Idiopathic Eosinophilic Esophagitis Research Articles

COMPLICATIONS OF EOSINOPHILIC ESOPHAGITIS

SESSION TITLE: Medical Student/Resident Cardiothoracic Surgery Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Idiopathic eosinophilic esophagitis is a chronic immune mediated eosinophilic infiltration of the esophageal mucosa. Clinical presentation is in the form of dysphagia and esophageal food impaction (1). Esophageal dissection is a complication which can occur spontaneously or secondary to a clinical complication of food impaction, Boerhaave syndrome or diagnostic and therapeutic interventions. Case reports have highlighted esophageal dissection including spontaneous dissection (2). Association between chronic inflammatory conditions and thromboembolism is well known, however there is only one case report of venous thromboembolism (VTE) occurring in eosinophilic esophagitis (3). CASE PRESENTATION: A 40-year-old male with no known past medical history presented to our emergency department with complaints of continuous chest pain, persistent emesis (occasionally blood tinged), dysphagia and odynophagia after eating ribs at a barbeque one day prior. The patient had no reported history of allergies, atopy, rhinitis, or asthma. Laboratory evaluation revealed leukocytosis of 11.0 k/uL with an eosinophil percentage of 1.8%. CT chest revealed food impaction in the esophagus with an incidental finding of right upper lobe acute pulmonary emboli (PE). The patient was admitted to the MICU for emergent endoscopy which revealed a large mucosal tear and food bolus impaction in the distal esophagus. Cold biopsies were taken. Patient was started on a heparin drip in MICU. Persistent chest pain led to an esophageal barium study which showed a double barrel sign suggestive of intramural esophageal dissection. Cardiothoracic surgery was consulted, patient was kept NPO for 72 hours and treated with a proton pump inhibitor for spontaneous resolution of esophageal dissection. Repeat esophageal barium study confirmed resolution and patient was restarted on enteral nutrition. The patient was discharged after being able to tolerate a soft diet and switched to an oral anticoagulation agent. Following up in two weeks, the patient remained asymptomatic and biopsy confirmed eosinophilic esophagitis. DISCUSSION: To our knowledge, this is the first reported case in which a patient presented with all of the above categories of complications, both local (food impaction and esophageal dissection) and systemic (VTE). This unique clinical presentation made the medical management increasingly challenging. In our case the patient was started on a heparin drip in the MICU for continuous monitoring in case the need for emergent repeat endoscopy or surgical intervention arose. Though conservative management with proton pump inhibitors and nil per mouth is the mainstay of management, surgery must be considered if esophageal perforation or mediastinal abscess occur. CONCLUSIONS: Surgery must be considered if esophageal perforation or mediastinal abscess occur. Reference #1: 1. Desai TK1, Stecevic V, Chang CH, Goldstein NS, Badizadegan K, Furuta GT. Association of eosinophilic inflammation with esophageal food impaction in adults. Gastrointest Endosc. 2005 Jun;61(7):795-801. Reference #2: 2. Straumann A1, Bussmann C, Zuber M, Vannini S, Simon HU, Schoepfer A. Eosinophilic esophagitis: analysis of food impaction and perforation in 251 adolescent and adult patients. Clin Gastroenterol Hepatol. 2008 May;6(5):598-600. doi: 10.1016/j.cgh.2008.02.003. Epub 2008 Apr 14 Reference #3: 3. Patricia D. Jonesa, b Stephan Mollc Evan S. Dellona, b. Pulmonary Embolism in a Patient with Eosinophilic Esophagitis: Causal or Coincidental? Case Rep Gastroenterol 2013;7:82–88 DISCLOSURES: No relevant relationships by Michael Hoffman, source=Web Response No relevant relationships by Benjamin Mba, source=Web Response No relevant relationships by Heba Naseem, source=Web Response No relevant relationships by Rabab Nasim, source=Web Response No relevant relationships by Marcus Stammen, source=Web Response

PPI Trial for Eosinophilic Esophagitis: Chaos in the Community.

Despite consensus eosinophilic esophagitis (EoE) statement published in 2011 calling for a 2-month trial of protons pump inhibitor (PPI), the guidelines are not followed by many. We studied the practice patterns in our community and response to a PPI retrial in patients previously diagnosed with "idiopathic EoE." All patients presenting to the senior author's practice with suspected EoE from 2011 to 2015. Two cohorts were studied: (1) patients diagnosed in the community as "idiopathic EoE"; (2) treatment naïve patients given a PPI trial at University of South Florida. PPI responsive eosinophilia was defined after 2 months of high dose PPIs after initial diagnosis of mucosal eosinophilia and histologic response of <15 eosinophils per HPF. SPSS v19.0 was used to calculate mean difference and odds ratios (OR) and 95% confidence intervals. In total, 78 patients met inclusion criteria, 46 patients had outside diagnosis of "idiopathic EoE," and 41 patients received a PPI trial at University of South Florida. In total, 34/46 (73.9%) community patients were placed on a PPI, 3/46 (6.5%) were placed on elimination diets, 31/46 (67.4%) steroids, and 21/46 (45.7%) were treated with both steroids/PPIs. Fewer patients received PPI trials in the community 3/46 (6.5%) versus 26/34 (76.5%) at our center [OR, 46.6 (95% CI, 11.3-191.5); P<0.0001]. In total, 12/26 (46.2%) were PPI responders on our retrial despite previously being diagnosed with idiopathic EoE. The group initially diagnosed at our center had a higher PPI response rate 12/15 (80%) versus 12/26 (46.2%) in the community group [OR, 7.58 (1.42, 40.55; P=0.018)]. The importance of a PPI trial is misunderstood and may be confused with the more traditional PPI trial for gastroesophageal reflux disease. This algorithm is critical and should be done before empiric steroids/diet therapies.

You Are What You Eat: A Case of Nematode-Induced Eosinophilic Esophagitis

A 41 year old man with a past medical history of allergic rhinitis and asthma presented to gastroenterology clinic for the evaluation of dysphagia that had developed over the previous year. He had difficulty swallowing solids especially thick solids like steak. He did not have any difficulty with swallowing liquids or soft foods. His symptoms were intermittent. He otherwise denied chest pain, regurgitation and nausea. He subsequently underwent upper GI endoscopy. The findings in his esophagus were significant for ringed esophagus, longitudinal furrows and white plaques in the entire esophagus concerning for eosinophilic esophagitis. In the stomach, a roundworm was found and removed. Pathology of the esophagus was significant for 100 eosinophils per high-power field in all biopsies. In addition, the worm was identified as nematode, likely Anisakidae species. Of note, patient did not have peripheral eosinophilia. Due to the findings of Anisakiasis, patient was treated with a 6-week course of Albendazole. He subsequently underwent repeat upper GI endoscopy after completion of his anti-parasitic treatment. The esophageal mucosal findings were improved from initial endoscopy with pathology showing marked improvement in mucosal eosinophilia of only 9 eosinophils per high-power field. In addition, patient's dysphagic symptoms also improved. This is the first case report of Nematode-induced eosinophilic esophagitis which improved with anti-parasitic treatment.Figure 1Figure 2Figure 3Human anisakiasis is acquired through eating raw fish. Infestation with living larvae caused by eating parasitized fish often times results in gastroenteritis with cases reported in the literature. This is often characterized by peripheral eosinophilia along with eosinophilic infiltration of the digestive tract and nonspecific gastrointestinal symptoms of abdominal pain, vomiting and diarrhea. It mainly involves the stomach and small intestine with no reported cases of eosinophilic esophagitis caused by Anisakidea. The symptoms of anisakiasis-induced eosinophilic esophagitis overlap with idiopathic eosinophilic esophagitis and therefore there has to be a high index of suspicion for nematode as a potential etiology of eosinophilia as this will affect the patient's management. This is especially important as endoscopic removal of the larvae is the first step in the treatment of eosinophilic esophagitis in addition to antiparasitic medications.

Current Management of Eosinophilic Esophagitis 2015.

Eosinophilic esophagitis (EoE) is a chronic inflammatory condition characterized by esophageal dysfunction and eosinophilic infiltrate (≥15/hpf) in the esophageal epithelium and the absence of other potential causes of eosinophilia. The prevalence is increasing and is the most common cause of solid food dysphagia in children and young adults. This article will review the diagnosis and management of EoE based on consensus conferences, systematic reviews, and meta-analysis and highlights seminal studies in our evolving treatment of this disease. However, all answers are not available and I will remark about the lessons learned in my clinical practice seeing EoE patients over the last 25 years. The complicated etiology of the complaint of dysphagia in EoE patients will be reviewed. The importance of utilizing endoscopy, biopsies, and barium esophagram to help define the 2 phenotypes (inflammatory, fibrostenosis) of EoE will be highlighted. The controversy about PPI-responsive esophageal eosinophilia will be discussed and contrasted with idiopathic EoE. Finally, the 3 treatment options for EoE (drugs, diet, dilation) will be reviewed in detail and a useful clinical management algorithm presented.

The natural history of steroid-naïve eosinophilic esophagitis in adults treated with endoscopic dilation and proton pump inhibitor therapy over a mean duration of nearly 14 years

Despite the vast focus of research in eosinophilic esophagitis (EoE), the natural history of untreated EoE remains undefined. Current expert consensus panels are calling for natural history studies to define long-term risks, adverse events, and progression of the disease. To address the natural course and long-term adverse events of EoE. Retrospective, single-center study. Tertiary-care center. A cohort of patients from the year 1988 initially diagnosed as having congenital esophageal stenosis who were later reclassified as having EoE. Ninety-five patients, with 13 meeting entrance criteria for idiopathic EoE with follow-up >5 years. Anti-acids and esophageal dilation. Clinical response, adverse events, long-term clinical outcomes, and progression of disease. Thirteen patients (mean age at diagnosis 30.3 years, 10 male) were evaluated over a 13.6-year mean follow-up (range 5-24 years). All patients experienced daily dysphagia, with 12 presenting with food impactions. Patients were treated with esophageal dilation (64% Maloney, 34% Savary, 2.5% through-the-scope balloon) and daily anti-acids. Patients were initially treated with an average of 3.2 dilations over the first year (range 1-6) to achieve a luminal size of 15.8mm (range 14-18mm). They were maintained successfully with dilations every 2 years, on average, based on symptoms. Two patients not adhering to recommended dilation schedules experienced repeat impactions. One adverse event from a mucosal tear required hospitalization (1 of 157, 0.6%). Seven of 13 had Barrett's esophagus, average length 2.4 cm (range 1-4 cm), 3 on initial EGD and 4 identified over a mean duration of 9.4 years. No patient developed dysplasia or malignancy. Retrospective, small sample. The course of EoE over a 13.6-year mean duration, although persistent, appears benign and not associated with cancer risk. A program of regular esophageal dilations based on symptom recurrence appears to be a safe, long-term treatment.

The Small-Caliber Esophagus: Radiographic Sign of Idiopathic Eosinophilic Esophagitis

To evaluate a small-caliber esophagus at barium esophagography with idiopathic eosinophilic esophagitis (IEE) and determine if there is a useful threshold diameter for suggesting this diagnosis. The institutional review board approved this retrospective study and waived informed consent. This study was HIPAA compliant. A search of the radiology database (by using the search term small-caliber esophagus) revealed 10 patients with a small-caliber esophagus at barium esophagography who had IEE (defined as more than 20 eosinophils per high-power field in endoscopic biopsy specimens). Images were reviewed to characterize findings and determine the length of narrowing. Luminal diameters were measured at three levels for nine patients and nine control subjects, and mean diameter, range, and standard deviation were determined at each level. An analysis of variance test was performed to determine whether the difference between the range of mean thoracic esophageal diameters in patients with IEE versus that in control subjects was significant. All 10 patients had long-segment but variable-length narrowing of the thoracic esophagus (mean length, 15.4 cm) with tapered margins. The mean diameter at the aortic arch, carina, and one vertebral body above the gastroesophageal junction was 13.9, 14.3, and 15.1 mm, respectively, for patients with small-caliber esophagus versus 20.2, 30.3, and 28.7 mm for control subjects. The mean overall diameter was 14.7 mm for patients with small-caliber esophagus versus 26.3 mm for control subjects. In the nine patients in whom the luminal diameter was measured, the mean thoracic esophageal diameter was 20 mm or less; all nine control subjects had a mean thoracic esophageal diameter greater than 20 mm. The difference in the range of mean thoracic esophageal diameters between these two groups was highly significant (P < .0001), so 20 mm was a useful threshold diameter for suggesting this diagnosis. The small-caliber esophagus of IEE is characterized at barium esophagography by long-segment but variable-length narrowing of the thoracic esophagus, with a mean length of 15.4 cm, a diameter of 20 mm or less, smooth contours, and tapered margins.

