bluuebunny/crossref_metadata_2025_split huggingface dataset:
A139 SUBMUCOSAL TUNNELING ENDOSCOPIC RESECTION (STER) FOR ESOPHAGEAL GIST: A CASE REPORT
Authors: DASHTI A , Jiang S X , Winter R , Trasolini R 
Published: February 2025

Abstract

Background
Gastrointestinal stromal tumors (GISTs) are rare mesenchymal tumors found throughout the gastrointestinal tract, with esophageal GISTs being particularly uncommon. Surgical resection is the standard treatment option, though it is associated with significant morbidity. Submucosal Tunneling Endoscopic Resection (STER) is a minimally invasive technique for per-oral subepithelial tumor removal with preservation of the surrounding esophagus and no need for thoracoscopy or mediastinoscopy. Herein, we report a successful case of STER for esophageal GIST in an elderly Canadian patient.

Aims
To present the successful management of an esophageal GIST using submucosal tunneling endoscopic resection.

Methods
Case report and literature review.

Results: Case Report
An 80-year-old man with dysphagia underwent an EUS for a 1.5 cm subepithelial lesion identified in his mid-esophagus on EGD. EUS showed a hypoechoic lesion arising from the muscularis propria. Biopsy confirmed a spindle cell tumor, C-KIT positive consistent with GIST. The patient was offered transthoracic surgical resection but declined given the associated risks and complications. An interval CT scan demonstrated a 4 mm increase in the size of the tumor. The patient was referred for consideration of endoscopic resection. He ultimately underwent submucosal tunneled endoscopic resection of the GIST with no complications. The procedure was performed by creating a mucosal flap over the GIST via submucosal tunnelling with subsequent traction assisted full thickness myotomy surrounding the lesion while preserving the capsule, followed by clip closure of the mucosotomy. Pathology confirmed R0 resection with low mitotic rate. A routine esophagram post-procedure showed no contrast leakage, and the patient was discharged the following day.

Literature Review
STER is a minimally invasive technique for resection of gastrointestinal subepithelial lesions first reported in 2012. It offers several advantages including preservation of GI tract function, rapid recovery time, and low adverse event rate but requires careful lesion selection and technical facility with endoscopic submucosal dissection, myotomy and defect closure. Studies have demonstrated high rates of complete resection with low complication risks, particularly in treating small to medium-sized tumors. To our knowledge, this case represents the first reported use of STER in Canada.

Conclusions: Conclusions
STER is a minimally invasive option for resection of subepithelial lesions. In this case it was used effectively with readily available equipment in a Canadian hospital. It reduces recovery time, preserves esophageal structure, and minimizes complications.

Funding Agencies
None
A141 TREATMENT OPTIONS FOR LYMPHOCYTIC ESOPHAGITIS: A SYSTEMATIC REVIEW OF CASE REPORTS AND CASE SERIES
Authors: Nguyen B A , Jowhari F 
Published: February 2025

Abstract

Background
Lymphocytic esophagitis (LyE) is a novel rare disorder characterized by intraepithelial lymphocytic infiltration of the esophagus in a peripapillary distribution without granulocytes, first described by Rubio et al. in 2006. No systematic reviews or randomized controlled trials have been published to date on the treatment options for LyE.

Aims
To describe the current state of evidence published to date for the treatment of lymphocytic esophagitis.

Methods
We performed a systematic review according to PRISMA guidelines, searching MEDLINE, Embase, Scopus, and Web of Science. Descriptive statistics were performed after extracting data on the study design, patient characteristics, treatment modalities, and outcomes (symptomatic, endoscopic, and histologic). The absence of randomized controlled trials and heterogeneity in outcome measures precluded the ability to perform a formal meta-analysis.

Results
A total of 39 articles (36 case reports, 3 case series) from 2012-2024 were selected for analysis. Proton pump inhibitors (PPIs) were the most common initial therapy used in 73.2% of patients (60/82), followed by topical steroids in 26.8% (22/82). A greater proportion of patients experienced a symptomatic, histologic and endoscopic response from initial use of topical steroids as monotherapy or part of PPI/Steroids combination therapy compared to PPIs alone. Histologic response was highest in the steroid monotherapy group (Table 1). Symptomatic recurrence was more common after initial use of topical steroids (as monotherapy or part of combination therapy) compared to PPIs alone (Table 1) but the samples sizes were very small. Initial endoscopic dilation improved symptoms in 90% (9/10) of patients and 66.7% (4/6) had successful stricture resolution, but 25% of patients experienced symptomatic recurrence. Other therapies for LyE included Vedolizumab, Botox injection, Sucralfate and Tacrolimus. The average follow-up duration was 8.98 months.

