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The identification of eosinophilic gastroenteritis in prednisone-dependent eosinophilic bronchitis and asthma

DOI: 10.1186/1710-1492-7-4

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Abstract:

Eosinophilic gastrointestinal disease (EGID) is characterized by identification of abnormal eosinophilic infiltration on morphologic evaluation of gastrointestinal tissues obtained by biopsy or resection from patients with gastrointestinal complaints [1]. EGIDs are classified according to the site involved (i.e., esophageal, gastric, small intestinal, colonic, or multiple). Esophagus is increasingly being recognized as a site of involvement with eosinophils accumulating in the mucosal, muscular, serosal, diffuse, or transmural areas [2]. The diagnosis for eosinophilic esophagitis and other EGIDs is established after ruling out other causes of an eosinophilic disease, particularly atopy, parasitic infestations, vasculitis, and hypereosinophilic syndrome (HES) [3]. We report the association of eosinophilic gastroenteritis and eosinophilic bronchitis in a young patient with prednisone-dependent asthma and some features of lymphocytic hypereosinophilic syndrome and the sensitivity of a novel monoclonal antibody directed against eosinophil peroxidase (EPX-mAb) [4] as an unambiguous means with which to detect both infiltrating tissue eosinophils and eosinophil degranulation in gastrointestinal tract biopsies. The patient provided written informed consent for publishing this manuscript.A 23-year old woman was referred for assessment of cough, wheeze, shortness of breath, and chest tightness. She had frequent bloating, belching and loose stools. The symptoms had started two years prior to presentation with new onset sinus congestion, cough, wheeze and 40lb weight loss. Shortly after returning from a trip to Belize in the summer of 2008, her symptoms worsened and were associated with peripheral eosinophilia (4.9 × 109/L) and diffuse peripheral pulmonary infiltrates. She had some features of chronic eosinophilic pneumonia; however, there was no clinical or laboratory evidence of vasculitis or hypereosinophilic syndrome (table 1). She did not have evidence of lymph node enlarg

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