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Endoscopic mucosal resection: tips and tricks for gastrointestinal trainees.
Herman, T, Megna, B, Pallav, K, Bilal, M
Translational gastroenterology and hepatology. 2023;:25
Abstract
Endoscopic mucosal resection (EMR) is a minimally invasive, specialized endoscopic technique that is useful in resecting superficial gastrointestinal lesions that are unable to be removed by standard polypectomy. This is typically accomplished using a submucosal injection that lifts the lesion away from the muscularis propria to allow for safe resection of the polyp, either via piecemeal or en bloc resection. Over the years, several techniques exist to perform EMR including conventional EMR or hot EMR, cold EMR and underwater EMR. Despite its established advantages and safety over conventional techniques such as surgery, the adoption of endoscopic resection (and thus the education and training of gastroenterology trainees) is lagging. The goal of this article is to offer a comprehensive review of the basic principles of colonic EMR. We review the concepts of optical diagnosis including the various polyp classification systems available to determine the polyp morphology and histology. We also discuss the technical aspects of performing colonic EMR. We also outline the common adverse events associated with EMR including bleeding, perforation, postpolypectomy syndrome, and residual or recurrent polyps, and discuss preventative measures that can be taken to mitigate adverse events. Lastly, we offer practical tips for trainees who want to undertake EMR in their clinical practice.
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Prospective randomized controlled study on the effects of Saccharomyces boulardii CNCM I-745 and amoxicillin-clavulanate or the combination on the gut microbiota of healthy volunteers.
Kabbani, TA, Pallav, K, Dowd, SE, Villafuerte-Galvez, J, Vanga, RR, Castillo, NE, Hansen, J, Dennis, M, Leffler, DA, Kelly, CP
Gut microbes. 2017;(1):17-32
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Abstract
Probiotics are believed to be beneficial in maintaining a healthy gut microbiota whereas antibiotics are known to induce dysbiosis. This study aimed to examine the effects of the probiotic Saccharomyces boulardii CNCM I-745 (SB), the antibiotic Amoxicillin-Clavulanate (AC) and the combination on the microbiota and symptoms of healthy humans. Healthy subjects were randomized to one of 4 study groups: SB for 14 days, AC for 7 days, SB plus AC, Control (no treatment). Participants gave stool samples and completed gastro-intestinal symptom questionnaires. Microbiota changes in stool specimens were analyzed using 16s rRNA gene pyrosequencing (bTEFAP). Only one subject withdrew prematurely due to adverse events. Subjects treated by S boulardii + AC had fewer adverse events and tolerated the study regimen better than those receiving the AC alone. Control subjects had a stable microbiota throughout the study period. Significant microbiota changes were noted in the AC alone group during antibiotic treatment. AC associated changes included reduced prevalence of the genus Roseburia and increases in Escherichia, Parabacteroides, and Enterobacter. Microbiota alterations reverted toward baseline, but were not yet completely restored 2 weeks after antibiotherapy. No significant shifts in bacterial genera were noted in the SB alone group. Adding SB to AC led to less pronounced microbiota shifts including less overgrowth of Escherichia and to a reduction in antibiotic-associated diarrhea scores. Antibiotic treatment is associated with marked microbiota changes with both reductions and increases in different genera. S. boulardii treatment can mitigate some antibiotic-induced microbiota changes (dysbiosis) and can also reduce antibiotic-associated diarrhea.
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Effects of polysaccharopeptide from Trametes versicolor and amoxicillin on the gut microbiome of healthy volunteers: a randomized clinical trial.
Pallav, K, Dowd, SE, Villafuerte, J, Yang, X, Kabbani, T, Hansen, J, Dennis, M, Leffler, DA, Newburg, DS, Kelly, CP
Gut microbes. 2014;(4):458-67
Abstract
BACKGROUND Interactions between the microbial flora of the intestine and the human host play a critical role inmaintaining intestinal health and in the pathophysiology of a wide variety of disorders such as antibiotic associated diarrhea, Clostridium difficile infection, and inflammatory bowel disease. Prebiotics can confer health benefits by beneficial effects on the intestinal microbiome, whereas antibiotics can disrupt the microbiome leading to diarrhea andother side effects. AIM: To compare the effects of the prebiotic, polysaccharopeptide from Trametes versicolor, to those of the antibiotic,amoxicillin, on the human gut microbiome METHODS Twenty-four healthy volunteers were randomized to receive PSP, amoxicillin, or no treatment (control).Stool specimens were analyzed using bTEFAP microbial ecology methods on seven occasions over 8 weeks from each participant in the active treatment groups and on three occasions for the controls. RESULTS Twenty-two of 24 participants completed the protocol. PSP led to clear and consistent microbiome changes consistent with its activity as a prebiotic. Despite the diversity of the human microbiome we noted strong microbiome clustering among subjects. Baseline microbiomes tended to remain stable and to overshadow the treatment effects.Amoxicillin treatment caused substantial microbiome changes most notably an increase in Escherichia/Shigella. Antibiotic associated changes persisted to the end of the study, 42 days after antibiotic therapy ended. CONCLUSIONS The microbiomes of healthy individuals show substantial diversity but remain stable over time.The antibiotic amoxicillin alters the microbiome and recovery from this disruption can take several weeks. PSP from T. versicolor acts as a prebiotic to modulate human intestinal microbiome composition.