Conclusions
For patients with histologically confirmed LyE, both PPIs and topical steroids are viable options for symptomatic relief, with topical steroids showing higher symptomatic and histologic improvement. Balloon dilation may alleviate dysphagia in cases of obvious strictures. Given the limited available data, further research, including randomized controlled trials, is necessary to better define optimal treatment targets (histologic vs. symptomatic outcomes) and to formally compare treatment efficacies.
Table 1: Initial treatment response and symptomatic recurrence

Funding Agencies
None
A142 ENDOSCOPIC ULTRASOUND-GUIDED GASTROENTEROSTOMY: A CASE SERIES AND REVIEW OF LITERATURE
Authors: Shamatutu C , Trasolini R 
Published: February 2025

Abstract

Background
Gastric outlet obstruction (GOO) refers to the clinical syndrome of epigastric pain and postprandial vomiting due to mechanical obstruction in the distal stomach or proximal duodenum. Management is undertaken to alleviate symptoms with the aim of maintaining nutritional status and improving quality of life. Endoscopic gastroduodenal stenting and surgical gastroenterostomy (SGE) are two established methods in the management of GOO. Enteral stenting is associated with stent malfunction such as migration and obstruction often requiring reintervention; SGE is associated with a higher degree of morbidity and mortality compared to endoscopic approaches. Endoscopic ultrasound-guided gastroenterostomy (EUS-GE), with the placement of a lumen-apposing metallic stents (LAMS) from the stomach to the small bowel distal to the obstruction, has emerged as an alternative approach in the management of GOO.

Aims
To describes a case series of patients who underwent EUS-GE and review the relevant literature.

Methods
This was a single-centre retrospective case series of 9 patients with GOO who underwent EUS-GE at Vancouver General Hospital. We looked at technical success, clinical success, and adverse outcomes. Technical success was defined as ability to place a LAMS between the stomach and the small bowel. Clinical success was defined as the patient’s ability to tolerate oral intake.

Results
A total of 9 patients with GOO underwent EUS-GE. The median age was 65. 5 were females (55%) and 4 (45%) were males. GOO was due to malignant tumors or metastases in 8 cases (89%) and in one case was due to afferent limb syndrome after pancreaticoduodenectomy. The technical and clinical success rate was 100%. The stents had a diameter of 15 mm in 7 cases (77%). The stents had a saddle length of 10mm in 7 cases (77%). All cases were performed under general anesthesia. There were no adverse outcomes. The median time to discharge was 8 days. At the time of the study, 5 patients had deceased, with a mean survival of 17 weeks.
We identified two systematic reviews and meta-analyses looking at EUS-GE. The majority of data comes from retrospective studies. They assessed 285 and 260 patients. Technical success was achieved in 92-93.5% of cases, clinical success was achieved in 90% across both studies, adverse outcomes occurred in 12% of cases in both studies.

Conclusions
EUS-GE is an alternative endoscopic approach in the management of GOO with the ability to ameliorate symptoms of GOO and improve quality of life. It is less invasive than SGE and provides a more durable approach compared to endoscopic stenting. We describe a series of patients at VGH who underwent EUS-GE with a technical and clinical success rate similar to that described in the literature. Further randomized studies comparing the different modalities of treatment for GOO are needed.

Funding Agencies
None
A144 EOSINOPHILIC GASTRITIS: A SERIES OF CHILDREN FROM BC CHILDREN’S HOSPITAL USING NASPGHAN/ESPGHAN CRITERIA
Authors: Greaves A , Bush J , Avinashi V 
Published: February 2025

Abstract

Background
Eosinophilic gastritis (EoG) involves eosinophilic infiltration of the stomach, leading to symptoms without identifiable secondary causes. It can occur with Eosinophilic Esophagitis (EoE) or independently (non-EoE EGID). Common symptoms include abdominal pain, vomiting, fatigue, and edema. Recent North American Society of Pediatric Gastroenterology, Hepatology and Nutrition/European Society of Pediatric Gastroenterology, Hepatology and Nutrition (NASPGHAN/ESPGHAN) criteria (Jan 2024) define EoG as &gt;30 eosinophils per high-power field (hpf).

Aims
This study aimed to identify and review cases of gastric eosinophilia at BC Children’s Hospital over a five-year period, examining clinical details of those meeting the new NASPGHAN/ESPGHAN criteria.

