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Background: Eosinophilic esophagitis (EoE) is a chronic disease characterized histologically by > 15 eosinophils per high-power field (eos/hpf). Esophageal mucosal mast cells have been implicated in EoE pathogenesis. The association of atopy with EoE has been established but has not been correlated with levels of serum tryptase. The lack of concurrent atopy in some patients suggests the possibility that atopy may either be the related subtype of EoE or may be a sign of comorbidities. No study has looked at whether patients present with different phenotypes/comorbid disease when they have evidence of elevated serum tryptase. We hypothesized that these patients differ with respect to presentation and comorbidities with more refractory GI disease., Aims: To examine whether elevations of serum tryptase associate with different, more severe clinical presentations in EoE patients which may be explained via mast cell activation., Materials and Methods: Retrospective chart review identified 72 patients with EoE with results for serum tryptase between 2015 and 2016. Patients were classified as Tryptase HI (tryptase > 10.9 µg/l) and Tryptase LO (< 10.9 µg/l). Clinical characteristics and treatment response were compared using univariate analysis and multivariate regression between the groups., Results: Out of 72 patients, 12 were tested as Tryptase HI (16.7%, 95% CI 8.1-25.3%). Tryptase HI was associated frequently with asthma (P = 0.0003), urticaria (P = 0.002), arthralgia (P = 0.005), sinusitis (P = 0.03), nausea/vomiting (P = 0.046), and eosinophilic gastrointestinal disease (P = 0.001). Asthma and arthralgia were found to be significantly associated with Tryptase HI (P = 0.0013, P = 0.0098, respectively). Mucosal eosinophil counts and tryptase levels were not correlated (R 2 0.095, P = 0.77). Tryptase did not resolve with resolution of esophageal eosinophilia., Conclusions: We found that EoE patients with elevated tryptase levels more commonly presented with asthma, urticaria, arthralgia, nausea/vomiting, sinusitis, and more distal eosinophilia. This indicates that atopy in EoE patients warrants further exploration. The lack of correlation between histologic remission and reduction of serum tryptase levels post-treatment suggests that mast cell activation may be an independent, yet associated disease. More study into this unique association is warranted.

Background: Eosinophilic esophagitis (EoE) remains difficult to classify because of varying presentations. Not uncommonly, patients present with symptoms of esophageal dysfunction and have esophageal changes on endoscopy resembling EoE but without >15 eosinophils/HPF. Patients with low numbers of eosinophils in esophageal biopsy specimens may have esophageal changes and symptomatic disease brought about by eosinophil granule protein deposition without recognizable intact cells., Aim: To determine whether extracellular eosinophil granule protein deposition is present in the esophagi of patients with low eosinophil numbers who have clinical symptoms and characteristic endoscopic esophageal changes of EoE including ringed esophagus (RE)., Methods: Esophageal biopsy specimens were studied from eight EoE patients with >15 eosinophils per high power field (HPF) and nine patients with RE (<15 eosinophils/HPF). The specimens were analyzed for eosinophil granule proteins, major basic protein 1 (eMBP1) and eosinophil-derived neurotoxin (EDN), by indirect immunofluorescence., Results: Both EoE and RE showed positive EDN and eMBP1 extracellular deposition; control esophagus showed minimal or none. Comparing EoE and RE, extracellular EDN and eMBP1 were similar except that EDN in EoE was greater in the distal esophagus., Conclusions: This study highlights the importance of assessing eosinophil granule protein deposition in esophageal disease with potential eosinophil involvement. Persistent/progressive esophageal changes may be brought about by eosinophil granule proteins despite low numbers of intact cells. The meaning of "resolution" in EoE may need to be redefined based on numbers of esophageal eosinophils, extracellular eosinophil granule protein deposition, and subsequent clinical course of patients.

Background: Radiofrequency atrial fibrillation ablation (AFA) is commonly performed in patients with atrial fibrillation. It is imperative to develop a strategy for the early detection of esophageal lesions secondary to AFA. The current protocol is to obtain cross-sectional imaging before and immediately after the procedure. If patients have evidence of esophageal inflammation, they undergo esophagogastroduodenoscopy (EGD). We hypothesized that esophageal abnormalities seen on imaging immediately post-ablation are a poor predictor of the damage seen during EGD., Methods: Patients referred for EGD following AFA from 1/2009 to 11/2010 were included. Two endoscopists reviewed and scored the EGD images. Two radiologists reviewed the post-AFA imaging studies. For computed tomography (CT) scans, esophageal inflammation was scored from 0 to 2. For T2 and delayed magnetic resonance imaging (MRI) pictures, esophageal enhancement was scored from 0 to 2, with the circumference involved as 0, <50%, or >50%, and the length of esophageal enhancement in mm., Results: In total, 76 patients were included; 22 patients had only endoscopic images and 54 had both endoscopic and radiologic images for review. Of the post-AFA imaging studies, 16 were CTs and 60 were MRIs. The kappa score for the inter-rater agreement of esophageal inflammation on EGD was 0.4584 (moderate). For MRIs, the kappa scores for T2 images were 0.1980 and 0.2857 for edema and circumference, respectively. For delayed images, the kappa scores were 0.2687 and 0.3101 for edema and circumference, respectively. The kappa scores were negative between EGD score by T2 edema (-0.2104) and circumference (-0.2212), and between EGD score and delayed edema (-0.0588) and circumference (-0.0446). When measures were treated as dichotomous, the overall agreement between CT measures and EGD scores was kappa = 0, for T2 measures and EGD kappa = -0.2963, 95% confidence interval (CI) (-0.5643, -0.0282), and between delayed measures kappa = -0.0244, 95% CI (-0.1420, -0.0932)., Conclusions: There was no agreement between immediate imaging and the endoscopic findings of esophageal inflammation after AFA. A longer period of time between AFA and obtaining an imaging study may be useful in detecting patients with significant esophageal injury who should undergo EGD to assess for complications of AFA. Further studies are needed in order to determine the best modalities and optimal timing to detect post-AFA esophageal damage in an attempt to prevent the formation of atrial-esophageal fistulas.

Background: Both gastroesophageal reflux disease and allergy/atopy have been implicated in the pathogenesis of eosinophilic esophagitis (EoE). There are no prospective studies comparing treatment of EoE with acid suppression versus topical corticosteroids., Objective: To determine the outcome of adult eosinophilic esophagitis patients treated with esomeprazole versus topical fluticasone., Design: Prospective randomized controlled trial., Setting: Academic medical center., Participants: Adults (18-80) diagnosed with EoE by symptoms of dysphagia and esophageal biopsies with >or=15 eosinophils/hpf., Interventions: Subjects were randomized to esomeprazole (40 mg by mouth every morning) or aerosolized, swallowed fluticasone (440 mcg by mouth twice a day) for 8 weeks., Main Outcome Measurements: Improvement in dysphagia (8-point scale), esophageal eosinophil infiltration before and after treatment, prevalence of GERD measured by validated questionnaire and baseline pH study., Results: About 56% (14/25) had acid reflux by pH study. There was no difference between treatment groups in improvement in dysphagia scores [3/12 (25%) of the esomeprazole group versus 6/12 (50%) in the fluticasone group, P = 0.40]. Eosinophil infiltration decreased with treatment in both groups, and there was no difference in the amount of decrease between groups (P = 0.70)., Limitations: Small sample size, unexpectedly high drop-out rate., Conclusions: Gastroesophageal reflux disease is common in adult eosinophilic esophagitis patients. Dysphagia improves and esophageal eosinophilic infiltration decreases with either treatment. There was no difference in degree of improvement in dysphagia or eosinophil infiltration in patients treated with either topical fluticasone or oral esomeprazole. GERD may be important in the pathogenesis of adult EoE.

Background: Exercise-triggered asthma (ETA) develops when physical activity triggers asthma symptoms during or directly after exercise. In patients prone to symptoms of supra-esophageal reflux, exercise may trigger gastroesophageal reflux (GER), resulting in such symptoms., Aims: To determine the prevalence of abnormal pH in patients with ETA and to determine whether acid suppression improves symptoms in ETA patients., Methods: We performed a randomized double-blind trial of rabeprazole versus placebo in the treatment of patients with ETA. Patients underwent treadmill protocol to determine their VO(2 max). Next, pH testing was initiated while undergoing a 30-min treadmill program exercising them at 65% of their VO(2 max). They were subsequently randomized to rabeprazole or placebo for 10 weeks. At the end of 10 weeks, exercise testing was repeated., Results: A total of 31 patients completed the study (20 asthmatics, 11 non-asthmatics). Twenty-two out of 30 (73%) subjects had abnormal pH studies. For all subjects, rabeprazole improved symptoms more than placebo (P = 0.03). The association was stronger in the pH-positive group (P = 0.009)., Conclusion: Acid reflux is common in ETA patients. Many patients with exercise-related respiratory symptoms are misdiagnosed as chronic asthmatics. Exercise-related symptoms improve with the use of acid suppression. This study suggests that ETA patients may benefit from acid suppression.

Eosinophilic Esophagitis (EE) is an emerging cause of esophageal food impaction (EFI) not accounted for in previous studies. We sought to determine the causes of EFI in a recent cohort with recognition of EE. A retrospective chart review of all patients with EFI during the past 5 years was performed. Etiology was determined by endoscopy report, pathology results, and follow-up studies. A total of 85 EFIs occurred, in 79 patients (55 men, 30 women, age 18-100). The most common etiologies of EFI were Schatzki's ring (n = 18), peptic stricture (n = 18), EE (n = 9), esophagitis (n = 9), and no underlying diagnosis (n = 20). EE was significantly more frequent in men (P < .025) and those <50 years old (P < .025). There was a significant difference in the age at which men (median age = 44) and women (median age = 71) present with EFI (P < .001). The etiology of EFI differs significantly by age and gender. This information may be useful in evaluation and management of EFI.

Clinical gastrointestinal manometry studies are currently performed with multilumen water-perfused polyvinyl or strain gauge sensor solid-state catheters. A disposable catheter incorporating air-filled balloons has been developed with performance characteristics suitable for esophageal and anorectal manometry studies. Our aim was to compare esophageal and anorectal pressure measurements using this newly developed catheter with measurements obtained using standard solid-state or water-perfused catheters. Measurements of resting LES pressure, esophageal contraction amplitudes, and anorectal rest and squeeze pressures were obtained in 10 healthy volunteers using a solid-state esophageal catheter, a water-perfused anorectal catheter, and air-filled balloon esophageal and anorectal catheters. Correlation coefficient analysis demonstrated that LES pressures, esophageal contraction amplitudes, and anorectal resting and squeeze pressures were not significantly among between the different catheters. We conclude that recently developed air-filled balloon esophageal and anorectal manometry catheters provide very similar measurements of LES, esophageal body, and anorectal sphincter pressures compared to presently used manometry catheters.