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Celiac disease or non-celiac gluten sensitivity? An approach to clinical differential diagnosis.
Kabbani, TA, Vanga, RR, Leffler, DA, Villafuerte-Galvez, J, Pallav, K, Hansen, J, Mukherjee, R, Dennis, M, Kelly, CP
The American journal of gastroenterology. 2014;109(5):741-6; quiz 747
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Plain language summary
Differentiating between celiac disease (CD) and non-celiac gluten sensitivity (NCGS) is challenging, as both conditions respond to a gluten-free diet but present different clinically. At present, an effective diagnostic protocol specific to NCGS is not available. The aim of this review is to develop a diagnostic algorithm to differentiate CD from NCGS. Records of 238 subjects who presented with gluten-responsive symptoms were reviewed. This study resulted in a clinical model for efficient differential diagnosis of CD and NCGS. On the basis of this model, unnecessary endoscopies could have been avoided in over 60% of subjects. This model offers clinicians a stepwise algorithm for diagnosis and management of patients who present with symptoms responsive to gluten exclusion.
Abstract
OBJECTIVES Differentiating between celiac disease (CD) and non-celiac gluten sensitivity (NCGS) is important for appropriate management but is often challenging. METHODS We retrospectively reviewed records from 238 patients who presented for the evaluation of symptoms responsive to gluten restriction without prior diagnosis or exclusion of CD. Demographics, presenting symptoms, serologic, genetic, and histologic data, nutrient deficiencies, personal history of autoimmune diseases, and family history of CD were recorded. NCGS was defined as symptoms responsive to a gluten-free diet (GFD) in the setting of negative celiac serology and duodenal biopsies while on a gluten-containing diet or negative human leukocyte antigen (HLA) DQ2/DQ8 testing. RESULTS Of the 238 study subjects, 101 had CD, 125 had NCGS, 9 had non-celiac enteropathy, and 3 had indeterminate diagnosis. CD subjects presented with symptoms of malabsorption 67.3% of the time compared with 24.8% of the NCGS subjects (P<0.0001). In addition, CD subjects were significantly more likely to have a family history of CD (P=0.004), personal history of autoimmune diseases (P=0.002), or nutrient deficiencies (P<0.0001). The positive likelihood ratio for diagnosis of CD of a >2× upper limit of normal IgA trans-glutaminase antibody (tTG) or IgA/IgG deaminated gliadan peptide antibody (DGP) with clinical response to GFD was 130 (confidence interval (CI): 18.5-918.3). The positive likelihood ratio of the combination of gluten-responsive symptoms and negative IgA tTG or IgA/IgG DGP on a regular diet for NCGS was 9.6 (CI: 5.5-16.9). When individuals with negative IgA tTG or IgA/IgG DGP also lacked symptoms of malabsorption (weight loss, diarrhea, and nutrient deficiencies) and CD risk factors (personal history of autoimmune diseases and family history of CD), the positive likelihood ratio for NCGS increased to 80.9. CONCLUSIONS On the basis of our findings, we have developed a diagnostic algorithm to differentiate CD from NCGS. Subjects with negative celiac serologies (IgA tTG or IgA/IgG DGP) on a regular diet are unlikely to have CD. Those with negative serology who also lack clinical evidence of malabsorption and CD risk factors are highly likely to have NCGS and may not require further testing. Those with equivocal serology should undergo HLA typing to determine the need for biopsy.
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Kinetics of the histological, serological and symptomatic responses to gluten challenge in adults with coeliac disease.
Leffler, D, Schuppan, D, Pallav, K, Najarian, R, Goldsmith, JD, Hansen, J, Kabbani, T, Dennis, M, Kelly, CP
Gut. 2013;(7):996-1004
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Abstract
OBJECTIVE Coeliac disease is defined by gluten responsiveness, yet there are few data on gluten challenge (GC) in adults on a gluten-free diet. Lack of data regarding the kinetics of responses to gluten is a limitation in clinical practice and research when GC is performed. DESIGN 20 adults with biopsy-proven coeliac disease participated. The study included two run-in visits followed by a 14-day GC at a randomly assigned dose of 3 or 7.5 g of gluten/day. Study visits occurred 3, 7, 14 and 28 days after starting GC. Duodenal biopsy was performed during the run-in and at days 3 and 14 of GC. Villous height to crypt depth ratio (Vh:Cd) and intraepithelial lymphocyte (IEL) count/100 enterocytes were measured by two pathologists. Antibodies to tissue transglutaminase and deamidated gliadin peptides, lactulose to mannitol ratio (LAMA) and symptoms were assessed at each visit. RESULTS Significant reduction in Vh:Cd (2.2-1.1, p<0.001) and increase in IELs (32.6-51.8, p<0.001) were seen from baseline to day 14. Antibody titres increased slightly from baseline to day 14 of GC but markedly by day 28. LAMA did not change significantly. Gastrointestinal symptoms increased significantly by day 3 and returned to baseline by day 28. No differences were seen between the two gluten doses. CONCLUSIONS 14 day GC at ≥ 3 g of gluten/day induces histological and serological changes in the majority of adults with coeliac disease. These data permit accurate design of clinical trials and indicate that many individuals will meet coeliac diagnostic criteria after a 2-week GC.