen in the anti-IgE-treated group at V2 (P<0.05) and V4 (P<0.05) compared with the placebo group. During the pollen season, patients with placebo showed an increase of ECP compared with baseline (V2: +30.3 μg/L; V3: +134.2 μg/L, P< 0.005; V4: +79.0 μg/L, P< 0.05), and stable levels of tryptase, IL-6 and IL-8. Treatment with anti-IgE resulted in stable ECP values and a significant decrease of tryptase compared with V1 (baseline): V2: −80.0 μg/L (P< 0.05); V3: −56.3 μg/L, which persisted after the pollen season with V4: −71.6 μg/L (P< 0.05). After the pollen season, a decrease of IL-6 was observed in both groups (V4 placebo group: −37.5 ng/L; V4 anti-IgE group: −42.9 ng/L, P< 0.01).


The combination of SIT and anti-IgE is associated with prevention of nasal ECP increase and decreased tryptase levels in nasal secretions.

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