History Of Eosinophilic Esophagitis Research Articles

S2264 A Case of Progressive Untreated Eosinophilic Gastrointestinal Disorder Complicated by Eosinophilic Myocarditis

Introduction: Eosinophilic gastrointestinal diseases (EGID) are immune-mediated conditions characterized by GI dysfunction and histological evidence of eosinophilic infiltration. While usually confined to the GI tract, severe inflammation can involve multiple organ systems, typically under the umbrella term of hypereosinophilic syndrome (HES). Patients can present with cardiac involvement such as eosinophilic myocarditis which results in an uncommon, but potentially lethal complication. We present a case of a patient with prior history of eosinophilic esophagitis (EoE) subsequently presenting with diffuse EGID complicated by eosinophilic myocarditis. Case Description/Methods: A 63-year-old female with a history of EoE and breast cancer post mastectomy presented with acute epigastric and chest pain. The patient had biopsy-proven EoE which was managed with PPI in the past. On physical examination, she had diffuse abdominal tenderness. Labs were remarkable for peripheral eosinophilia peaking at 57%. Initial high sensitivity troponin I was 300 ng/L without EKG changes, and ultimately peaked at 7821 ng/L. CT of the abdomen and pelvis showed thickening of the stomach, duodenum, and jejunum. Left heart catheterization revealed LAD disease without obstructive disease. EGD demonstrated severe inflammation, erythema, and eosinophilic infiltration in the gastric body, antrum, and throughout the duodenum. High dose steroids were initiated with subsequent improvement in symptoms, serum troponin, and complete resolution of peripheral eosinophilia. Patient followed up as an outpatient, where cardiac MRI confirmed eosinophilic myocarditis, and she was started on Mepolizumab for maintenance therapy and prevention of relapse. Discussion: EGID are increasingly prevalent disorders that can result in significant morbidity and mortality without prompt diagnosis. This patient had a history of EoE and developed diffuse GI involvement and subsequent eosinophilic myocarditis. Her presentation as atypical chest pain suggestive of NSTEMI resulted in delay of initiation of steroids until after heart catheterization. Our case suggests that without glucocorticoid suppression, eosinophilia can cause widespread tissue infiltration and damage. The majority of these patients have chronic disease that require long term maintenance therapy. Mepolizumab has been demonstrated to be an effective agent for hypereosinophilic disorders. When managing EGID, it is pertinent to recognize early involvement of systemic eosinophilic infiltration.Figure 1.: EGD.

The Prevalence of Dysphagia and Food Impactions is High in Atopic Patients Without a Known History of Eosinophilic Esophagitis (EoE)

While EoE is associated with atopic disease, the prevalence of EoE symptoms in patients with atopic conditions is unknown. The objective of this pilot study was to assess the prevalence of dysphagia and food impaction in atopic patients compared to healthy controls.

Onset of eosinophilic esophagitis during a clinical trial program of oral immunotherapy for peanut allergy

Onset of eosinophilic esophagitis during a clinical trial program of oral immunotherapy for peanut allergy

Eosinophilic esophagitis: definition, epidemiology and quality of life

Eosinophilic esophagitis (EoE) is a clinicopathological disease defined by symptoms of esophageal dysfunction and ≥15 eosinophils/HPF after excluding other causes of esophageal eosinophilia. Increasing attention has been paid by clinicians and researchers after its first description in 1978. Many consensuses and guidelines have been issued over the years, as gastroenterologists did not reach an agreement on EoE definition, especially regarding the controversial responsiveness to proton pump inhibitor (PPI) therapy. Of note, recent evidence suggests that the incidence and prevalence of EoE have been increasing through the years: many risk factors have been advocated as possible reasons for this, although further studies are needed. In this brief review, we will first cover the history of EoE in the literature, with a focus on its varying definition throughout the years. Then, we will discuss EoE epidemiology, emphasizing potential risk factors explaining its increasing incidence and prevalence. Last, we will deal with the quality of life of adult and pediatric patients with EoE.

S2008 A Case of Esophageal Adenocarcinoma in a Young Male With Longstanding Untreated Eosinophilic Esophagitis

INTRODUCTION: Eosinophilic Esophagitis (EoE) has been increasing in incidence over the last decade due to the increasing number of EGD with biopsies preformed. Up to 6.5% patients undergoing EGD for any indication are diagnosed with EoE and 22% in patients for dysphagia. EoE is present in all age groups but peak incidence is bimodal, in first and third decades of life. Here we describe a case of esophageal adenocarcinoma in a patient with history of EoE. CASE DESCRIPTION/METHODS: A 42 year-old male (BMI 27 kg/m2) with PMHx of untreated EoE for 10 years presented to the ED for food bolus impaction a few hours after eating pork. No history of alcohol or tobacco use. Emergent EGD was performed with successful removal of solid food bolus in middle third of the esophagus. There were endoscopic mucosal changes consistent with EoE (EoE-EREFS: Edema 1, Rings 2, Exudates 1, Furrows 1 and Stricture 0) within the entire esophagus and a nodularity appreciated at the GEJ. Biopsies obtained from proximal and distal esophagus showed more than 50 and 100 eosinophils/per HPF respectively. The GEJ lesion showed high grade dysplasia in the settings of goblet cell metaplasia. Repeat EGD 3 weeks later revealed a medium sized fungating and ulcerated mass at the GEJ which was circumferential and partially obstructing. The biopsies showed esophageal adenocarcinoma with indeterminate HER2 oncogene expression, staged as T3N1 based on mini-probe EUS. Oncology classified the patient as cT3N1Mx. The patient received chemo-radiation (5-fluorouracil/oxaliplatin) over 37 days followed by robotic assisted laparoscopic Ivor Lewis esophagogastrectomy with left gastric hepatic artery and celiac lymphadenectomy with successful remission, T0N0. Patient remained in clinical remission at 6 months follow up. DISCUSSION: An estimated 17,500 new cases of esophageal cancer were reported in 2016. Incidence was 4 in 100,000 and increases with age starting from 0.2 in 100,000 at age 30 increasing to 26 in 100,000 at age 80. Mortality was 3.9 in 100,000 deaths and has a 5 year survival of 18.9%. Current risk factors for development of esophageal cancer are alcohol, smoking, and obesity. No clear genetic factors have been associated with development and it is unknown if EoE is a risk factor. However, chronic inflammation and structural changes may be a contributor to malignancy and further research should focus on this area given diseases mortality rates.Figure 1.: A. Food Bolus at Middle Third of the Esophagus B. Abnormal Mucosa at the Gastro-Esophageal Junction C. Gastric Cardia, retroflex view: Mass.Figure 2.: Proximal esophagus shows increased intraepithelial eosinophils, consistent with eosinophilic esophagitis.Figure 3.: GE Junction biopsy shows adenocarcinoma arising in the background of barrett’s esophagus.

S3146 Patients With Eosinophilic Esophagitis (EoE) and Persistent Extra-Esophageal GI Symptoms Should Be Evaluated for Eosinophilic Gastritis (EG) and Eosinophilic Duodenitis (EoD)

INTRODUCTION: Eosinophilic gastrointestinal (GI) disorders (EGIDs) are chronic inflammatory conditions characterized by aberrant accumulation and activation of localized tissue eosinophils and mast cells. While Eosinophilic Esophagitis (EoE) is the best understood of the EGIDs, there is growing understanding of Eosinophilic Gastritis (EG) and Duodenitis (EoD) and evidence that they may be more prevalent than previous estimates. Though EoE is defined in part by esophageal dysfunction, patients with EoE often present with extra-esophageal symptoms which may not be attributable to isolated esophageal inflammation. EG/EoD may be underdiagnosed in these patients due to non-routine biopsy and histopathologic evaluation of gastric and duodenal mucosa. We reviewed gastric and duodenal biopsies in patients with known EoE and persistent non-esophageal symptoms to determine the frequency of EG/EoD in this population. METHODS: 27 patients at the University of Utah with a known history of EoE, persistent extra-esophageal symptoms, and a history of gastric and duodenal biopsies were identified, and retrospectively reviewed. Histopathologic evaluation was performed and eosinophil counts and chronic inflammation were assessed. Eosinophilic gastritis and duodenitis were defined as the presence of ≥30 eosinophils/high-powered field (hpf) in 5 and 3 hpfs in the stomach and duodenum, respectively. RESULTS: Of the 27 patients, 17 (63%) met histologic criteria for EG and/or EoD (4 combined EG/EoD, 13 EoD). The most common non-esophageal symptoms among these 17 patients were abdominal pain, nausea and bloating. 3 of the 17 patients had been diagnosed with irritable bowel syndrome in addition to EoE. Of the 10 patients not meeting histologic criteria for EG/EoD, 4 were subsequently found to have gastroparesis, 1 was on high dose NSAIDs and 1 was subsequently found to have mast cell activation syndrome. CONCLUSION: In this retrospective study, 63% of patients with EoE and chronic extra-esophageal GI symptoms were found to meet histologic criteria for EG/EoD. This high discovery rate suggests that gastric and duodenal biopsies should be performed and evaluated for eosinophils in patients with EoE and extra-esophageal symptoms, including those with persistent abdominal pain, nausea, bloating or a diagnosis of functional GI disease.

