Volume 7, Issue 4 , Pages 370-371, April 2009
Eosinophilic Esophagitis: From Rookie of the Year to Household Name
Article Outline
Eosinophilic esophagitis (EE) is now past the stage of being a hot new disease. It is close to becoming part of the list of standard diseases that all gastroenterologists should recognize and be able to treat. Part of the reason for such a rapid evolution has been how much we have learned about this disease. For example, a food allergy–based etiology has been well-characterized in patients.1 Typical clinical, demographic, and endoscopic criteria have been described to point toward diagnosis.2, 3, 4 Effective medical treatments based on either allergen avoidance and/or pharmacologic suppression of the allergic reaction and a safe means of stricture dilation have been described.5, 6, 7 An elegant animal model has been developed.8 There are already natural history data for the disease.9 Finally, both the immunologic and genetic pathways in EE have been elucidated to a large degree.10, 11, 12 The fact that all this information could be obtained within 15 years of the disease description is a testament to modern science and a handful of investigators who have made EE one of their life's passions.
Once these important steps in disease characterization have occurred, then one of the next areas of study is in understanding how the disease penetrates the population at large. More specifically, physicians need to know basic epidemiologic information such as how common is the disease, what races are more likely to be affected, are there specific geographic or socioeconomic predispositions to disease occurrence, and how adaptable are previously published and presumably specific disease attributes to a population as a whole. In this issue of the Journal, 2 excellent studies start to address these questions. In the article by Franciosi et al,13 the largest pediatric base of patients with EE from Children's Hospital of Philadelphia is studied. Through an elegant process known as geocoding, the authors analyze several distribution characteristics of their large population of patients. They convincingly confirm smaller scale studies demonstrating that EE is a predominantly white male–based disease. EE was also found to be more of a suburban than urban disease. Notably, although it appears to be a disease more of higher socioeconomic suburban populations when compared with appropriate general gastroenterology and allergy control groups, race unfortunately becomes an important confounder, so they are unable to dissect this possibility, as likely as it might seem.
The second study by Veerappan et al14 takes a different epidemiologic approach to EE. In their large and readily accessible adult military population at Walter Reed Army Medical Center, the authors are able to determine a prevalence of disease. Somewhat alarmingly, these investigators found a 6.5% prevalence of EE in patients undergoing endoscopy. This is a high number when compared with prior data from Sweden showing a 0.4% prevalence, albeit in more of a general population as opposed to those patients having an indication for endoscopy. Similar to the data of Franciosi et al,13 these authors also demonstrate a male predominance. They also confirm smaller study data that the typical endoscopic findings of EE, specifically rings, furrows, and white plaques, are very common, that dysphagia is the most common symptom in these patients, and that a history of asthma is a strong predictive factor for the presence of EE. Although the percentage of white patients with EE was also high (60%), it did not differ from controls.
One of the joys of analyzing articles in depth and knowing the literature reasonably well, however, is seeing the subtext of important studies such as these. Furthermore, because a disease is studied in a broad population, not only is it an opportunity to confirm the common characteristics of a disease, but it is also a chance to start to appreciate the variations. As a result, much of the strength of these studies comes not only in their population-based confirmation of EE as more likely a white male disease, but in the obverse that there will still be a sizable population of patients with EE who do not fit the typical pattern. For example, both studies point to sizable non-white population of EE patients. In the study by Franciosi et al,13 16.4% of patients are non-white. It would be nice to know the breakdown, but we have to assume that at least African-Americans are represented, as are probably other ethnic groups. This is further confirmed in the study by Veerappan et al,14 in which 10 of the 25 (40%) patients with EE are African-American. Although this latter study might suffer from the issue of reliably differentiating allergy-based EE from acid reflux–based EE, specifically in the African-American patients who tended to have less dysphagia and were less likely to have endoscopic features typical of EE (only 20%), we have to assume at least some of these patients had allergy-based disease. This study is also important in demonstrating that the typical endoscopic findings of EE as outlined above, although helpful, are not entirely specific. More precisely, control patients in this study exhibited these furrows, rings, and white plaques in 1%–9% of non-EE patients, depending on the finding.
