Anti-IgE treatment of eosinophil-associated gastrointestinal disorders

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Presentation transcript:

Anti-IgE treatment of eosinophil-associated gastrointestinal disorders Shabnam Foroughi, MD, Barbara Foster, MS, NaYoung Kim, MD, Leigh B. Bernardino, RN, Linda M. Scott, CRNP, Robert G. Hamilton, PhD, Dean D. Metcalfe, MD, Peter J. Mannon, MD, Calman Prussin, MD Journal of Allergy and Clinical Immunology Volume 120, Issue 3, Pages 594-601 (September 2007) DOI: 10.1016/j.jaci.2007.06.015 Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 1 Effect of omalizumab on peripheral blood eosinophil counts. Peripheral blood AECs were determined at baseline (week 0) and every 2 weeks thereafter for the duration of the study. The actual values for each time point (A), as well as the value as a percentage of the preomalizumab baseline (B), are shown. Journal of Allergy and Clinical Immunology 2007 120, 594-601DOI: (10.1016/j.jaci.2007.06.015) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 2 Effect of omalizumab on tissue eosinophil counts. Esophagogastroduodenoscopy was performed at baseline and again after 16 weeks of omalizumab therapy, and the median number of eosinophils per hpf in the duodenum (A), gastric antrum (B) and body (C), and esophagus (D) were determined. Data are shown as the median value for each subject. Journal of Allergy and Clinical Immunology 2007 120, 594-601DOI: (10.1016/j.jaci.2007.06.015) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 3 Efficacy of omalizumab in blocking IgE. Changes in the levels of serum free IgE (A), basophil-associated IgE (B), FcɛRI expression by peripheral blood basophils (C), myeloid DCs (mDC; D), and pDCs (E) are shown. The above were determined at baseline and again after 16 weeks of omalizumab. Free IgE was determined at baseline and serially thereafter. ∗P < .005 for each time point relative to baseline. Fluorescence intensity was quantitated as molecules of equivalent phycoerythrin (MEPE). Journal of Allergy and Clinical Immunology 2007 120, 594-601DOI: (10.1016/j.jaci.2007.06.015) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 4 Efficacy of omalizumab in blocking basophil activation. Basophil CD63 expression after in vitro activation by anti-IgE (A) and allergen (data not shown) was measured, and the EC50 was calculated for each, respectively (B and C). D and E, Constitutive basophil CD63 expression without or with added IL-3. F, Basophil CD63 expression after N-formyl-methionine-leucine-phenylalanine activation. The results were determined at baseline and again after 16 weeks of omalizumab. Journal of Allergy and Clinical Immunology 2007 120, 594-601DOI: (10.1016/j.jaci.2007.06.015) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 5 Efficacy of omalizumab in blocking immediate hypersensitivity. Wheal (A) and erythema (B) after food and aeroallergen titration skin testing at baseline and after 16 weeks of omalizumab. Each result is the mean of 2 skin tests. Journal of Allergy and Clinical Immunology 2007 120, 594-601DOI: (10.1016/j.jaci.2007.06.015) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 6 Effect of omalizumab on EGID symptom scores. A, EGID symptom scores at baseline, midstudy (weeks 7-8), and end of study (weeks 15-16). B, EGID symptom scores were calculated as a percentage of the baseline value for each subject. ∗P < .005 for each time point relative to baseline. Journal of Allergy and Clinical Immunology 2007 120, 594-601DOI: (10.1016/j.jaci.2007.06.015) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions