Introduction

Obscure gastrointestinal bleeding (OGIB) is defined as gastrointestinal bleeding of unknown origin that persists or recurs despite a negative finding from an initial bidirectional endoscopy. According to recent guidelines, capsule endoscopy was recommended first in overt OGIB, but it is unclear when it is appropriate to perform capsule endoscopy in overt OGIB patients.

Aims & Methods

We aimed to analyze clinical outcomes with regard to the timing of capsule endoscopy in overt OGIB patients. We conducted a single-center retrospective study enrolling patients who had undergone capsule endoscopy for overt OGIB between February 2010 to December 2021. We included hospitalized patients who underwent capsule endoscopy for overt OGIB after negative bidirectional endoscopy. We investigated the diagnostic yield of capsule endoscopy, rebleeding rate, length of hospital stay, initial hemoglobin, and the amount of blood transfusion with regard to the timing of capsule endoscopy.

Results

A total of 118 patients underwent capsule endoscopy to assess overt OGIB. The diagnostic yields in the groups that underwent capsule endoscopy < 48h and > 48h from the last overt OGIB were 50.0% and 22.0%, respectively (P=0.017). Rebleeding rate and the length of hospital stay were not significantly different between the two groups. Initial hemoglobin level in the group who underwent capsule endoscopy > 48h group was lower than in the < 48h group (8.8±3.0 vs. 10.7±3.7, P=0.015).

Conclusion

Performing capsule endoscopy within 48 hours from the last overt OGIB resulted in a higher diagnostic yield. Performing capsule endoscopy within 48 hours may improve the clinical outcomes of patients with overt OGIB.

Introduction

Autoimmune Atrophic Gastritis (AAG) is a chronic immune-mediated condition that mainly affects the body and fundus of the stomach. AAG is often under-diagnosed due to the slow progression of the disease and a variable spectrum of symptoms. Recent data suggests a potential role of altered gastric microbiota in the natural history of AAG, due to the potential overgrowth of bacteria linked to the development of neoplastic complications (neuroendocrine tumors- NETs and gastric cancer) (1,2). Moreover, the same data hypothesizes the use of fecal microbiota as a possible non-invasive marker to diagnose and monitor AAG. Thus, we aimed to prospectively characterize the salivary and fecal microbiota of patients with AAG to provide further insights in this field.

Aims & Methods

We collected salivary and fecal samples from consecutive patients with an established diagnosis of AAG, enrolled at the Gastroenterology Unit of Azienda Ospedale Università Padova from March to June 2023 at the time of endoscopic follow-up examination. All patients needed to be off Proton-Pump Inhibitors, antibiotics, and probiotics for at least one month before enrolment. Stool samples were collected by the patients on the day of the endoscopy, transferred in a buffer solution, and stored at -20°C. Oral samples were collected through salivary commercial kits and freezed at -20°C. Both salivary and faecal samples were analyzed by BMR Genomic (Padua, Italy) that amplified the V3-V4 hypervariable ribosomal RNA region. Sequencing of the 16S rRNA gene V3- V4 region was performed using the Illumina MiSeq. Preliminary analyses were conducted on individual fecal samples compared to an internal population of healthy subjects (provided by BMR genomics) using Qiime2 tools. Shannon–Wiener index was used to calculate α-diversity and then the microbial biodiversity index (MBI) and Dysbiosis Index (DI). Mann–Whitney tests were performed to verify statistical differences in the α-diversity across AAG patients and healthy subjects.

Results

We enrolled 15 AAG patients with a mean age of ± 63 ± 11 years (9/15 females). OLGA 2 stage was reported in 10/15 patients. Sixty percent of the patients showed a MBI between 7.11 and 12.45, indicating that each sample contained phylogenetically similar species. The remaining patients have an index greater than 12.45 compared to the healthy population. More than half of the patients had dysbiosis (>0.082). The highest indices of dysbiosis were found in patients with a history of NET (n=3), gastric cancer (n=1), and previous HP- infection and OLGA 3 stage (n=1). Firmicutes, Bacteroidetes, and Proteobacteria were more frequent phyla found in the fecal samples, whereas Enterobacteriaceae and Streptococcaceae were the most common bacterial families (13/15, 87%). In particular, Klebsiella and Campylobacter pathogens genera were found in some samples. Streptococcus and Prevotella were the most abundant genera found in the salivary samples.

