title: Effect of omalizumab on adenosine 5'-monophosphate responsiveness in subjects with allergic asthma.
abstract: 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 PC(20) (provocative concentration required to produce a 20% fall in FEV(1)) 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 PC(20) 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 PC(20) 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.
authors.affiliation: Sección de Alergología, Hospital Universitario Dr. Peset, Valencia, Spain. prieto_jes@gva.es
authors.forename: L
authors.initials: L
authors.lastname: Prieto
authors.forename: V
authors.initials: V
authors.lastname: Gutiérrez
authors.forename: C
authors.initials: C
authors.lastname: Colás
authors.forename: A
authors.initials: A
authors.lastname: Tabar
authors.forename: C
authors.initials: C
authors.lastname: Pérez-Francés
authors.forename: L
authors.initials: L
authors.lastname: Bruno
authors.forename: S
authors.initials: S
authors.lastname: Uixera
mesh_terms: D000249:Adenosine Monophosphate / Q000494:pharmacology*; D000293:Adolescent; D000328:Adult; D000368:Aged; D000888:Antibodies, Anti-Idiotypic; D000911:Antibodies, Monoclonal / Q000494:pharmacology* / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D001249:Asthma / Q000188:drug therapy / Q000276:immunology*; D001985:Bronchial Provocation Tests; D016084:Bronchoconstriction / Q000187:drug effects* / Q000276:immunology; D016085:Bronchoconstrictor Agents / Q000494:pharmacology*; D005260:Female; D006801:Humans; D008168:Lung / Q000187:drug effects / Q000502:physiology; D008297:Male; D016210:Methacholine Chloride / Q000494:pharmacology; D008875:Middle Aged; D000069444:Omalizumab; D012130:Respiratory Hypersensitivity / Q000188:drug therapy / Q000276:immunology*
chemical_list: D000888:Antibodies, Anti-Idiotypic; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D016085:Bronchoconstrictor Agents; D016210:Methacholine Chloride; D000069444:Omalizumab; D000249:Adenosine Monophosphate