High Intraepithelial Eosinophil Counts in Esophageal Squamous Epithelium Are Not Specific for Eosinophilic Esophagitis in Adults

The histologic criterion of >20 eosinophils per high power field (hpf) is presently believed to establish the diagnosis of idiopathic eosinophilic esophagitis (IEE). This is based on data that the number of intraepithelial eosinophils in gastroesophageal reflux disease (GERD) is less than 20/hpf. This study tests this belief. Pathology records were searched for patients who had an eosinophil count >20/hpf in an esophageal biopsy. This patient population was biased toward adults with GERD who had routine multilevel biopsies of the esophagus. The clinical, radiological, and manometric data and biopsies were studied. Forty patients out of a total of 3,648 reports examined had an eosinophil count >20/hpf in squamous epithelium of an esophageal biopsy. Analysis of these 40 cases indicated that 6 (15%) patients had IEE, 2 (5%) had coincident IEE and GERD, 28 (70%) had GERD, and 2 (5%) each had achalasia and diverticulum. There was no significant difference among these groups in terms of maximum eosinophil number, biopsy levels with >20 esoinophils/hpf, presence of eosinophilic microabscesses, involvement of surface layers by eosinophils, and severity of basal cell hyperplasia and dilated intercellular spaces. All histologic features presently ascribed to IEE can occur in other esophageal diseases, notably GERD. As such, the finding of intraepithelial eosinophilia in any number is not specific for IEE. When a patient with GERD has an esophageal biopsy with an eosinophil count >20/hpf, it does not mean that the patient has IEE.

Gastroesophageal Reflux Disease–Associated Esophagitis Induces Endogenous Cytokine Production Leading to Motor Abnormalities

Gastroesophageal reflux disease is a condition frequently associated with esophagitis and motor abnormalities. Recent evidence suggests that proinflammatory cytokines, such as interleukin (IL)-1beta and IL-6, may be implicated because they reduce esophageal muscle contractility, but these results derive from in vitro or animal models of esophagitis. This study used human esophageal cells and tissues to identify the cellular source of cytokines in human esophagitis investigate whether cytokines can be induced by gastric refluxate, and examine whether esophageal tissue- or cell-derived mediators affect muscle contractility. Endoscopic mucosal biopsy specimens were obtained from patients with and without esophagitis, organ-cultured, and undernatants were assessed for cytokine content. The cytokine profile of esophageal epithelial, fibroblast, and muscle cells was analyzed, and esophageal mucosa and cell products were tested in an esophageal circular muscle contraction assay. The mucosa of esophagitis patients produced significantly greater amounts of IL-1beta and IL-6 compared with those of control patients. Cultured esophageal epithelial cells produced IL-6, as did fibroblasts and muscle cells. Epithelial cells exposed to buffered, but not denatured, gastric juice produced IL-6. Undernatants of mucosal biopsy cultures from esophagitis patients reduced esophageal muscle contraction, as did supernatants from esophageal epithelial cell cultures. The human esophagus produces cytokines capable of reducing contractility of esophageal muscle cells. Exposure to gastric juice is sufficient to stimulate esophageal epithelial cells to produce IL-6, a cytokine able to alter esophageal contractility. These results indicate that classic cytokines are important mediators of the motor disturbances associated with human esophageal inflammation.