Methods
Pathology reports from August 2019-2024 were reviewed to identify cases meeting EoG criteria. Clinical details, including symptoms, EoE association, food allergies, laboratory findings, and treatments, were analyzed.

Results
A total of 31 cases were identified, with 4 having secondary causes of eosinophilia (ulcers, liver transplant, Crohn’s disease). Of the remaining 27 EGID cases, 8 had both EoE and EoG, while 18 had non-EoE EGID (13 confined to the stomach, 5 involving both the stomach and duodenum).
1. Mean age: 6.3 years (EoE-EGID) vs. 8.7 years (non-EoE EGID)
2. Gender: EoE-EGID showed male predominance (67%), while non-EoE EGID was equally prevalent in males and females (50%).
3. IgE-based food allergies were common in both groups (58% vs. 67%).
4. Iron deficiency anemia was significantly more prevalent in non-EoE EGID (61% vs. 11%) and hypoalbuminemia (39% vs. 11%).
5. Nausea and vomiting were more frequent in EoE (55%), with dysphagia at 44%. Non-EoE cases had these symptoms less frequently (22%).
6. Treatment varied, including steroids, proton pump inhibitors (PPI), and dietary elimination. 80% of EoE-EGID cases were prescribed steroids or diet, compared to 35% and 45% for non-EoE EGID.

Conclusions
Eosinophilic gastritis was found in 27 patients in the past 5 years. Symptoms are quite non-specific and even overlap between EoE and non-EoE EGID cases. While EoG patients are more likely to present with iron deficiency anemia and hypoalbuminemia, these are far from universal. Further research is necessary to better understand the natural history of this condition which can also better guide disease specific treatment.

Funding Agencies
None
A146 THROAT TROUBLES: CASE REPORT OF LYMPHOCYTIC ESOPHAGITIS IN A CHILD WITH DYSPHAGIA.
Authors: Alzahrani I A 
Published: February 2025

Abstract

Background
Lymphocytic esophagitis (LE) is a rare and poorly understood inflammatory condition of the esophagus.it is characterized by presence of lymphocyte within esophageal mucosa. It has unique histologic phenotype characterized by increased intraepithelial lymphocytes in the absence or minimal presence of intraepithelial granulocytes. It is unclear whether LE is a unique primary inflammatory esophageal disease or a marker of an underlying esophageal or systemic immune-mediated disease process. Clinical presentations range from asymptomatic to dysphagia, heartburn, chest pain, nausea, vomiting, strictures, and food bolus impaction. Given the rarity of the disease, the incidence is not well known, with one study reporting incidence of LE 0.1% of total esophageal biopsies based on the results of a large pilot study in the United States of more than 40,000 patients.

Aims
To report on a patient with lymphocytic esophagitis who exhibited chronic dysphagia.

Methods
We describe a 6-year-old male, who has a history of coughing and choking with solid foods, as well as dysphagia. Although he has not experienced food impactions, he occasionally vomits undigested food. He was evaluated previously for eosinophilic esophagitis (EoE), with an unremarkable esophagogastroduodenoscopy (EGD). He was diagnosed with gastroesophageal reflux disease (GERD) in his first weeks of life due to projectile vomiting and arching of the back after feeding. He started on proton pump inhibitors (PPIs) at 7 weeks old, continuing until he was 2 years old, with initial vomiting persisting but gradually improving over time.

Results
He had an upper endoscopy again at 6 years which was unremarkable macroscopically. Pathology showed features of lymphocytic esophagitis in upper/mid/distal esophagus and focal basal spongiosis in mid esophagus, no intra-epithelial eosinophils are detected in all esophageal segments. He was started on proton pump inhibitors (PPIs) with good clinical response and improvement of dysphagia and reflux symptoms.

Conclusions
We present a patient with a history of chronic dysphagia and histological findings of LE. LE is a rare subtype of chronic esophagitis, that can include a wide range of clinical presentations. It should be considered in the differential diagnosis of dysphagia or reflux symptoms. Patients with LE can respond to proton PPI therapy and this should be the first line of therapy. However, steroid therapy should be considered for PPI non-responder LE patients. This case raises the importance of heightened awareness regarding the clinical presentation of LE and emphasizes the need for increased recognition of this condition. Although LE seems to have a chronic but benign course, more research is needed to better understand the pathophysiology and natural history of this condition.

