An esophageal stricture is one of the complications that may develop during cancer treatment in children. Although more commonly associated with radiotherapy, recurrent mucositis has also been implicated. Presented herein is a case of a patient with acute lymphoblastic leukemia who suffered recurrent attacks of severe mucositis. Initial management of ensuing dysphagia included antifungal treatment for candida esophagitis. A subsequent upper endoscopy due to persistence of dysphagia revealed the presence of an esophageal stricture. Our aim in presenting this case is to emphasize the importance of considering a diagnosis of esophageal stricture in patients receiving anti-cancer treatment; early endoscopic intervention may be warranted in some patients.

Background.

Specific dietary components have been associated with gastroesophageal reflux disease (GERD) in Europe and the United States. However, the relationship between dietary components and GERD in Chinese still remains unclear. Methods. A total of 268 patients who were newly diagnosed as reflux esophagitis (RE) in Outpatient Endoscopy Center of Tongji Hospital were recruited. In addition, 269 sex- and age-matched subjects were also recruited as controls. The body measurements were determined, and the dietary intake during the previous year was evaluated using food frequency questionnaire (FFQ). Stepwise multiple logistic regression analysis was performed to examine the association between nutrients and RE.

Results.

After adjustment for WC, WHR, total energy intake, and demographics, there were a positive dose-response relationship between RE and calcium, meat, oils, and salt and a negative dose-response relationship between RE and protein, carbohydrate, calories from protein (%), vitamin C, grains and potatoes, fruits, and eggs.

Conclusion.

High intake of meat, oils, salt, and calcium is associated with an increased risk for RE while high intake of protein, carbohydrate, calories from protein (%), vitamin C, grains and potatoes, fruits, and eggs correlates with a reduced risk for RE.

PURPOSE OF REVIEW:

With the increasing recognition of eosinophilic esophagitis (EoE) over the past two decades, pharmacologic and dietary therapies have emerged as primary management options. The effectiveness of the elimination dietary therapy supports the conceptual definition of EoE as an antigen/immune-mediated esophageal disease. This manuscript reviews the three types of dietary therapy: an elemental formula diet with complete elimination of table foods, an allergy testing-directed elimination diet and an empiric elimination diet based on common food allergens.

RECENT FINDINGS:

Recent prospective studies have demonstrated symptomatic and histologic response to an elimination diet in adults with EoE that is comparable with response rates previously reported in children. Retrospective, comparative data in pediatric EoE have identified the elemental diet as offering the greatest likelihood of histologic disease remission compared with either allergy testing-directed or empiric elimination diets. The long-term goal of each dietary approach is the eventual identification of a single or limited number of trigger foods, thereby allowing a return to as regular a diet as possible.

SUMMARY:

Studies continue to support dietary therapy as an important and effective therapy for EoE. Although topical steroids continue to be a mainstay of therapy, none are presently Food and Drug Administration-approved for EoE. In addition, many patients are reluctant to utilize pharmacologic therapy on a chronic basis. Further research is necessary to better understand and optimize the use of diet therapy for EoE.

Several studies have shown that interleukin (IL)-13 is induced in the esophageal biopsies of eosinophilic esophagitis (EoE) patients and promotes esophageal eosinophilia in mice, following an IL-13 challenge. However, the role of IL-13 has not been clearly investigated in allergen-induced EoE. Accordingly, we tested the hypothesis that IL-13 is required in allergen-induced EoE. Mice deficient in IL-13, STAT (signal transducer and activator of transcription)6 and both IL-4/IL-13 genes with their respective controls were challenged with Aspergillus extract, and IL-5 gene deficient with their control were challenged with recombinant IL-13, intranasally. The lung and esophageal eosinophils, mast cells and collagen accumulation were examined. Herein, we report that intranasal delivery of IL-13 promotes IL-5-dependent esophageal eosinophilia. However, allergen-induced EoE is not impaired in the IL-13 gene-deficient mice. In addition, wild-type and IL-13 gene-deficient mice demonstrated a comparable level of mast cells and collagen accumulation in the esophagus, following allergen-induced experimental EoE. Similarly, we found that esophageal eosinophilia in IL-4/IL-13 double gene-deficient and STAT6 gene-deficient mice were also not reduced following allergen-induced experimental EoE. In contrast, lung eosinophilia was significantly reduced in mice deficient in IL-13, both IL-4/IL-13 and STAT6 genes following allergen challenge. In conclusion, our data establish that allergen-induced EoE pathogenesis is independent of IL-13, whereas IL-13 is required for allergen-induced lung eosinophilia.Immunology and Cell Biology advance online publication, 21 May 2013; doi:10.1038/icb.2013.21.

GOALS:: To evaluate sources of upper gastrointestinal bleeding (UGIB) at an urban US hospital and compare them to sources at the same center 20 years ago, and to assess clinical outcomes related to source of UGIB.

BACKGROUND::

Recent studies suggest changes in causes and outcomes of UGIB. STUDY:: Consecutive patients with hematemesis, melena, and/or hematochezia undergoing upper endoscopy with an identified source at LA County+USC Medical Center from January 2005 to June 2011 were identified retrospectively.

RESULTS::

Mean age of the 1929 patients was 52 years; 75% were male. A total of 1073 (55%) presented with hematemesis, 809 (42%) with melena alone, and 47 (2%) with hematochezia alone. The most common causes were ulcers in 654 patients (34%), varices in 633 (33%), and erosive esophagitis in 156 (8%), compared with 43%, 33%, and 2% in 1991. During hospitalization, 207 (10.7%) patients required repeat endoscopy for UGIB (10.6% for both ulcers and varices) and 129 (6.7%) died (5.2% for ulcers; 9.2% for varices). On multivariate analysis, hematemesis (OR=1.38; 95% CI, 1.04-1.88) and having insurance (OR=1.44; 95% CI, 1.07-1.94) were associated with repeat endoscopy for UGIB. Varices (OR=1.53; 95% CI, 1.05-2.22) and having insurance (OR=4.53; 95% CI, 2.84-7.24) were associated with mortality.

