AGA Technical Review on Gastric Intestinal Metaplasia-Natural History and Clinical Outcomes.
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ABSTRACT:
SUBMITTER: Gawron AJ
PROVIDER: S-EPMC7375032 | biostudies-literature | 2020 Feb
REPOSITORIES: biostudies-literature
Publications
AGA Technical Review on Gastric Intestinal Metaplasia-Natural History and Clinical Outcomes.
Gawron Andrew J AJ Shah Shailja C SC Altayar Osama O Davitkov Perica P Morgan Douglas D Turner Kevin K Mustafa Reem A RA
Gastroenterology 20191206 3
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Project description: Not available
| S-EPMC7425600 | biostudies-literature
Project description:BackgroundGastric intestinal metaplasia (GIM) is a precursor to gastric adenocarcinoma (GAC). In the United States, there is no consensus on the utility of surveillance for GIM, and minority populations most affected by GAC are understudied. Our aims were to define clinical and endoscopic features, surveillance practices, and outcomes in patients with GIM in a multicenter safety-net system.MethodsWe identified patients with biopsy-proven GIM between 2016-2020 at the three medical centers comprising Los Angeles County Department of Health Services. Demographics, findings at index esophagogastroduodenoscopy (EGD) first showing GIM, recommended interval for repeat EGD, and findings at repeat EGD were abstracted. Descriptive statistics were performed to characterize our cohort. T-tests and chi-squared (χ2) tests were used to compare patients with and without multifocal GIM.ResultsThere were 342 patients with newly-diagnosed biopsy-proven GIM, 18 (5.2%) of whom had GAC at index EGD. Hispanic patients comprised 71.8% of patients. For most patients (59%), repeat EGD was not recommended. If recommended, 2-3 years was the most common interval. During a median time to repeat EGD of 13 months and cumulative follow-up of 119 patient-years, 29.5% of patients underwent at least one repeat EGD, of whom 14% had multifocal GIM not previously detected. Progression to dysplasia or GAC was not detected in any patients.ConclusionIn a predominantly minority population with biopsy-proven GIM, there was a 5% incidence of GAC on index EGD. Though progression to neither dysplasia nor GAC was detected, there was significant variability in endoscopic sampling and surveillance practices.
| S-EPMC10197307 | biostudies-literature
Project description:Gastric cancer (GC) remains one of the most common causes of mortality worldwide. Intestinal metaplasia (IM) is one of the preneoplastic gastric lesions and is considered an essential predisposing factor in GC development. Here we present a review of recent most relevant papers to summarize major findings on the molecular alterations in gastric IM. The latest progress in novel diagnostic methods allows scientists to identify various types of molecular alterations in IM, such as polymorphisms in various genes, changes in the expression of micro-RNAs and long noncoding RNAs, and altered microbiome profiles. The results have shown that some of these alterations have strong associations with IM and a potential to be used for screening, treatment, and prognostic purposes; however, one of the most important limiting factors is the inhomogeneity of the studies. Therefore, further large-scale studies and clinical trials with standardized methods designed by multicenter consortiums are needed. As of today, various molecular alterations in IM could become a part of personalized medicine in the near future, which would help us deliver a personalized approach for each patient and identify those at risk of progression to GC.
| S-EPMC8199079 | biostudies-literature
Project description:BackgroundGastric cancer (GC) has a poor prognosis with wide variation in survival rates across the world. Several studies have shown premalignant lesions gastric atrophy (GA) and intestinal metaplasia (IM) influence gastric cancer risk. This systematic review examines all available evidence of the risk of GC in patients with GA or IM and explores the geographical variation between countries.MethodsEMBASE, MEDLINE, Web of Science and the Cochrane Library were searched for relevant articles published to June 2016 investigating the risk of GC in individuals with GA or IM. Analysis was performed to determine variation based on geographical location. Study quality was assessed using the Newcastle-Ottawa Scale and heterogeneity between studies was also evaluated.ResultsFifteen relevant articles were identified, in which there were eight studies of GC incidence in GA and nine in IM cohorts (two articles investigated both GA and IM). The incidence rate of GC in patients with GA ranged from 0.53 to 15.24 per 1000 person years, whereas there was more variation in GC incidence in patients with IM (0.38 to 17.08 per 1000 person years). The greatest GC incidence rates were in Asian countries, for patients with GA, and the USA for those with IM (15.24 and 17.08 per 1000 person years, respectively). The largest studies (four over 25,000 person years) had an incidence rate range of 1.0-2.5 per 1000 person years, however, in general, study quality was poor and there was marked heterogeneity.ConclusionOverall there is a wide variation in annual incidence rate of GC from premalignant lesions. With the recent introduction of surveillance guidelines for gastric atrophy and intestinal metaplasia in the Western world, future assessment of this risk should be performed. Furthermore, substantial heterogeneity supports the need for more robust studies in order to pool results and determine the overall incidence rate of gastric cancer for patients with these premalignant lesions.
