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Volume 2, Issue 7, Pages 568-575 (July 2004)


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Clinical and immunopathologic effects of swallowed fluticasone for eosinophilic esophagitis

Richard J Noel, Philip E Putnam, Margaret H Collins, Amal H Assa’ad§, Jesus R Guajardo§, Sean C Jameson§, Marc E Rothenberg§Corresponding Author Informationemail address

Abstract 

Eosinophilic esophagitis (EE) is a recently recognized clinical disorder that is understood poorly. We aimed to determine the efficacy of swallowed fluticasone propionate on the immunopathologic features associated with EE. A retrospective analysis was performed on 20 pediatric patients with EE. Inclusion criteria specified a peak eosinophil density of ≥24 cells per 400× field in the esophagus and treatment with swallowed fluticasone between 2 endoscopic assessments. Histologic specimens were examined for eosinophil and CD8+ lymphocyte infiltration, papillary lengthening, and proliferation of the basal layer as determined by monoclonal anti—Ki-67 (MIB-1) antibody staining. The mean time interval between endoscopic assessments was 4.8 months. The patients were divided equally between allergic and nonallergic groups based on the results of skin-prick testing. All of the nonallergic patients responded to fluticasone propionate. The endoscopic appearance of the mucosa improved and microscopic evaluation showed markedly reduced eosinophil infiltration, reduced basal layer hyperplasia documented by a reduced number of MIB-1+ cells, and a reduced number of CD8+ lymphocytes. However, allergic patients were relatively refractory to therapy; 20% had a partial response, whereas 20% had no detectable improvement. Esophageal eosinophil levels before and after therapy in all patients strongly correlated with the level of epithelial cell proliferation as measured by MIB-1 staining. Collectively, these results suggest that patients treated with swallowed fluticasone have improved endoscopic, histologic, and immunologic parameters associated with EE. However, patients with identifiable allergies who fail dietary elimination may have a blunted response to treatment.

 Division of Pediatric Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA

 Division of Pathology, Department of Pediatrics, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA

§ Division of Allergy and Immunology, Department of Pediatrics, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA

Corresponding Author InformationAddress requests for reprints to: Marc E. Rothenberg, M.D., Ph.D., Cincinnati Children’s Hospital Medical Center, Division of Allergy and Immunology, 3333 Burnet Avenue, Cincinnati, Ohio 45229-3039 USA; fax: (513) 636-3310

 Supported in part by the Burroughs Wellcome Fund and National Institutes of Health grants T32 DK07727 and R24 DK 064403.

PII: S1542-3565(04)00240-X


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