Real–World Experience With Peanut Oral Immunotherapy: Lessons Learned From 270 Patients

This retrospective record review reports observations on the treatment of 270 patients with peanut allergy with peanut oral immunotherapy (POIT).The study included 270 patients between the ages of 4 and 18 years who received POIT in a single practice between 2009 and 2017. A total of 96.7% of patients had a history of an immunoglobulin E–mediated reaction, 70.7% had experienced anaphylaxis, 26% had a peanut-specific immunoglobulin E (PSIgE) concentration of >100 kU/mL, and 9.6% had a positive peanut challenge result within 2 years of inception of POIT. No patient was excluded on the basis of severity of previous reaction(s) or PSIgE concentration. Patients with a history of eosinophilic esophagitis or gastroenteritis were excluded.The treatment protocol began with 2.5 µg of peanut protein. Dose increases were administered under direct observation. Patients reached a target dose of 3000 mg of peanut protein, underwent a 6000-mg challenge, and then began a 2000-mg maintenance dose administered at home 1 to 2 times per day for a minimum of 3 years. The treatment team made dose adjustments and decisions regarding discontinuation of therapy on the basis of collaborative clinical judgment. Patients and caregivers were instructed to report any adverse reactions more significant than transient, self-limited oral pruritis or abdominal discomfort.A total of 214 of 270 patients (79%) completed POIT dose escalation. Age (P < .001) and PSIgE (P < .001) correlated inversely with completion of dose escalation. For each year increase in patient age after 5, there was a 17% decrease in the odds ratio of reaching the escalation target (P < .001). One hundred epinephrine-treated reactions occurred in 63 patients (23%) during escalation. Intermittent asthma and higher PSIgE levels increased the risk of epinephrine-treated reactions (P = .035 and .019, respectively). Eosinophilic esophagitis–like oral immunotherapy–related syndrome occurred in 37 patients (13.7%). Intermittent asthma and higher PSIgE levels increased the risk of eosinophilic esophagitis–like oral immunotherapy–related syndrome (P = .014 and <.001, respectively). After 3 years of maintenance treatment, 14 patients were able to achieve sustained peanut unresponsiveness, defined as tolerance of 6000 mg of peanut protein after avoiding peanut for 30 days. The best predictors of sustained unresponsiveness were a pretreatment PSIgE level <20 kU/L and a prechallenge PSIgE level <1 kU/L.In an allergy office practice, 79% of patients were able to complete a POIT desensitization protocol and maintain a desensitized state with daily peanut dosing.This study demonstrates that patients can achieve successful peanut desensitization despite a history of previous reaction(s) or markedly elevated PSIgE levels. Epinephrine-treated reactions did occur during POIT, demonstrating that risk of significant allergic reactions was not eliminated. Reduced likelihood of achieving the target dose with increasing age makes early intervention attractive. Additional future studies are necessary to improve risk assessment and identification of patients likely to achieve sustained unresponsiveness.

