Eosinophilic esophagitis (EoE) is a clinicopathologic condition of increasing recognition and prevalence. In 2007, a consensus recommendation provided clinical and histopathologic guidance for the diagnosis and treatment of EoE; however, only a minority of physicians use the 2007 guidelines, which require fulfillment of both histologic and clinical features. Since 2007, the number of EoE publications has doubled, providing new disease insight. Accordingly, a panel of 33 physicians with expertise in pediatric and adult allergy/immunology, gastroenterology, and pathology conducted a systematic review of the EoE literature (since September 2006) using electronic databases. Based on the literature review and expertise of the panel, information and recommendations were provided in each of the following areas of EoE: diagnostics, genetics, allergy testing, therapeutics, and disease complications. Because accumulating animal and human data have provided evidence that EoE appears to be an antigen-driven immunologic process that involves multiple pathogenic pathways, a new conceptual definition is proposed highlighting that EoE represents a chronic, immune/antigen-mediated disease characterized clinically by symptoms related to esophageal dysfunction and histologically by eosinophil-predominant inflammation. The diagnostic guidelines continue to define EoE as an isolated chronic disorder of the esophagus diagnosed by the need of both clinical and pathologic features. Patients commonly have high rates of concurrent allergic diatheses, especially food sensitization, compared with the general population. Proved therapeutic options include chronic dietary elimination, topical corticosteroids, and esophageal dilation. Important additions since 2007 include genetic underpinnings that implicate EoE susceptibility caused by polymorphisms in the thymic stromal lymphopoietin protein gene and the description of a new potential disease phenotype, proton pump inhibitor-responsive esophageal eosinophila. Further advances and controversies regarding diagnostic methods, surrogate disease markers, allergy testing, and treatment approaches are discussed.

/pdf/eosinophilic-esophagitis-updated-consensus-recommendations-16knxh59cv.pdf

Eosinophilic esophagitis: Updated consensus recommendations for children and adults

Epidemiology and Natural History of Eosinophilic Esophagitis

https://www.gastrojournal.org/article/S0016-5085(14)00217-0/pdf

Efficacy of Dietary Interventions for Inducing Histologic Remission in Patients With Eosinophilic Esophagitis: A Systematic Review and Meta-analysis

Objective:To determine the natural history of treated and untreated eosinophilic esophagitis (EE) and examine the presenting symptoms of EE.Patients and Methods:Retrospective and prospective chart review of all patients diagnosed with EE at The Children's Hospital of Philadelphia. EE was def

14 years of eosinophilic esophagitis: clinical features and prognosis.

https://www.cghjournal.org/article/S1542-3565(13)01304-9/pdf

Prevalence of eosinophilic esophagitis in the United States.

To the Editor: The association between Helicobacter pylori (H. pylori) and gastroesophageal reflux disease (GERD) in adult patients has been fiercely debated. In recent years, epidemiologic studies in adults have documented a decrease in H. pylori infection rate and an increase in GERD rate, suggesting that the bacterium has a protective effect against GERD. To date, the relationship between H. pylori infection and GERD in children has not been adequately evaluated. In the present study, we investigated this relationship in H. pyloriinfected children before initiation of eradication therapy, by performing a retrospective review of all upper endoscopy reports, between 1998 and 2004. In all procedures, biopsies from the esophagus and/or the gastric mucosa were obtained irrespective of the mucosal appearance. Positive H. pylori infection status (test group) was defined as positive histology and positive urease test (CLO test). Children without infection constituted the control group. Statistical calculation for adequate power to compare between the groups suggested a sample size of 50 patients for test group and 100 patients for the control group (Stata 7.0; College statistics, TX). The groups were matched for sex, age, and clinical symptoms. Histology was reevaluated by an experienced pathologist who was blinded to the patient’s clinical and histologic diagnosis. Esophagitis was graded according to various histologic markers including the thickness of the basal layer (as a % of mucosal thickness), the length of the papilla (as a % of mucosal thickness), and the degree of inflammatory infiltrate. The study was approved by the local IRB committee. Two-tailed w analysis was performed to compare the 2 groups. A total of 150 charts were evaluated (50-test group and 100control group). The mean age was 11.8±3.5 years. Male to female ratio was 1.2:1.0, with no difference between the groups for both data. Overall, there was no significant difference in the rate of esophagitis between the groups (10% and 18% for test and control, respectively; P=0.297; relative ratio=1.1; 0.96, 1.25). Similarly, no significant difference was noted in the rate of esophageal inflammation at any level (mild, moderate, or severe) between test and control groups (70%, 12%, and 8% vs. 67%, 11%, and 4%, respectively; P>0.45). Gastritis was identified in all children from the test group, but in only 55 children from the control group (100% vs. 55%, P=0.000). None of the patients had atrophic gastritis. Indeed, the interaction between H. pylori infection and reflux esophagitis in adult and pediatric patients has been of great debate in the literature. In the present study, we demonstrated no difference in the rate of reflux esophagitis between H. pylori-infected and H. pylori-naive children. Concurring with our results, several pediatric studies showed no association between H. pylori infection and reflux esophagitis, preeradication or posteradication therapy. On the other hand, Nijevitch et al reported that esophagitis was significantly lower in asthmatic children infected with H. pylori organisms compared with H. pylori-negative children. The differing results may be explained by various confounding factors existing in the previous studies, such as different ethnic groups, different disease severity, and/or different clinical conditions (asthma, neurologically impaired children, etc). From published data in adults and children, it is apparent that the true association between H. pylori infection and GERD is far from being clear. It has already been shown that other factors such as anatomic location, the type of gastritis, ethnicity, and bacterial antigen (CagA status), may all play a significant role in this association. For example, antral gastritis and/or pangastritis can significantly affect the recovery of gastric acid secretion capacity after eradication therapy, but those factors were not evaluated in the present study. To summarize, our study results showed no difference in the severity of esophagitis (mild, moderate, and severe) between H. pylori-positive and H. pylori-negative children. The findings further suggest that GERD and H. pylori infection in children may coexist, but are independent of each other. Moreover, our data emphasizes that the presence of H. pylori infection does not influence the histologic characteristic of GERD even at the highest degree of esophagitis. Because there is not a single diagnostic test that is considered as the gold standard for GERD in children, we chose to establish the diagnosis by histology. This test may have restricted our patient population to only children at the higher disease spectrum of GERD (histologically proven esophagitis), rather than to include the children with nonerosive reflux disease diagnosed clinically and/or by pH study. In short, our findings demonstrated a lack of significant interaction between H. pylori infection and histologic esophagitis in children before therapy. We suggest that it is unlikely that H. pylori infection plays a significant role in the pathophysiology of GERD. Larger prospective studies in children are needed to further establish the interaction between H. pylori infection and GERD.

Does Helicobacter pylori protect children from reflux disease

Treatment for NASH: the value of histology.

The prevalence of eosinophilic esophagitis in children from wv: a review of the last decade

Eosinophilic esophagitis disease in children from West Virginia: a review of the last decade (1995-2004).

Background
Symptoms of vomiting and dysphagia in children with eosinophilic esophagitis may be related to the development of mucosal fibrosis.

Fluticasone and Food Allergen Elimination Reverse Sub-epithelial Fibrosis in Children with Eosinophilic Esophagitis

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