Eosinophilic esophagitis (EoE) is a chronic, food antigen-driven gastrointestinal disease that is characterized by esophageal eosinophilia. Currently, there are no Food and Drug Administration (FDA)-approved treatments for EoE, but the two most commonly prescribed therapies include topical corticosteroids and food elimination diets. Clinical trials have revealed a significant proportion of cases that are resistant to topical corticosteroids, and although we define EoE as a food antigen-driven disease, not all patients with EoE respond to elimination diets or even elemental diets. The varied response to treatments highlights the heterogeneity of EoE and the need for new treatment strategies. Despite the clinical differences in treatment response, predicting the outcome remains difficult since factors including age, histologic severity at diagnosis, atopic history, and anthropometrics are not predictive of treatment response. In our practice at an academic pediatric referral center, we observe distinct clinical EoE phenotypes, including cases with atopy, connective tissue disorders, or responsiveness to a proton pump inhibitor. Similar to the work in progress with asthma, stratification of patients with EoE by clinical phenotypes and/or molecular endotypes will likely assist with therapy selection and prediction of natural history. Molecular analysis with gene expression panels also shows promise in helping us classify patients based on molecular endotypes. In additional to the clinical and molecular classifications, more accurate histologic diagnostic criteria for EoE may help us tease out small differences between patient cohorts. Despite the leaps in knowledge over the past decade regarding EoE pathogenesis, it remains a challenge to predict the response to treatment. Future studies focused on molecular, genetic, and immunologic analyses of larger patient cohorts are needed to assist in identifying EoE phenotypes and endotypes as we attempt to improve patient outcomes in pediatric EoE.
Nonalcoholic fatty liver disease (NAFLD) is the most common cause of elevated liver enzymes in children in the United States. Screening for NAFLD in children with obesity is recommended by several published guidelines, but the application of these recommendations in pediatric weight management programs is uncertain. Our study aimed to describe the screening practices for NAFLD in a large pediatric weight management program. During 2014, 1312 patients were seen, with a liver enzyme panel obtained in 847 (64.5%). Only 47/847 (5.5%) had elevated liver enzymes twice the upper limit of normal. Of the 47, 33 (70%) patients had persistently elevated liver enzymes. Of those 33, 22 (67%) had further exclusionary laboratory testing. Screening for NAFLD is challenging even in a pediatric weight management program with clearly established protocols. Those with elevated liver enzymes do not always complete recommended exclusionary testing. Barriers to completing further evaluation need to be addressed.
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