2373 Failure of Occam’s Razor: A Rare Trifecta of Causes for Elevated Liver Enzymes

INTRODUCTION: Unexplained abnormal liver function tests in a patient are a common reason for referral to a hepatologist. Patients may often have coexisting liver diseases, and require a liver biopsy for definitive diagnosis to guide treatment. We present a patient with celiac disease, fatty liver disease, and a delayed diagnosis of autoimmune hepatitis, highlighting the need to recognize anchoring bias. CASE DESCRIPTION/METHODS: A 55 year-old male, with a history of eosinophilic esophagitis and obesity, was referred a hepatologist for elevated liver enzymes. The patient was asymptomatic and consumed two units of alcohol per week. His BMI was 30, and he did not have stigmata of chronic liver disease and hepatomegaly. Labs showed total bilirubin 2.0mg/dL, ALP 59U/L, AST 132U/L, ALT 392U/L, albumin 4.3g/dL, and INR 1.3. Complete serologic evaluation for secondary causes of liver disease including viral hepatitis and autoimmune screen, alpha 1 antitrypsin, iron studies and ceruloplasmin were negative. Tissue transglutaminase (tTG) antibody was greater than 150U/mL and EGD revealed Modified-Marsh 3 pathologic changes suggestive of celiac disease. Liver ultrasound showed steatosis without cirrhosis and transient hepatic elastography suggested mild fibrosis (6.7kPa). Transaminases and tissue tTG antibody increased to more than 10 times the upper limit of normal despite adherence to a gluten-free diet. Liver biopsy confirmed evidence of autoimmune hepatitis with mild fibrosis and steatosis. The patient was commenced on immunosuppression with significant improvement in liver function tests. DISCUSSION: Liver involvement in celiac disease accounts for 9% of patients with unexplained, mildly elevated transaminases and has the potential to impact the clinical course of established liver disease. Primary biliary cholangitis and autoimmune hepatitis are also associated with celiac disease. Due to the high prevalence of elevated liver enzymes in celiac disease, it is reasonable to delay liver biopsy and monitor for improvement of liver enzymes with exclusion of dietary gluten. A liver biopsy to rule out coexisting liver diseases is warranted in patients with celiac disease with severely elevated transaminases or failure to respond to a gluten free diet. Clinicians must maintain a high index of suspicion for concurrent autoimmune liver disease especially in patients with a history of other autoimmune diseases. 1) Rubio-Tapia, A., Murray, JA. Liver involvement in celiac disease. Minerva Medica, 2008 Dec; 99(6): 595–604.

Eosinophilic esophagitis presenting with spontaneous esophageal rupture: a case report

BackgroundEosinophilic esophagitis, once considered a rare disorder, has been increasingly recognized as a leading cause of dysphagia and food impaction in children and adults over the last few decades. It predominantly occurs in young men with a history of atopy. Dysphagia and food impaction are the most common presentations. However, rarely, spontaneous perforation (Boerhaave’s syndrome) may occur in association with eosinophilic esophagitis.Case presentationA 40-year-old white woman with known history of eosinophilic esophagitis, who was non-compliant with treatment, presented with chest pain and developed acute spontaneous transmural esophageal perforation while eating a snack. Surgical repair was required.ConclusionIn a relatively young patient who presents with spontaneous esophageal perforation, eosinophilic esophagitis should always be ruled out as subsequent treatment may prevent recurrent perforation.

Eosinophilic Esophagitis in Children and Adolescents

Eosinophilic esophagitis (EoE) is an inflammatory disorder of the esophagus characterized by symptoms of esophageal dysfunction in association with histologic evidence of eosinophilic infiltration of the esophageal mucosa. The diagnosis is based on esophageal biopsies showing more than 15 eosinophils per high-power field in the absence of pathologic gastroesophageal reflux. It can present with a wide array of upper gastrointestinal tract symptoms. Babies and toddlers typically present with feeding intolerance or refusal, vomiting, and failure to thrive. Older children often present with abdominal pain and reflux symptoms, whereas adolescents and adults typically present with solid-food dysphagia and/or food impaction. Diagnosis is also supported by a family history of EoE and other allergy-based disorders, such as asthma, seasonal allergies, and atopy. Topical corticosteroids and dietary elimination are acceptable first-line treatment approaches. This review contains 7 figures, 5 tables, and 51 references. Key words: dysphagia, elimination diets, endoscopic dilation, eosinophilic esophagitis, eotaxin-3, feeding dysfunction, interleukin-5, proton pump inhibitor–responsive esophageal eosinophilia, swallowed fluticasone, viscous budesonide