| S-EPMC5725642 | biostudies-literature
Project description: Not available
| S-EPMC10824166 | biostudies-literature
Project description:Evidence suggests that Helicobacter pylori plays a role in gastric cancer (GC) initiation. However, epidemiologic studies on the specific role of other bacteria in the development of GC are lacking. We conducted a case-control study of 89 cases with gastric intestinal metaplasia (IM) and 89 matched controls who underwent upper gastrointestinal endoscopy at three sites affiliated with NYU Langone Health. We performed shotgun metagenomic sequencing using oral wash samples from 89 case-control pairs and antral mucosal brushing samples from 55 case-control pairs. We examined the associations of relative abundances of bacterial taxa and functional pathways with IM using conditional logistic regression with and without elastic-net penalty. Compared with controls, oral species Peptostreptococcus stomatis, Johnsonella ignava, Neisseria elongata and Neisseria flavescens were enriched in cases (odds ratios [ORs] = 1.29-1.50, P = .004-.01) while Lactobacillus gasseri, Streptococcus mutans, S parasanguinis and S sanguinis were under-represented (ORs = 0.66-0.76, P = .006-.042) in cases. Species J ignava and Filifactor alocis in the gastric microbiota were enriched (ORs = 3.27 and 1.43, P = .005 and .035, respectively), while S mutans, S parasanguinis and S sanguinis were under-represented (ORs = 0.61-0.75, P = .024-.046), in cases compared with controls. The lipopolysaccharide and ubiquinol biosynthesis pathways were more abundant in IM, while the sugar degradation pathways were under-represented in IM. The findings suggest potential roles of certain oral and gastric microbiota, which are correlated with regulation of pathways associated with inflammation, in the development of gastric precancerous lesions.
| S-EPMC8770574 | biostudies-literature
Project description:AimIntestinal metaplasia (IM) and gastric atrophy (GA) are precancerous lesions in the stomach. There is a large debate on natural course of these lesions and surveillance strategy in these patients. This meta-analysis was aimed to find the most appropriate follow up and the rate of progression from IM and GA to GC.MethodsThis meta-analysis is followed and reported according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Electronic databases including EMBASE, PubMed, Web of Science databases, Scopus, and the Cochrane Library were searched until July 2018. Cochran's Q test and I-square (I2) test were used to examine heterogeneity across included studies. We pooled data using random-effect or fixed effect models indicated as incidence rate or proportion with 95% confidence intervals (CI). The variables of study included demographic data, endoscopy interval, follow up interval and time, GA and IM type and GC stage. Moreover, incidence rate of GC and progress rate, regress and persistence proportion in both GA and IM patients were assessed.ResultsOverall, 68 original articles out of 32981 citations were included in our meta-analysis. The pooled GC incidence rate in patients with GA was 1.24 (95% CI, 0.80, 1.76; I2: 83.6%) cases per 1,000 person-years. The rates of later diagnosis of IM and gastric dysplasia in patients with GA were estimated as 41.42 (95% CI, 3.11, 64.45; I2: 95.6%) and 6.23 (95% CI, 2.34, 11.46; I2: 83.0%) cases per 1,000 person-years, respectively. The pooled regressed proportion was 32.23 (95% CI, 18.07-48.02; I2: 94.0%) and the persistence proportion was 38.83 (95% CI, 20.20-59.13; I2: 97.0%) per 100 observations in GA patients. In IM studies, the pooled incidence rate of GC was 3.38 (95% CI, 2.13, 4.85; I2: 93.4%) cases per 1,000 person-years. The progressed rate to dysplasia in IM patient was estimated to be 12.51 (95% CI, 5.45, 22.03; I2: 95.1%) cases per 1,000 person-years. The pooled regressed proportion was 31.83 (95% CI, 25.48-38.51; I2: 91.0%) and the persistence proportion was 43.46 (95% CI, 32.52-54.71; I2: 96.0%) per 100 observations in IM patients.ConclusionOverall, the incidence of GC in patients with IM and GA are low but there is heterogeneity in data with the highest rate in Asian, males with those with incomplete IM. There is probability of regression or persistence without progression in patients with IM and GA who receive appropriate management.