Idiopathic Eosinophilic Esophagitis and Eosinophilic Gastroenteritis Successfully Treated with Azathioprine or 6-Mercaptopurine

Background: Idiopathic eosinophilic esophagitis (EE) is an increasingly recognized inflammatory disorder of the esophagus. The inflammatory pattern of EE is predominately associated with a TH 2-type allergic response. The disease has often chronic recurrent character and requires long-term treatment with topical or systemic corticosteroids. The aim of our study was to determine whether in severe cases with long-term systemic corticosteroid-dependency an immuno-modulating treatment may have a steroid-sparing effect? Methods: In three patients with proven severe idiopathic EE (1/3 also suffered from eosinophilic gastroenteritis) and chronically corticosteroid-dependency, we prospectively studied the clinical and histological response under treatment with azathioprine (2mg/kg BW po/die) or 6-mercaptopurine (1mg/kg BW po/die). Results: All patients experienced both symptomatical and histological relapse once steroid doses were tapered on several occasions. After administration of azathioprine in 2 patients and 6-mercatopurine in one patient, steroids could be stopped in all 3 patients without clinical relapse. Subsequent histological examinations showed complete disappearance of eosinophilic infiltration over a time span of months up to 8 years. One patient who stopped his treatment with azathioprine relapsed and became again steroid-dependent. In the follow-up, steroids could be stopped again after azathioprine had been reinstituted. In one patient, high blood counts of eosinophilic cells had been originally measured which also disappeared under azathioprine treatment. Conclusions: In severe steroid-dependent cases of idiopathic eosinophilic esophagatis and eosinophilic gastroenteritis, an immuno-modulationg treatment with purine analogues may be an helpful alternative to glucocorticoid therapy. At least in our patients, long-term use of immuno-modulating drugs was overall well tolerated and decreased morbidity due to EE. It could be speculated that the beneficial effect of azathioprine/6-mercaptopurine in treating EE is associated with their pro-apoptotic effect on T-lymphocytes.

Idiopathic Eosinophilic Esophagitis in Adults: The Ringed Esophagus

To retrospectively assess the findings of idiopathic eosinophilic esophagitis (IEE) at barium studies and determine the frequency of the ringed esophagus in patients with this condition. The institutional review board approved all aspects of this retrospective study and did not require informed consent from patients whose records were included in the study. The study was compliant with the Health Insurance Portability and Accountability Act. A review of the pathology and radiology databases at the authors' institution revealed 14 patients (11 men and three women; mean age, 41.3 years) with IEE (defined as more than 20 eosinophils per high-power field in biopsy specimens) who had undergone barium studies and endoscopy. The radiographs were reviewed for strictures, esophagitis, or other abnormalities. The endoscopic reports, clinical records, and laboratory data were also reviewed and compared with the radiographic findings. Seven of the 14 patients (50%) had a history of allergies, and two of nine patients with complete blood cell counts (22%) had peripheral eosinophilia. Thirteen patients (93%) had dysphagia, six (43%) had food impactions, and six (43%) had reflux symptoms. Ten patients (71%) had a total of 11 strictures at barium studies (two in the upper part of the esophagus, two in the middle part, three in the distal part, one in the middle and distal parts, and three at the gastroesophageal junction). The strictures had a mean length of 5.1 cm. In seven patients (50%), the strictures contained multiple fixed ringlike indentations that produced a ringed esophagus. The ringlike indentations appeared as multiple, fixed, closely spaced, concentric rings traversing the stricture. Four patients (28%) had esophagitis. Of 13 patients who underwent recumbent imaging, 10 (77%) had hiatal hernias and nine (69%) had reflux. Eight of the 10 patients (80%) with strictures underwent endoscopic dilation procedures, which resulted in only temporary relief of dysphagia. The findings suggest that most patients with IEE have esophageal strictures, often with distinctive ringlike indentations that produce a ringed esophagus.

Three brothers with dysphagia caused by eosinophilic esophagitis

Idiopathic eosinophilic esophagitis (EE) is a chronic inflammatory disorder of the esophagus characterized by dense infiltration of eosinophils within the squamous epithelium. It is distinct from the eosinophilic infiltration of the esophagus associated with GERD and eosinophilic gastroenteritis. The pathogenesis of EE is not entirely clear. There is a strong association with allergies, and it may be a response to environmental allergens, particularly food allergens. Personal and family histories of allergic diseases were noted in 62% to 85% of patients. It is more frequently reported in pediatric patients but can be present at any age, and the incidence in adults appears to be increasing. More than three fourths of reported patients are maleda predilection not yet explained. This report describes 3 adult brothers with dysphagia; in all 3 cases, EE was ultimately diagnosed. Although the true prevalence of the EE is unclear, data from an Australian population suggest that it may be approximately 0.01%. If there is no familial component to the disease, the probability that 3 brothers would develop EE is 10 . Given the low probability of such an occurrence, our 3 patients highlight and suggest potential hereditary and genetic features in the pathogenesis of EE. This is an association that has not been reported.