Eosinophilic Esophagitis in Children and Adolescents

Eosinophilic esophagitis (EoE) is an inflammatory disorder of the esophagus characterized by symptoms of esophageal dysfunction in association with histologic evidence of eosinophilic infiltration of the esophageal mucosa. The diagnosis is based on esophageal biopsies showing more than 15 eosinophils per high-power field in the absence of pathologic gastroesophageal reflux. It can present with a wide array of upper gastrointestinal tract symptoms. Babies and toddlers typically present with feeding intolerance or refusal, vomiting, and failure to thrive. Older children often present with abdominal pain and reflux symptoms, whereas adolescents and adults typically present with solid-food dysphagia and/or food impaction. Diagnosis is also supported by a family history of EoE and other allergy-based disorders, such as asthma, seasonal allergies, and atopy. Topical corticosteroids and dietary elimination are acceptable first-line treatment approaches. This review contains 7 figures, 5 tables, and 51 references. Key words: dysphagia, elimination diets, endoscopic dilation, eosinophilic esophagitis, eotaxin-3, feeding dysfunction, interleukin-5, proton pump inhibitor–responsive esophageal eosinophilia, swallowed fluticasone, viscous budesonide

CO-35: ALPHA-1 Antitrypsin deficiency : a novel cause of isolated systolic resistant hypertension?

Background Alpha-1 Antitrypsin (AAT), a serine protease of the SERPIN superfamily inhibits various tissue proteases such as neutrophil elastase and proteinase 3. Mutations in the corresponding gene, SERPINA1, are at the origin of AAT deficiency (AATD). The most frequent manifestations of AATD are panacinar emphysema and chronic liver disease. AATD has been occasionally associated with aneurysms and dissection of large vessels. Compared to matched controls, AATD patients homozygous for the common Z variant have larger ascending aortas with abnormal elastic properties (Vizzardi et al. Heart 2012 ; 98: 1354–58). However, so far, increased arterial stiffness and isolated systolic hypertension have not been documented in AATD patients. We describe the case of a young patient with isolated systolic refractory hypertension associated with a mild, atypical form of AATD, and discuss the potential link between both entities. Methods A 43-year-old non-smoker man was referred at the hypertension consultation for severe, early-onset resistant hypertension with very high pulse pressure, despite intake of eight antihypertensive drugs. He reported a history of eosinophilic esophagitis and left popliteal stent for lower limb arteriopathy. Results In a context of moderate increase in ALAT ( Genetic testing confirmed the presence of the frequent Z variant of SERPINA1 at the heterozygous state, in the absence of AAT-related liver or pulmonary disease. Sitting office blood pressure was 160/50mmHg. Body mass index was 31.3kg/m 2 . Clinical examination was otherwise unremarkable. Mean day – and night-time ambulatory blood pressre were 142/58 and 115/43mmHg, respectively. Blood and urine analysis, urinary metanephrines and abdominal CT-angiography were normal. Echocardiography showed mild concentric left ventricular hypertrophy (LVMI : 134g/m 2 ). Carotid-femoral pulse wave velocity (SphygmoCor ® ) was markedly increased (14.2 m/s; age-adjusted reference values : 4.6–9.8 m/s). By contrast, detailed assessment of retinal and sublingual capillaries showed no evidence of microvascular dysfunction. Conclusions This case report suggests that increased arterial stiffness and isolated systolic hypertension are an integral part of the spectrum of AATD-related vascular abnormalities. Conversely, AATD may be considered in the differential diagnosis of resistant hypertension, especially in the presence of increased pulse pressure in a young patient. Future perspectives include indepth blood pressure and vascular characterization of a cohort of patients with both heterozygous and homozygous AATD.