Conclusion

Patients with AAG were found to have a great proportion of Firmicutes and Bacteroidetes, which aligns with the literature (3,4). Moreover, a dominant of Proteobacteria, especially Enterobacteriaceae commonly associated with proinflammatory states, was found. (5) Our preliminary data showed a possible positive association between higher degrees of dysbiosis and a previous history of NET or gastric cancer.

References

1. Parsons BN, Ijaz UZ, D'Amore R, Burkitt MD, Eccles R, Lenzi L, Duckworth CA, Moore AR, Tiszlavicz L, Varro A, Hall N, Pritchard DM. Comparison of the human gastric microbiota in hypochlorhydric states arising as a result of Helicobacter pylori-induced atrophic gastritis, autoimmune atrophic gastritis and proton pump inhibitor use. PLoS Pathog. 2017 Nov 2;13(11):e1006653.

2. Conti L, Annibale B, Lahner E. Autoimmune Gastritis and Gastric Microbiota. Microorganisms. 2020 Nov 19;8(11):1827.

3. Castaño-Rodríguez N, Goh KL, Fock KM, et al. Dysbiosis of the microbiome in gastric carcinogenesis. Sci Rep. 2017;7(1):15957.

4. Conti L, Borro M, Milani C, Simmaco M, Esposito G, Canali G, Pilozzi E, Ventura M, Annibale B, Lahner E. Gastric microbiota composition in patients with corpus atrophic gastritis. Dig Liver Dis. 2021 Dec;53(12):1580-1587.

5. Rizzatti G, Lopetuso LR, Gibiino G, Binda C, Gasbarrini A. Proteobacteria: A Common Factor in Human Diseases. Biomed Res Int. 2017;2017:9351507.

Disclosure

Nothing to disclose

Introduction

The degree of fibrosis during colorectal ESD varies and sometimes makes the procedure itself difficult. Preoperative prediction of fibrosis is expected to help develop a reliable strategy.

Aims & Methods

Of 1309 colorectal ESD lesions performed at our hospital between April 2012 and September 2022, 953 lesions larger than 20 mm were included after excluding post-treatment recurrence, SMT, and other conditions. Intraoperative fibrosis was classified into F0 (none), F1 (mild), and F2 (severe).

Results

Fibrosis was observed in 192 (20.1%) patients (F1; 143, F2; 49). The tumor diameter (median, range) was 23 (20-135), 30 (20-210), and 35 (20-115) mm in F0, F1, and F2 groups, respectively. The rate of the cecum (%) was 13.3 : 29.4 : 16.3, which was higher in F1. Overall, bleeding was observed in 17 patients (1.8%) and perforation in 3 patients (0.3%), and the frequency was similar in each group. The curative resection rate (%) was 98.4:91.6:59.2, with F2 being significantly inferior. The long treatment time (≥120 minutes) (%) was 1.7 : 9.1 : 46.9, showing a significant difference between F0 vs F1 and F1 vs F2, and the dissection speed (mean±SD, mm²/min) was 25.9±14.5 : 23.2±13.6 : 15.3±10.6, which was significantly slower in F2. The predictive factors of F1 and F2: straddling the folds, prior biopsy, lesion diameter, site, and morphology, were included in the study, and multivariate analysis showed that the predictive factors of F1 were straddling folds (OR;2.07,95%CI;1.39-3.11), lesion diameter ≥50mm (OR;4.68,95%CI;2.45-8.94), biopsy (OR;6.44,95%CI;3.32-12.5), NGPD (OR;4.31,95%CI;2.37-7.83), and cecum(OR;3.73,95%CI;2.35-5.92). The predictive factors of F2 were straddling folds (OR;2.34,95%CI;1.21-4.51), lesion diameter ≥50 mm (OR;7.29,95%CI;3.03-17.5), biopsy (OR;5.07,95%CI;1.81-14.1), and protruded type (OR;6.44,95%CI;3.23-12.8).