Endoscopy in eosinophilic esophagitis: “feline” esophagus and perforation risk

Background & Aims : Idiopathic eosinophilic esophagitis is an underdiagnosed disease with typical endoscopic findings, which have not been well described. Methods : Charts and pathology reports at two tertiary care centers from June 1993 to April 2002 were reviewed to describe the endoscopic findings of this disease and to correlate them with clinical characteristics. Eight patients were identified as having eosinophilic esophagitis based on clinical symptoms and pathology reports. Results : Soft and subtle ring(s) in the esophagus were found in 7 of 8 patients. In 3 of 8 patients, the esophagus appeared rigid. Mucosal rents occurred with simple passage of the endoscope in 5 of 8 patients. One patient developed a perforation after simple passage of the endoscope. Endoscopic findings can be normal or very subtle in these patients, and the findings can easily be missed during endoscopy. Tearing of the esophagus can occur with simple passage of the endoscope or biopsy even in the absence of overt rings. A minimum of 8 weeks of medical therapy (proton pump inhibitor, histamine antagonists, immunosuppressants) should be undertaken before considering dilation because of the high risk involved with the procedure and the good response to medical therapy. Conclusions : We recommend considering dilation only in patients with eosinophilic esophagitis who do not respond to medical therapy and have rings that appear to be obstructing the lumen.

Infiltrating eosinophils and eotaxin: their association with idiopathic eosinophilic esophagitis

Idiopathic eosinophilic esophagitis (IEE) is a very rare disease characterized by thickening and eosinophil infiltration of the esophagus. The most potent chemotactic factor for eosinophils is eotaxin, and its pathophysiologic significance in IEE needs to be elucidated. To study the association between eotaxin and IEE. We examined eotaxin expression in the esophagus of an IEE patient in comparison to controls by immunohistochemistry using a monoclonal antibody for human eotaxin. We also measured the free eotaxin level and the total (free and bound-form) eotaxin level in blood by enzyme-linked immunosorbent assay before and after the initiation of steroid therapy. Most of the infiltrating eosinophils in the affected esophageal tissue showed immunohistochemical staining with anti-eotaxin antibody. In blood samples, the free eotaxin level was slightly elevated before treatment, whereas the total eotaxin level was within the normal range. Unexpectedly, the total eotaxin level increased dramatically after the initiation of steroid therapy, whereas the increase of free eotaxin was modest. Infiltrating eosinophils that express eotaxin and the changes of blood eotaxin levels during steroid therapy suggest that eotaxin may be associated with IEE.

Eosinophils express functional IL-13 in eosinophilic inflammatory diseases.

IL-13 is an immunoregulatory and effector cytokine in allergic diseases such as bronchial asthma. A variety of immune and non-immune cells are known as IL-13 producers. In this study we investigated whether and under what conditions human eosinophils generate IL-13. Freshly isolated highly purified peripheral blood eosinophils from patients with several eosinophilic inflammatory diseases and from normal control individuals were investigated. We observed that blood eosinophils from patients suffering from bronchial asthma, atopic dermatitis, parasitic infections, hypereosinophilic syndrome, and idiopathic eosinophilic esophagitis expressed IL-13, as assessed by ELISA, ELISPOT assay, flow cytometry, and immunocytochemistry. By using nasal polyp tissues and immunohistochemistry, we demonstrated IL-13 expression in eosinophils under in vivo conditions. In contrast, blood eosinophils from control individuals as well as blood neutrophils from both eosinophilic and control patients did not produce detectable IL-13 levels. However, when blood eosinophils from control individuals were stimulated with GM-CSF or IL-5 in vitro, they generated IL-13 mRNA and protein, suggesting that IL-13 expression by eosinophils under inflammatory conditions is a cytokine-driven process. Stimulation of blood eosinophils containing IL-13 by eotaxin resulted in a rapid release of this cytokine. Eosinophil-derived IL-13 was functional, as it increased the surface expression of the low affinity IgE receptor (CD23) on purified B cells. In conclusion, human eosinophils are able to produce and release functional IL-13 in eosinophilic inflammatory responses.