Eosinophilic Esophagitis and Crohnʼs Disease: An Unbalanced Co-Existence

Eosinophilic Esophagitis (EoE) and Crohn's Disease (CD) occurring simultaneously is rare. Our literature search revealed only two documented cases of co-existing EoE and CD, with very limited evidence supporting an association. We present two additional cases to demonstrate these distinct immunemediated diseases can occur together, and propose a unique hypothesis about their immunopathogenic relationship. Case 1: A 27 year old Caucasian female with a 4-year history of CD, whose biologic therapy had been held during pregnancy, presented to our hospital with an abdominal abscess and obstruction. After discharge, her biologic therapy was resumed. Two months later, she had improvement in her CD symptoms but reported new symptoms of solid food dysphagia. EGD revealed changes compatible with EoE. After an 8-week proton pump inhibitor trial, repeat esophageal biopsies showed persistent eosinophilia consistent with a diagnosis of EoE. Case 2: A 30 year old Caucasian male with a history of EoE well controlled on topical budesonide presented to our clinic for a second opinion regarding his 5-year history of fistulizing CD on methotrexate. EGD and colonoscopy confirmed quiescent EoE but active Crohn's ileitis. History was remarkable for several failed CD therapies including immunomodulators and biologics, over which time his EoE remained well controlled. He was subsequently placed on vedolizumab for CD, and topical budesonide was continued for EoE. While it is accepted that CD and EoE are driven primarily by Th1 and Th2-mediated immune responses, respectively, much of the pathophysiology of these two conditions is not yet fully understood. These responses are fostered by differing and often competing cytokine profiles, and it is therefore conceivable that a Th1-mediated condition could help quell a Th2-mediated condition, and vice versa. This is supported by recent advances via epigenetics studies in patients with EoE and inflammatory bowel disease. Our cases present two young, Caucasian patients with co-existent severe CD and EoE. In each case, one of the conditions is quiescent while the other is exacerbated. Patient 1, developed symptoms leading to the diagnosis of EoE only after her CD went into remission with aggressive biologic therapy. Patient 2 manifested treatment-refractory CD when his EoE was well controlled. Our clinical observation questions whether treating one condition can worsen the other as the immune response shifts between Th1 and Th2, or, possibly, whether EoE could be a marker for aggressive CD. As evidenced by recent epigenetics studies, the answers to these questions are undoubtedly complex. Until further advancements, it is important to recognize the potential interplay of diseases such as EoE and CD when managing these complex cases.

899 Endoscopic Esophageal Epiphrenic Diverticulum Inversion by Using the Submucosal Tunneling Technique

instances, a bipolar coagulation probe set at 25 watts was employed to progressively burn a tract into, but not through, the food boluses. Constant contact pressure with the center of the food bolus was crucial to avoid iatrogenic thermal injury to the surrounding mucosa. Next, a tri-prong anchor device was inserted and deployed into the tract. This ensured secure anchoring of the food bolus from within, ultimately allowing for successful en bloc bolus extraction via traction pull. Reinspection of the first patient’s esophagus demonstrated a narrowed esophageal lumen with linear furrows and circular rings, suggestive of eosinophilic esophagitis. Esophageal biopsies were obtained for confirmation of diagnosis. The second patient’s esophagus also demonstrated linear furrows and circular rings, consistent with his known history of eosinophilic esophagitis. Clinical Implications: Esophageal food impaction can be refractory to standard retrieval techniques despite prolonged efforts. In such instances, the newly described burn-anchor method can be useful at extracting the challenging food bolus in a relatively safe and efficient manner. We stress the importance of airway protection when attempting such maneuvers, as patient safety

Diagnostic yield of allergy testing in Pediatric Eosinophilic Esophagitis: a 10 year experience at a tertiary care centre

Background Eosinophilic Esophagitis (EoE) is a disease in children characterized by esophageal dysfunction and eosinophilic infiltration [1]. Patients frequently present with an atopic history; therefore, allergy testing by both skin prick and food patch testing are often performed. However, the utility of allergy testing remains unclear [1,3]. Treatment with topical corticosteroids may be needed for clinical and histologic improvement if allergic triggers are not identified [1,2]. However, the natural history of EoE suggests that this condition is chronic and may recur when corticosteroids are withdrawn [2]. Therefore, treatment with dietary/aeroallergen avoidance is preferable to reduce the need for oral corticosteroids, while preventing exacerbation of EoE [3]. This study aims to describe the atopic characteristics of a pediatric cohort with EoE over a 10 year period at a tertiary care center.