Funding Agencies
None
A149 LYTIC PHAGE REDUCES COLITIS SEVERITY IN MICE COLONIZED WITH IBD-ASSOCIATED E. COLI NRG857C
Authors: Jackson K , Galipeau H , Hann A , Zangara M , Bording-Jorgensen M , Coombes B , Hosseinidoust Z , Verdu E 
Published: February 2025

Abstract

Background
Current therapies for inflammatory bowel disease (IBD) suppress inflammation rather than inhibiting the underlying drivers. Treatment failures can lead to dose escalation and risk of adverse effects. Bacteria with pathogenic potential, like adherent-invasive Escherichia coli (AIEC), have been postulated as one possible microbial driver in Crohn’s disease (CD), however, targeting these bacteria with precision in IBD remains challenging. Most antibiotics have broad-spectrum activity and disturb the background microbiome, which may exacerbate inflammation.

Aims
We aimed to assess whether and how bacteriophage, specific for a CD-associated bacterium, improves colitis severity in gnotobiotic mouse models.

Methods
Adult germ-free C57BL/6 mice were colonized with altered Schaedler-flora (ASF) and E. coli NRG857c (NRG), a CD-associated isolate. After 3 weeks, mice were treated with an NRG-specific lytic phage (1x109 PFU/dose; daily or TIW) or vehicle (PBS) for 2 weeks (n=6/group) and then exposed to 1 cycle of dextran sulfate sodium (2%; DSS) in drinking water. Additional PBS-treated mice (n=6) not exposed to DSS served as controls. Phage treatment was also tested in a spontaneous model of colitis using C57BL/6NTac-Il10em8Tac (IL-10-/-) mice, treated weekly with phage. In both models, mice were monitored daily for weight, stool consistency, and occult blood. Fecal contents were cultured to determine bacterial load, and the expression of NRG fimS was quantified using qPCR as an assessment of bacterial virulence. At endpoint, colon tissues were collected for histological and immunohistochemistry analysis to quantify colitis severity and NRG infiltration, respectively.

Results
In ASF and NRG colonized mice, phage treatment reduced clinical symptoms (p&lt; 0.001, p&lt;0.001) and histological scores (p&lt; 0.0001, p&lt; 0.001) of chemical and spontaneous colitis respectively. A1-log reduction in NRG bacterial load was observed in phage-treated mice (p&lt; 0.001), and reisolated NRG exhibited a reduced FimS ON/OFF ratio (p-value &lt; 0.01). Immunohistochemistry revealed reduced infiltration of NRG into the lamina propria following phage treatment, with greater accumulation in the epithelium.

Conclusions
Our results demonstrate that lytic phage targeting a CD-associated bacterium attenuates colitis in two gnotobiotic mouse models. Whereas this model did not lead to complete eradication of the disease-driving agent, phage treatment was associated with a reduction in a known AIEC virulence factor, attenuating colitis severity. The data suggest alternative mechanisms should be considered when translating phage therapy to treat IBD in clinical trials.

Funding Agencies
CIHRFarncombe Innovation Fund
A150 THE PARKINSON’S DISEASE-ASSOCIATED MUTATION LRRK2 G2019S INCITES NEUTROPHILIC INFLAMMATION AND INCREASED TISSUE DAMAGE IN A MOUSE MODEL OF INFECTIOUS COLITIS.
Authors: Oliveira N L , Pei J , Recinto S J , Kazanova A , Queiroz-Junior C , Li Z , Ribeiro C T , Milnerwood A J , Desjardins M , Thanabalasuriar A , Stratton J A , Gruenheid S 
Published: February 2025

Abstract

Background
The gut-brain axis is an area of intense interest in Parkinson’s disease (PD) research. PD is characterized by inflammation and gastrointestinal (GI) dysfunction, such as recurrent constipation, dysphagia, and intestinal bacterial overgrowth. GI symptoms in PD appear decades before motor symptoms. Mutations in the protein leucine-rich repeat kinase 2 (LRRK2) are associated with increased risk for PD and inflammatory bowel disease. Among them, the LRRK2 Gly2019Ser is the most common PD-associated mutation. It is unknown whether and how the LRRK2 mutation affects intestinal inflammation susceptibility or pathogenesis of PD.

Aims
To understand how the LRRK2 mutation affects intestinal inflammation susceptibility or pathogenesis of PD.

Methods
LRRK2 knock-in G2019S (GKI) and WT mice were infected with the mouse-specific pathogen Citrobacter rodentium and intestinal immune response was evaluated by single cell RNA sequencing (scRNAseq), flow cytometry, and ELISA.