These studies then help move the field of EE in several important regards. They confirm general demographic and clinical consensus15 characteristics of the disease, and they push us further in the direction of understanding EE as a common disease in our population. These studies, however, also help us to understand that as in many diseases, there is no absolute, and thus, the diagnosis of EE should be based not on one test but on a compendium of compatible diagnostic factors that include demographic, clinical, and laboratory-based criteria as well as appropriate treatment response. Important in this theme is the side observation that the number of eosinophils per high-power field, the sine qua non of the diagnosis, has also been extensively questioned, with high numbers potentially seen in gastroesophageal reflux disease.16 Conversely, esophageal eosinophil counts in some allergy-based EE patients might fall below defined lower limits as defined in the literature.17 Perhaps the time will come when widespread genetic analysis is reliable and available to diagnose EE, but even in these times of rapid medical advance, these studies underscore some of the basics of medicine: that in a disease that will clearly affect a relatively large part of our population, it is important to recognize not only the common scenarios but also use our good medical judgment to diagnose those patients with atypical presentations or characteristics so that we might help all patients with this rapidly evolving disease.
References
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- Eosinophilic esophagitis: a prevalent disease in the United States that affects all age groups. Gastroenterology. 2008;134:1316–1321
- Prevalence and predictive factors of eosinophilic esophagitis in patients presenting with dysphagia: a prospective study. Am J Gastroenterol. 2007;102:2627–2632
- Histopathologic variability and endoscopic correlates in adults with eosinophilic esophagitis. Gastrointest Endosc. 2006;64:313–319
- Eosinophilic esophagitis: a 10-year experience in 381 children. Clin Gastroenterol Hepatol. 2005;3:1198–1206
- Comparison of oral prednisone and topical fluticasone in the treatment of eosinophilic esophagitis: a randomized trial in children. Clin Gastroenterol Hepatol. 2008;6:165–173
- Esophageal strictures in adult eosinophilic esophagitis: dilation is an effective and safe alternative after failure of topical corticosteroids. Endoscopy. 2008;40:161–164
- Epicutaneous antigen exposure primes for experimental eosinophilic esophagitis in mice. Gastroenterology. 2005;129:985–994
- Natural history of primary eosinophilic esophagitis: a follow-up of 30 adult patients for up to 11.5 years. Gastroenterology. 2003;125:1660–1669
- Eotaxin-3 and a uniquely conserved gene-expression profile in eosinophilic esophagitis. J Clin Invest. 2006;116:536–547
- Esophageal remodeling develops as a consequence of tissue specific IL-5-induced eosinophilia. Gastroenterology. 2008;134:204–214
- Interplay of adaptive th2 immunity with eotaxin-3/c-C chemokine receptor 3 in eosinophilic esophagitis. J Pediatr Gastroenterol Nutr. 2007;45:22–31
- A case-control study of sociodemographic and geographic characteristics of 335 children with eosinophilic esophagitis. Clin Gastroenterol Hepatol. 2009;7:415–419
- . The prevalence of eosinophilic esophagitis in an adult population undergoing upper endoscopy: a prospective study. Clin Gastroenterol Hepatol. 2009;7:420–426
- Eosinophilic esophagitis in children and adults: a systematic review and consensus recommendations for diagnosis and treatment. Gastroenterology. 2007;133:1342–1363
- High intraepithelial eosinophil counts in esophageal squamous epithelium are not specific for eosinophilic esophagitis in adults. Am J Gastroenterol. 2008;103:435–442
- The spectrum of pediatric eosinophilic esophagitis beyond infancy: a clinical series of 30 children. Am J Gastroenterol. 2001;96:2290
Conflicts of interest The author discloses no conflicts.
PII: S1542-3565(08)01113-0
doi:10.1016/j.cgh.2008.10.029
© 2009 AGA Institute. Published by Elsevier Inc. All rights reserved.
Volume 7, Issue 4 , Pages 370-371, April 2009