Idiopathic eosinophilic esophagitis is associated with a T-helper 2-type allergic inflammatory response

Idiopathic eosinophilic esophagitis is associated with a T-helper 2-type allergic inflammatory response

Idiopathic eosinophilic esophagitis is associated with a TH2-type allergic inflammatory response

Background: Idiopathic eosinophilic esophagitis (IEE) is a chronic-inflammatory disorder of the esophagus of unknown origin. The established cornerstone of diagnosis is a dense infiltration of the esophagus with eosinophils, but neither the precise pattern of inflammatory cell infiltration nor the mechanisms that likely contribute to induction and maintenance of the inflammatory response have been described. Objective: The intention of this study was to characterize the esophageal inflammatory infiltrate and the expression of cytokines in the esophagus in this disease. In addition, we searched for immunologic abnormalities of blood leukocytes to exclude major primary hyporeactive and hyperreactive conditions of the immune system. Methods: Infiltration of inflammatory cells in the esophagus, stomach, and duodenum was analyzed by immunohistochemistry through use of mAbs against lineage-associated molecules. Cytokine expression was measured by ELISA and immunohistochemical analysis. Lymphocyte subpopulations in blood were determined by means of flow cytometry. Results: High eosinophil infiltration into the esophageal squamous epithelium was observed in patients with IEE but not in control subjects. Interestingly, increased T-cell and mast cell numbers were also found within the epithelium in these patients. In contrast, the numbers of inflammatory cells were not increased in the stomach and duodenum in patients with IEE, suggesting a specific inflammatory process within the esophagus. Moreover, increased expression of IL-5 and TNF-α was observed in esophageal epithelial biopsy specimens. The distribution of lymphocyte subsets in the peripheral blood and their capacity to generate cytokines did not reflect the changes observed at the inflammatory site. Conclusions: IEE is a selective inflammatory response of the esophagus. T cells, IL-5, eosinophils, and IgE-mediated mechanisms appear to be involved, giving rise to the possibility that allergic reactions might play a role in the pathogenesis of the disease. (J Allergy Clin Immunol 2001;108:954-61.)

EUS and histopathologic correlates in eosinophilic esophagitis

Idiopathic eosinophilic esophagitis is part of a continuum of disorders that comprise eosinophilic gastroenteritis, a condition characterized by eosinophilic infiltration of the GI tract. 1 Talley NJ. Eosinophilic gastroenteritis. in: 6th ed. Sleisenger and Fordtran's gastrointestinal and liver disease. : WB Saunders Co, Philadelphia1998: 1679-1688 Google Scholar This is a presentation of a case of eosinophilic esophagitis and a review of published information regarding this disorder. This case highlights several unique features of this rare entity, including EUS findings not previously described.

Eosinophilic esophagitis: A subset of eosinophilic gastroenteritis.

Eosinophilic gastroenteritis (EG) was first described over 50 years ago. Despite its long history, it remains an ill-defined and poorly understood entity. EG can present in a number of ways, none of which are exclusive to the disorder. EG has features of allergy and immune dysregulation but does not clearly fit into the category of allergic or immune disorder. While EG has been reported to affect all locations and layers of the gastrointestinal tract, the vast majority of reported cases have demonstrated mucosal involvement of the gastric antrum and small intestine in addition to disease activity of other locations of the gastrointestinal tract. Recently, several reports have identified a disease consisting of an isolated esophageal eosinophilia. Eosinophilic esophagitis (EE), also known as primary eosinophilic esophagitis or idiopathic eosinophilic esophagitis, occurs in adults and in children and represents a subset of EG with an isolated severe esophageal eosinophilia. Patients with EE present with symptoms similar to those of gastroesophageal reflux but are unresponsive to antireflux medication. Reports have demonstrated that patients with EE respond to either dietary restriction or corticosteroids.

Eosinophil derived major basic protein deposition occurs in idiopathic eosinophilic esophagitis

Eosinophil derived major basic protein deposition occurs in idiopathic eosinophilic esophagitis

A case of idiopathic eosinophilic esophagitis with CT findings showing marked thickening of the esophageal wall.

A case of idiopathic eosinophilic esophagitis with CT findings showing marked thickening of the esophageal wall.