Adult versus pediatric eosinophilic esophagitis: important differences and similarities for the clinician to understand

Eosinophilic esophagitis (EoE) is recognized as a common, allergy-associated cause of chronic esophageal symptoms affecting both children and adults. Research has begun to shed light on its epidemiology with consistent results from various geographical areas. Differences in clinical presentation, endoscopic aspects and response to treatment have all been reported for patients of different ages, and the question as to whether adult and pediatric EoE are manifestations of a single entity or in fact two distinct disorders has been posed. The most relevant differences between pediatric and adult EoE come from evolutionary changes in the consequences of the disease, including fibrous remodeling, and the ability to express symptoms. However, most studies support a common pathogenesis and similar histopathological features for adult and pediatric patients, being the same diagnostic criteria applied to them. This article comprehensively reviews the most recently published information and addresses important questions about the natural history of EoE.

Intramural esophageal dissection after trans-esophageal echocardiogram

A 31-year-old man with history of eosinophilic esophagitis, maintained on topical fluticasone, was admitted with Staphylococcus aureus bacteremia. The patient had no dysphagia at presentation. He underwent trans-thoracic echocardiogram, which was inconclusive for vegetations. Trans-esophageal echocardiogram (TEE) was attempted, but was unsuccessful. At the third attempt to advance the 13mm probe beyond 30cm from the incisors, he developed chest pain followed by hematemesis. The procedure was terminated.

Eosinophilic Esophagitis

Eosinophilic esophagitis (EE) is a recently recognized form of pan-esophagitis, which is characterized by the presence of at least 15 eosinophils per high power field on esophageal histology. EE is closely associated with atopic disorders and occurs predominantly in male patients. Young children are more likely to be sensitized to food allergens whilst aeroallergen sensitization predominates in older children and adults--a pattern reminiscent of the "atopic march". EE presents with a diverse range of gastrointestinal symptoms, including regurgitation, vomiting, feeding difficulties or refusal in infancy, in addition to dysphagia and food bolus impaction in older children and adults. The diagnosis may also be ascertained incidentally in patients undergoing gastroscopy for other suspected gastrointestinal conditions, such as gastroesophageal reflux disease or celiac disease. Complications mainly relate to subepithelial remodeling and fibrosis which may result in dysmotility, dysphagia and esophageal strictures. The proportion of EE patients at risk of these complications is unknown due to a paucity of data on the natural history of EE. There are only few randomized controlled trials assessing the efficacy of treatment modalities for EE, which currently either involve food allergen elimination or use of swallowed aerosolized corticosteroids. This article aims to discuss the complex issues of the diagnosis and long-term management that confront clinicians who care for children with EE.

Progression of Symptoms and Endoscopic Findings with Age: Clues of the Natural History of Eosinophilic Esophagitis?

Progression of Symptoms and Endoscopic Findings with Age: Clues of the Natural History of Eosinophilic Esophagitis?

Combined Reflection Confocal Microscopy and Optical Coherence Tomography Imaging of Esophageal Biopsy

Reflection confocal microscopy (RCM) and optical coherence tomography (OCT) are two non-contact optical imaging technologies that provide images of tissue cellular and architectural morphology, which are both used for histopathologic diagnosis. We have developed a combined RCM and OCT system to compare the accuracy of these imaging techniques for diagnosing esophageal pathology and to evaluate the potential utility of merging the two modalities into a single imaging system. Clinical study was conducted on 32 human esophageal biopsy samples from 23 patients with various histories. Esophageal mucosa was differentiated from gastric mucosa, Barrett's esophagus with intestinal metaplasia was distinguished from normal esophagus, and eosinophils were distinguished from normal squamous cells in a patient with the history of eosinophilic esophagitis. Preliminary results demonstrate the feasibility of a co-registered multimodal RCM-OCT device and the potential of this combined technology to provide significantly more information about the microscopic morphology of tissue than either technique alone.