Conclusion

Colorectal ESD for fibrotic lesions was safe, but the curative resection rate was low in F2. F1-specific predictors were cecum and NGPD, and F2-specific predictors were protruded type, suggesting that the choice of surgeon and strategy should depend on the expected degree of fibrosis.

Introduction

The only effective treatment for celiac disease (CD) is lifelong compliance with a gluten-free diet. Lactobacilli and Bifidobacterium spp. may play a role in the breakdown of gluten. Ithas been demonstrated that Lactobacilli can detoxify gliadin peptides after partial digestion by human proteases. These findings could suggest the use of probiotics as complementary therapy for CD.

Aims & Methods

We designed a study to determine the potential effect of a combination of Lactobacillus (acidophilus HA-122, casei HA-108) and Bifidobacterium bifidum HA-132 on perception of symptoms and on the inflammatory-immunological markers in patients with active CD.
25 adult patients were randomized to receive bid of a probiotic combination of Lactobacilus and Biffidobacter for six weeks (13 pts) va a placebo group (12 pts) while being on gluten-free diet. Laboratory studies included routine blood tests, CD specific antibodies, determination of IL-1b, IL-6 and TNF-alpha. CD serology and duodenal histology were performed at baseline, at the end of treatment and at 30 days after therapy. Histological damage in intestinal biopsy samples was graded according to the Marsh modified classification. At baseline and follow-up visit, patients completed the Gastrointestinal Symptom Rating Scale (GSRS) questionnaire. Histological damage in intestinal biopsy samples was graded according to the Marsh modified classification.

Results

25 pacients, 13 in the probiotic associated arm, 12 in the placebo arm, with median age of 40, BMI 21.2, 18 with symptomatic CD (equal distribuited) and 7 with sublinical CD (4 in the probiotic arm, 9 in the placebo arm). Baseline serology: IGA tTG 1986.6 (group A) vs 1507.1 (placebo group). Baseline hystology (Marsh classification)- Marsh 3a 1 pacient in probiotic group, 2 in the placebo arm. 5 pts Mars 3b3 in group A and 2 in the placebo arm and 17 pts Marsh 3c (9 pts probiotic, 8 pts placebo). IELs density (mean range) was 44.5 in the first group vs 42.5
After treatment: clinical aleviation of indigestion and diareea (p=0.002), constipation (p=0. 0396), gastro-esophageal reflux (p=0.0493) and abdominal pain (p=0.0378)-superior in the probiotic associated treatment.
Serologic parameters: IgA tTG 0,96 in the probiotic arm vs 1,16 in the placebo (p=0.048), IgA EMA 1,05 vs 0,97 (p=0.028), IgG DGP 0,91 vs 1,12 (p=0.21).
Improvement of the inflamatory status: decrease of IL-1b, IL 6 and TNF-a was superior in the probiotic associated group (p=0.071, p=0.083, p=0.078).
Regarding the histologic response: IELs 0,83 vs 1.07 in the placebo arm (p=0.049).

Conclusion

Tests and the lymphocyte infiltrates in the mucosal biopsy specimen in uur study suggests that prebiotic/probiotic treatment may improve symptoms and serology in celiac disease.

Disclosure

I don t have any conflict of interest to declare

Introduction

Ozanimod (OZA) is approved for the treatment of moderately to severely active ulcerative colitis (UC). Approximately 30% of patients (pts) were clinical nonresponders after 10 wk of OZA treatment in the phase 3 True North (TN) study (NCT02435992), but ~50% of these OZA nonresponders achieved symptomatic response after 5–10 wk of additional OZA treatment during the open-label extension (OLE) study (NCT02531126).

Aims & Methods

This analysis evaluated the impact of TN baseline (BL) endoscopic disease activity on the durability of OZA response in Week (W) 10 OZA clinical nonresponders after extended induction during the OLE up to 4 years (OLE W190). Pts were categorized by BL Mayo endoscopy subscore (MES) as moderate (MES=2) or severe (MES=3). Symptomatic, clinical, and mucosal efficacy were assessed through OLE W190 using observed case (OC) and nonresponder imputation (NRI) analyses.

