Background: The objective of this study was to evaluate the effects of omalizumab on bronchoconstriction induced by methacholine and adenosine 5′-monophosphate (AMP). Methods: Thirty-four subjects with mild to moderate allergic asthma were randomized to receive placebo (n = 16) or omalizumab (n = 18) subcutaneously during 12 weeks. Airway responsiveness to AMP was measured at baseline and after 4 and 12 weeks of treatment, whereas the response to methacholine was measured at baseline and after 12 weeks of treatment. Results: After 4 weeks of treatment, the increase in AMP PC₂₀ (provocative concentration required to produce a 20% fall in FEV₁) was significantly greater in the omalizumab group than in the placebo group, the mean difference in the change between the groups being 1.52 doubling concentrations (95% CI, 0.25–2.79, p = 0.02). Compared with baseline, the mean AMP PC₂₀ values at 12 weeks were increased by 1.91 doubling concentrations with omalizumab (p < 0.001) and 1.01 doubling concentrations with placebo (p = 0.16), but changes were not significantly different between the treatment groups. Changes in methacholine PC₂₀ values were not significantly different between the omalizumab and placebo groups. Conclusions: In subjects with allergic asthma, omalizumab reduces the response to AMP without decreasing the response to methacholine. These findings are consistent with the conclusion that the contribution of IgE to the development of AMP bronchoconstriction is more important than their role in the induction of methacholine hyperresponsiveness.

Bronchoconstriction induced by inhaled adenosine 59-monophosphate in subjects with allergic rhinitis. L. Prieto, V. Gutie Ârrez, J. Lin Äana, J. Marõ Ân. #ERS Journals Ltd 2001. ABSTRACT: Adenosine and its related nucleotide, adenosine 59-monophosphate (AMP) induce bronchoconstriction in asthmatics, probably caused by histamine release from airway mast cells. The objective of this study was to determine the effect of inhaled AMP on lung function in subjects with allergic rhinitis.A total of 52 adults (28 subjects with allergic rhinitis, 14 asthmatics and 10 healthy subjects) were challenged with increasing concentrations of AMP and methacholine. Air¯ow was assessed after each concentration and the response to each bronchoconstrictor agent was measured by the provocative concentration required to produce a 20% fall (PC20) in forced expired volume in one second (FEV1).All 14 asthmatics, 10 subjects with allergic rhinitis and none of the healthy controls were hyperresponsive to AMP. Subjects with allergic rhinitis had higher prevalence of hyperresponsiveness to AMP than healthy controls (p=0.038). Although the prevalence of hyperresponsiveness for methacholine and for AMP in subjects with allergic rhinitis was similar (39% and 36%, respectively), four subjects had hyperresponsiveness to methacholine but not to AMP, whereas three subjects had hyperresponsiveness to AMP but not to methacholine.To conclude, inhaled adenosine 59-monophosphate causes airway narrowing in a signi®cantly higher proportion of subjects with allergic rhinitis than healthy volunteers. Furthermore, methacholine and adenosine 59-monophosphate hyperresponsiveness are not detected in the same individuals with allergic rhinitis, thus suggesting that responsiveness to the two bronchoconstrictor stimuli is not re¯ecting the same abnormalities of the airways. Eur Respir J 2001; 17: 64±70. Seccio  n de Alergologõ Âa and Universidad de Valencia, Valencia, Spain (The NAOMI project).

In subjects with allergic rhinitis, sensitization to perennial allergens is associated not only with lower methacholine threshold values, but also with lower prevalence and higher level of plateau than sensitization to pollen allergens.

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