CONCLUSION:

: Peptic ulcers decreased modestly over 2 decades, whereas varices continue as a common cause of UGIB at an urban hospital serving lower socioeconomic patients. Inpatient mortality, but not rebleeding requiring endoscopy, was higher with variceal than nonvariceal UGIB, indicating patients with variceal UGIB remain at risk of death from decompensation of underlying illness even after successful control of bleeding.

BACKGROUND:

To identify dose-volume parameters predictive for severity of acute esophagitis (CTC > grade 2) in locally-advanced non small-cell lung cancer (LA-NSCLC) patients treated with neoadjuvant concurrent hyperfractionated-accelerated chemoradiotherapy (HA-CRT) a retrospective analysis was performed. 88 patients were treated with HA-CRT followed by radical surgery. Predictive power of absolute oesophageal length, absolute and relative oesophageal volume included in the 95%-isodose, patient- and tumor-related factors for severity of acute esophagitis was assessed.

FINDINGS:

A total of 82 patients (93%) developed radiation-induced acute esophagitis. Grade 1 was documented in 1 (1%), grade 2 in 55 (67%), grade 3 in 23 (28%) and grade 4 in 3 (4%) patients, respectively. Absolute oesophageal volume included in the 95%-isodose (42.8 Gy) achieved 13.5 cm3 (range: 3 -- 29 cm3). Of the tested variables in univariate analysis, absolute oesophageal volume included in the 95%-Isodose was found to be the only significant variable (p = 0.03) predicting severe acute esophagitis (CTC > grade 2). For this volume a gradation scale of the likelihood of severity was built.

CONCLUSION:

Increase of absolute oesophageal volume included in the 95%-isodose correlates with severity of acute esophagitis in LA-NSCLC patients treated with neo-adjuvant concurrent HA-CRT.

Barrett's esophagus is characterized by the replacement of squamous epithelium by columnar epithelium that is intestinal metaplasia-positive or -negative in the distal esophagus. Gastroesophageal reflux disease, which is frequent and prolonged in esophageal atresia, probably plays a major role in the development of Barrett's esophagus through repeated mucosal damage. Long-term acid exposure contributes to carcinogenesis in Barrett's esophagus of intestinal type, but its effect on gastric metaplasia is less well defined. Recent studies have suggest that metaplasia arises in about 15% of patients with esophageal atresia, with a lag time to developing metaplasia from initial surgical correction of about 10 years. Preliminary data from an ongoing multicenter study including 88 patients with esophageal atresia aged 15-19 years showed gastric metaplasia in 42% of patients (29 fundic and 7 cardial metaplasia), while one patient presented intestinal metaplasia. Esophageal mucosal abnormalities can be observed in esophageal atresia patients at endoscopy despite the absence of symptoms. Whether prolonged, aggressive, acid suppression is beneficial in these situations remains to be determined. Barrett's metaplasia can be removed by endoscopic mucosal resection or destroyed with endoscopic ablative techniques, such as photodynamic therapy, radiofrequency ablation, and cryotherapy. The risk of developing esophageal carcinoma is still a controversial issue as only a few clinical cases have been reported in young adults with esophageal atresia. As late complications of esophageal atresia, particularly esophagitis and Barrett's esophagus, are increasingly being recognized, long-time systematic follow up of the esophageal mucosa including multistage biopsies is therefore required even in asymptomatic patients.

Esophageal dysmotility is a considerable long-term issue in patients born with esophageal atresia (EA). To better characterize it, the normal esophageal motility is briefly reviewed with emphasis on the specific defects in EA. Multiple studies attempted to describe the dysmotility seen in patients with operated EA using esophageal manometry. Recently, high-resolution manometry has improved our understanding of normal esophageal motility. Using this new technology, it is now possible to better characterize the esophageal motility of patients operated on for EA. Three different patterns are described and presented: aperistalsis, pressurization, and distal peristalsis. Up to now, it has not been possible to find a correlation between the dysmotility severity and the patient's symptomatology. Different pathophysiological hypotheses of esophageal dysmotility in that population are discussed. Developmental neuronal defects are certainly present from the beginning. Surgical trauma can also contribute to the dysmotility. Finally, defective esophageal acid clearance capacity is a cause of gastroesophageal reflux disease, but the resultant esophagitis can also impair the normal esophageal function. The evolution of esophageal dysmotility in patients with repaired EA is not known and further studies will be necessary to clarify it.

Streptocara spp. infections are reported to cause gastritis, proventriculitis, esophagitis, and pharyngitis in various waterfowls, especially diving ducks. In the present paper, we describe severe fatal diphtheritic pharyngitis and esophagitis caused by Streptocara incognita in three female mute swans (Cygnus olor) in Bosnia and Herzegovina. Prior to death, the swans were showing signs of lethargy, anorexia, and reluctance to move. At necropsy, in all swans severe diphtheritic pharyngitis and esophagitis with deep, dark red hemorrhagic ulcerations were observed. Numerous thin, white, up to 1-cm-long nematodes, identified as S. incognita, were observed embedded in the pharyngeal and esophageal mucosa under the diphtheritic membranes. Histopathology revealed severe fibrinonecrotic inflammation with numerous cross-sections of the parasites. To the authors' knowledge, this is the first report of severe, fatal streptocariasis in mute swans.