Results

Of the 226 W10 OZA clinical nonresponders who entered the OLE, 67 had moderate and 159 had severe endoscopic disease at BL. Pt characteristics were generally similar between groups, but more pts with severe vs moderate endoscopic activity had prior immunomodulator (52.8% vs 34.3%), anti–tumor necrosis factor (TNF; 45.9% vs 25.4%), or non–anti-TNF biologic (36.5% vs 19.4%) exposure. Some symptomatic response was observed in OZA W10 clinical nonresponders from BL to W10/OLE entry, which was greater in pts with moderate disease and further improved with extended OZA exposure by OLE W5 (moderate: 36.9% at W10 and 66.2% by OLE W5; severe: 23.8% at W10 and 47.9% by OLE W5). Similar patterns were observed with symptomatic remission but overall rates were lower (moderate: 6.2% at W10 and 26.2% by OLE W5; severe: 1.3% at W10 and 13.0% by OLE W5). Symptomatic response and remission rates after OLE W5 were generally similar in moderate and severe endoscopic activity groups, and rates were maintained throughout the OLE. Likewise, clinical and mucosal efficacy were durable and rates were generally similar between subgroups through OLE W190 (Table). Notably, higher endoscopic improvement rates were achieved through OLE W190 in pts with BL moderate endoscopic activity despite ~50% of these pts progressing to severe by TN W10. Similar data trends were observed in the NRI analysis.

Conclusion

Delayed response to OZA was observed in pts who did not achieve clinical response after 10 wk of OZA therapy, regardless of BL endoscopic activity. W10 nonresponders with moderate endoscopic activity responded faster with additional OZA exposure, whereas those with severe endoscopic activity needed longer exposure to OZA to achieve similar efficacy rates that were durable with continuous OZA exposure. These results suggest that some pts may require a longer induction on OZA but ultimately maintain durable OZA response.

Disclosure

Acknowledgment: This study was sponsored by Bristol Myers Squibb. Professional medical writing assistance was provided by Traci Stuve, MA, and Julie Ko, PharmD, of Peloton Advantage, LLC, an OPEN Health company, and funded by Bristol Myers Squibb.
PI: received lecture fees from AbbVie, Bristol Myers Squibb, Celgene, Celltrion, Dr. Falk Pharma, Ferring, Galapagos, Gilead, Janssen, MSD, Pfizer, Sandoz, Sapphire Medical, Shire, Takeda, Tillotts, and Warner Chilcott; received financial support for research from Celltrion, MSD, Pfizer, and Takeda; received advisory fees from AbbVie, Arena, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Celltrion, Eli Lilly, Genentech, Gilead, Hospira, Janssen, MSD, Pfizer, Pharmacosmos, Prometheus Biosciences, Roche, Samsung Bioepis, Sandoz, Takeda, TopiVert, VH2, Vifor, and Warner Chilcott.
RKC: consulted for AbbVie, Bristol Myers Squibb, Fresenius Kabi, Fzata, Janssen, Magellan Health, Option Care, Pfizer, Pharmacosmos, Samsung Bioepis, Sandoz, Sebela, and Takeda; scientific co-director of the CorEvitas Registry and executive committee member of the IBD Education Group; received financial support for research from Janssen.
TR: served on advisory boards for AbbVie, Bristol Myers Squibb, Celltrion, Eli Lilly, Ferring, Genentech, Intercept Health, Janssen, Merck, Pfizer, and Takeda; speaker for AbbVie, Bristol Myers Squibb, Eli Lilly, Janssen, Pfizer, and Takeda.
AS: declares no competing financial or nonfinancial interests.
PH: consultant and speaker for Boston Scientific, FujiFilm, MedWork, and Viatris.
SC: consultant for AbbVie, Bristol Myers Squibb, Janssen, and Pfizer.
ST, HW, MTO, and AJ: employees and/or shareholders of Bristol Myers Squibb.
DCW: received research funding from AbbVie, Amgen, Arena/Pfizer, Celgene/Bristol Myers Squibb, Genentech, and Janssen; lectured for AbbVie, Bristol Myers Squibb, Janssen, and Takeda; consulted for AbbVie, Arena/Pfizer, Celgene/Bristol Myers Squibb, Eli Lilly, Janssen, and Takeda.