Results
Results revealed that, at day 7 of infection, GKI mice had increased histopathology in colon after infection, compared to WT mice. The most prominent features were inflammatory infiltrate, edema, erosion, and goblet cells loss, although the control of infection was comparable, since the CFU counts were equal in both infected groups. Multiplex analysis of colon homogenates demonstrated that LRRK2 mutation changed cytokine production in response to the infection, including increase in G-CSF, CCL5, and decrease of IL-6 and CXCL2 levels. Myeloperoxidase ELISA in colon tissue showed a tendency to be higher in GKI mice, after infection, compared to WT mice. Single cell RNA sequencing (scRNAseq) of colonic LP cells demonstrated that after infection, LRRK2 G2019S mutation has a great impact in the number of differentially expressed genes (DEGs) on innate immune cells, such as neutrophils, monocytes, and NK cells. In fact, neutrophil was the only cell type proportionally significant after infection. Their DEGs were mostly upregulated and accounted for cell signalling, inflammatory pathways, myeloid leukocyte migration, and interferon response. In addition, flow cytometry revealed that after C. rodentium infection, GKI mice had increased neutrophil infiltration of colonic lamina propria (LP), compared to WT infected mice. Analysis in CD4 T cells by scRNA sequencing and RT-qPCR showed an increase in IL-17a expression, known for its G-CSF stimulating neutrophil migration effect.

Conclusions
Our results suggest that the LRRK2 GKI mutation promotes neutrophilic pathology in response to intestinal bacterial infection and this could be linked to an increase of IL-17a-mediated immune response.

Funding Agencies
Aligning Science Across Parkinson’s: ASAP - Michael Fox Foundation
A152 INTESTINAL INFLAMMATION DISRUPTS MICROBIAL ANTIGEN METABOLISM FACILITATING FOOD SENSITIZATION
Authors: Barbosa da Luz B , Rondeau L E , Muppidi P , Ling C , Dang R , Caminero A 
Published: February 2025

Abstract

Background
Patients with inflammatory bowel disease (IBD) report diverse food-related adverse reactions. Dairy is the most self-reported food intolerance in IBD. Emerging evidence suggests that altered diet-microbiota interactions can contribute to the development of IBD and adverse reaction to foods. We hypothesize that microbial alterations in IBD patients facilitate adverse reactions to foods.

Aims
To investigate the role of intestinal inflammation on microbial metabolism and food sensitization.

Methods
To investigate the effects of inflammation on microbial metabolism of food, eight-week-old C57BL6 mice were exposed to different concentrations (1.5 – 3.5%) of dextran sodium sulfate (DSS) for 5 days, then gavaged with dairy proteins. To study the role of inflammation in food sensitization, C57BL/6 mice were exposed to 3% DSS for 5 days, then sensitized to dairy proteins (6 mg casein/whey protein) using 4 oral administrations of cholera toxin (20 ug/mouse). After 1 week of recovery, sensitized mice were exposed to either a dairy-free or dairy containing diet for 7 days. Finally, the effects of inflammatory-mediated microbial alterations on food sensitivities were studied in gnotobiotic mice. Germ-free C57BL6 were colonized with DSS-inflamed microbiota or healthy SPF microbiota. After 3 weeks of colonization, the mice were sensitized to dairy proteins as described above, exposed to dairy and one cycle of DSS. Intestinal microbiota composition (16S sequencing) and function (digestion assays), and markers of intestinal inflammation (disease activity index, histological damage, cell infiltration and pro-inflammatory genes expression) were analyzed.

Results
DSS led to pronounced changes in the intestinal microbiota, impaired microbial capacity to degrade dairy proteins and increased systemic access of antigens. Inflammation also facilitated food sensitization characterized by immune cell infiltration (polymorphonuclear cells and CD3+) and mast cell proliferation in the colonic mucosa, and generation of systemic IgE and IgG levels. Dairy increased genes associated to immune cell recruitment and apoptosis in sensitized mice, and increased of apoptosis in the colon was confirmed by staining (TUNEL). Finally, mice colonized with microbiota from DSS-inflamed mice showed a worsening in inflammatory parameters during the dairy-diet intervention after sensitization. These results suggest that microbial alterations after inflammation facilitate the onset of food sensitivities and exacerbate food-mediated immune reactions in the colon.

Conclusions
Intestinal inflammation facilitates sensitization to foods by altering microbial antigen metabolism in the colon.

Funding Agencies
CCC