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Eosinophilic Gastrointestinal Diseases (Egids) Journal of Pediatric Gastroenterology and Nutrition 47:234–238 # 2008 by European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition Eosinophilic Gastrointestinal Diseases (EGIDs) EGIDs Working Group: ôGlenn T. Furuta, yyDavid Forbes, zzChris Boey, yC. Dupont, §§Phil Putnam, ôS.K. Roy, ÃAderbal Sabra´, jjAnadina Salvatierra, §Yuichiro Yamashiro, and ÃÃS. Husby ÃyDepartment of Paediatrics and Nutrition, Hospital Saint Vincent de Paul, Paris, France, {International Centre for Diarrhoeal Disease Research, Bangaldesh, Dhaka, §Probiotics Research Laboratory, Juntendo University School of Medicine, Tokyo, Japan, ôUniversity of Colorado School of Medicine, Denver, ÃÃDepartment of Paediatrics, Odense University Hospital, Odense, Denmark, {{School of Paediatrics and Child Health, University of Western Australia, Perth, {{Pediatric Gastroenterology and Hepatology, Department of Pediatrics, University of Malaya Medical Centre, Kuala Lumpur, Malaysia, and §§Department of Pediatrics, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH Eosinophilic gastrointestinal diseases (EGIDs) are a rarity of the diseases limits well-designed studies and heterogeneous group of diseases (eosinophilic esophagi- precludes consensus on histological features; in fact, only tis [EoE], eosinophilic gastroenteritis, and eosinophilic recently have studies explored the normal numbers of colitis) characterized by gastrointestinal symptoms and eosinophils in the different part of the gastrointestinal increased eosinophils in the intestinal mucosa; more tract (1,2). A gradient exists with respect to the normal important, other causes of gastrointestinal eosinophilia number of eosinophils per high power field (eos/HPF) in must have been ruled out for the diagnosis of EGIDs to be the gastrointestinal (GI) tract starting with the esophagus, confirmed. Original descriptions of EGIDs divided where there are none, and advancing to the terminal patients into subtypes with respect to the anatomical ileum, where more than 30 eos/HPF have been docu- location affected by eosinophilia; ie, mucosal (diarrhea mented. In most studies, specimens examined have been and bleeding), muscular (obstruction), and serosal derived from mucosal pinch biopsies that are limited to (ascites) disease. Recent descriptions characterize the 2 to 3 mm in depth, sections that typically only allow mucosal forms in more detail; patients affected by examination of only the superficial mucosa; deeper mucosal EGIDs present with a diverse set of symptoms eosinophilic infiltration likely occurs in certain circum- that reflect the organ-specific section of the intestinal stances but is unaccounted for presently. Geographic tract that is affected. EoE may present with feeding variation likely exists with respect to the number of intolerance, vomiting, food impaction, and dysphagia. eosinophils in the GI tract of healthy individuals, a Patients with eosinophilic gastroenteritis develop vague feature suggesting a role in host health and constitutive symptoms including abdominal pain, diarrhea, and immune defense. Finally, most analyses examining histo- bleeding. Eosinophilic colitis typically presents with logical features use only hematoxylin and eosin staining diarrhea and lower abdominal pain. In the most clearcut with little attention to other immunohistochemical circumstances, this categorization will provide speci- methods of assessment. Thus, the histological assessment ficity for the tissue involved, but in clinical practice a of the tissue is limited to a statement indicating increased wide variety of symptoms have been attributable to numbers of eosinophils in the lamina propria and or EGIDs. Thus, an open mind should be maintained when intraepithelial layer; the interpretation of this finding is these diseases are suspected. restricted to a small amount of data interpreting normal A number of reasons have led to a lack of clarity values and individual pathologist experience within defining the histopathology associated with EGIDs. The defined geographic locations. Address correspondence and reprint requests to Glenn T. Furuta, MD, ISSUES OF CONTROVERSY Section of Pediatric Gastroenterology, Hepatology, and Nutrition, The Children’s Hospital Denver, University of Colorado Denver, School of Medicine, 13123 E 16th Ave, B290, Aurora, CO 80045 (e-mail: With these initial descriptions in mind, a number of [email protected]). specific areas of controversy exist that continue to per- The authors report no conflicts of interest. plex practitioners and scientists alike. 