Introduction

Digestive hemorrhage is a frequent complication in advanced chronic kidney disease. Patients with end-stage renal disease (ESRD) are more likely to have gastrointestinal (GI) problems, including digestive bleeding of high or low origin.

Aims & Methods

The aim of our work is to study the particularities of HD in CKD patients.
This is a monocentric prospective analytical study over a period of 28 months: April 2020 to August 2022, including patients with HD with CKD at the dialysis stage or not, including renal transplant patients.
In order to be able to compare patients with ESRD with patients without ESRD, a control group of patients admitted for HD who had a GI endoscopy during the study period and with normal renal function were identified and grouped. In this group of patients, we took into account age, sex, indications, GI endoscopy results and ICU stay.
We also assessed all-cause mortality between the groups of CKD patients with HD versus the control group.

Results

A total of 378 patients underwent digestive exploration for HD. In this population, 46 (12.16%) patients with CKD were compared with 332 patients without RI.
70% (n=32) of the patients with RI were on chronic hemodialysis, 26% (n=12) had a GFR<60ml/min/1.73m2 but were managed without the aid of dialysis or transplantation, and 4% (n=2) patients were renal transplant recipients.
The most common etiologies in CKD patients were ulcer disease 65.2% (n=30); vascular ectasia 28.2% (n=13), gastritis 26% (n=12), esophagitis 10.8% (n=5); and tumors in 8.6% (n=4).
After statistical analysis patients with CKD had:
A higher risk of hemodynamic instability 69.5% (n=32) compared to the control group 11.14% (n=37) with p=0.002,
A higher rate of recurrence 26% (n=12) CKD patients compared to 9.6% (n=32) of the control group with a p=0.00.
A higher mortality rate 4.34% (n=2) in CKD patients compared to the control group 1.2% (n=4) with p=0.00.

Conclusion

GI bleeding in advanced chronic kidney disease is more severe it is accompanied by a higher risk of recurrence of ICU stay and mortality, hence the interest of prompt management and close monitoring. The main causes are peptic ulcer and vascular ectasia.

Clinical Case Summary

Introduction: Superior Mesenteric Vein (SMV) Thrombosis accounts for only 5% of all cases of intestinal ischemia. As opposed to acute mesenteric ischemia secondary to an arterial thrombus which has a more drastic presentation, SMV thrombus typically presents with non-specific signs and symptoms. Rarely, when venous congestion leads to bowel wall edema which can consequently head to intestinal obstruction.
Case presentation: We present the case of a 47-year-old male presenting with severe generalized abdominal pain and vomiting. Abdominal CT findings were suggestive of small bowel obstruction and venous thrombosis. CT angiogram confirmed SMV thrombus which was visualized as severe narrowing of the SMV at the midabdomen a few centimeters above the umbilicus, with consequent congestion and decreased contrast enhancement proximal to the area of narrowing. The patient was initially managed conservatively with anticoagulation, however the patient did not improve clinically. Since there were no signs of infarction or peritonitis that would warrant immediate surgical intervention, an alternative approach using endovascular technique was attempted. The patient underwent SMV stenting which subsequently relieved the obstruction.

References

1. Treatment of superior mesenteric and portal vein thrombosis with direct thrombolytic infusion via an operatively placed mesenteric catheter; https://pubmed.ncbi.nlm.nih.gov/1527918
2. A systematic review of the management of acute superior mesenteric vein thrombosis in adults https://mednexus.org/doi/full/10.1097/JP9.0000000000000051
3. Naffouj S, Al-Shammari M, Salgia R. Treatment of colonic varices with a superior mesenteric venous stent: a case report describing a unique approach. Gastroenterol Rep (Oxf). 2021 Feb 4;9(6):597-600. doi: 10.1093/gastro/goab003. PMID: 34925858; PMCID: PMC8677559
4. Vekariya P, Daneti D, Senthamizhselvan K, et al. (June 14, 2021) Acute Intestinal Obstruction as an Initial Presentation of Mesenteric Venous Thrombosis. Cureus 13(6): e15652. doi:10.7759/cureus.15652

Disclosure

None