234 Copyright © 2008 by Lippincott Williams & Wilkins.Unauthorized reproduction of this article is prohibited. EOSINOPHILIC GASTROINTESTINAL DISEASES 235 What Are the Best Diagnostic Criteria for These estimated that esophageal eosinophilia is present in about Diseases? 1% of the population (7). Whether the emergence of EoE represents increased recognition or increasing inci- Because the normal values across the world have yet to dence is still uncertain, although the data from Western be defined, the establishment of diagnostic criteria for Australia suggests that this is a new disease, accompanied EGIDs continues to pose challenges. Several studies in by more severe inflammation in the mucosa. North America have identified ranges of normal numbers With respect to other EGIDs, the data are less clear. of mucosal eosinophils, but broader definitions that Katz et al (8) reported 12 children with peripheral encompass more diverse settings are lacking. In addition, eosinophilia, iron deficiency anemia because of blood reports focus primarily on the enumeration of eosinophils loss in the stools, protein-losing enteropathy, and eosi- and little data exist characterizing distribution within the nophilic infiltration of the stomach and small intestine, mucosa. For instance, is it normal for eosinophils to what today would be called eosinophilic gastroenteritis. reside directly adjacent to epithelial cells? If the para- These patients were divided into 2 groups. In the first digm for histological assessment of polymorphonuclear group, the disease presented under the age of 1 year and cells in the classical inflammatory bowel disease is responded to the exclusion of milk from the diet. The adopted, the answer is no, but this issue has not been second group consisted of patients whose disease started fully addressed in the healthy intestinal mucosa. Because later in childhood and who did not respond to dietary eosinophils are normal residents of the intestinal mucosa, changes. They had atopy and immunoglobulin (Ig)E– whereas polymorphonuclear cells are not, significant mediated immediate hypersensitivity reactions to food. differences likely exist. In addition, a full consideration This report and others suggest that specific phenotypes of all diagnostic possibilities for pathological intestinal may exist within patient populations with EGIDs. eosinophilia always must be considered. Currently, the Few natural history data are published examining the finding of mucosal eosinophilia is met with the frequent long-term outcome of EGIDs in children or adults. assumption that it is secondary to food allergy or parasitic Clinical observation suggests that the condition may infection, but a number of other diseases have been resolve permanently with time, or more likely is charac- associated with this finding. terized by recurrent relapses. For instance, allergic eosi- nophilic proctocolitis and/or food-induced proctocolitis are significant causes of lower gastrointestinal bleeding What Is the Epidemiology of the EGIDs and Why in infants. It is thought that milk proteins are the etiologic Are They Seemingly Increasing, at Least in Certain agent inducing these findings but little has been done to Geographic Locations? determine the natural history or potential complications of these conditions. In fact, some patients may have a Because diagnostic criteria are lacking, answers remain relatively benign disorder called neonatal transient eosi- elusive. The absolute number of eos/HPF may indeed vary nophilic colitis (9). in different geographic environments, making absolute The rising prevalence reported of eosinophilic esopha- threshold numbers for the diagnostic evaluation difficult gitis mirrors the rise in allergic disease that has been to establish. occurring for the past 4 decades, probably reflecting an Because EGIDs are rare, scant population-based data increasing vulnerability to antigen sensitization (3). The are available on incidence, prevalence, and racial diver- increases in allergic disorders parallel a declining inci- sity of EGIDs, and most knowledge has been accumu- dence of infectious diseases. This gradient from infectious lated from isolated reports occurring in children and to allergic disease correlates with gradients from low to adults (3). The best-documented and most-studied EGID high socioeconomic status, large to small family size, and is EoE. The rapid rise in prevalence of EoE has been increasing body weight, and also with early day care documented in several populations and is consistent with attendance, exposure to animals, and the patterns of gut changing environmental exposure in vulnerable individ- microflora. Helminth exposure appears to be an important uals. EoE has been reported in North America, South mirror, and possibly a determinant of these changes. It has
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