| S-EPMC6660080 | biostudies-literature
Project description:Most patients with ulcerative colitis (UC) have mild-to-moderate disease activity, with low risk of colectomy, and are managed by primary care physicians or gastroenterologists. Optimal management of these patients decreases the risk of relapse and proximal disease extension, and may prevent disease progression, complications, and need for immunosuppressive therapy. With several medications (eg, sulfasalazine, diazo-bonded 5-aminosalicylates [ASA], mesalamines, and corticosteroids, including budesonide) and complex dosing formulations, regimens, and routes, to treat a disease with variable anatomic extent, there is considerable practice variability in the management of patients with mild-moderate UC. Hence, the American Gastroenterological Association prioritized clinical guidelines on this topic. To inform clinical guidelines, this technical review was developed in accordance with the Grading of Recommendations Assessment, Development and Evaluation framework for interventional studies. Focused questions included the following: (1) comparative effectiveness and tolerability of different oral 5-ASA therapies (sulfalsalazine vs diazo-bonded 5-ASAs vs mesalamine; low- (<2 g) vs standard (2-3 g/d) vs high-dose (>3 g/d) mesalamine); (2) comparison of different dosing regimens (once-daily vs multiple times per day dosing) and routes (oral vs rectal vs both oral and rectal); (3) role of oral budesonide in patients mild-moderate UC; (4) comparative effectiveness and tolerability of rectal 5-ASA and corticosteroid formulations in patients with distal colitis; and (5) role of alternative therapies like probiotics, curcumin, and fecal microbiota transplantation in the management of mild-moderate UC.
| S-EPMC6858923 | biostudies-literature
Project description:A subset of patients with ulcerative colitis (UC) present with, or progress to, moderate to severe disease activity. These patients are at high risk for colectomy, hospitalization, corticosteroid dependence, and serious infections. The risk of life-threatening complications and emergency colectomy is particularly high among those patients hospitalized with acute severe ulcerative colitis. Optimal management of outpatients or inpatients with moderate to severe UC often requires the use of immunomodulator and/or biologic therapies, including thiopurines, methotrexate, cyclosporine, tacrolimus, TNF-α antagonists, vedolizumab, tofacitnib, or ustekinumab, either as monotherapy or in combination (with immunomodulators), to mitigate these risks. Decisions about optimal drug therapy in moderate to severe UC are complex, with limited guidance on comparative efficacy and safety of different treatments, leading to considerable practice variability. Therefore, the American Gastroenterological Association prioritized development of clinical guidelines on this topic. To inform the clinical guidelines, this technical review was completed in accordance with the Grading of Recommendations Assessment, Development and Evaluation framework. Focused questions in adult outpatients with moderate to severe UC included: (1) overall and comparative efficacy of different medications for induction and maintenance of remission in patients with or without prior exposure to TNF-α antagonists, (2) comparative efficacy and safety of biologic monotherapy vs combination therapy with immunomodulators, (3) comparative efficacy of top-down (upfront use of biologics and/or immunomodulator therapy) vs step-up therapy (acceleration to biologic and/or immunomodulator therapy only after failure of 5-aminosalicylates, and (4) role of continuing vs stopping 5-aminosalicylates in patients being treated with immunomodulator and/or biologic therapy for moderate to severe UC. Focused questions in adults hospitalized with acute severe ulcerative colitis included: (5) overall and comparative efficacy of pharmacologic interventions for inpatients refractory to corticosteroids, in reducing risk of colectomy, (6) optimal dosing regimens for intravenous corticosteroids and infliximab in these patients, and (7) role of adjunctive antibiotics in the absence of confirmed infections.
| S-EPMC7117094 | biostudies-literature
Project description:Gastric intestinal metaplasia (GIM) represents a precancerous stage characterized by morphological and pathophysiological changes in the gastric mucosa, where gastric epithelial cells transform into a phenotype resembling that of intestinal cells. Previous studies have demonstrated that the intragastric administration of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) induces both gastric carcinoma and intestinal metaplasia in mice. Here, we show that MNNG induces GIM in three-dimensional (3D) mouse organoids. Our histological analyses reveal that MNNG-induced gastric organoids undergo classical morphological alterations, exhibiting a distinct up-regulation of CDX2 and MUC2, along with a down-regulation of ATP4B and MUC6. Importantly, metaplastic cells observed in MNNG-treated organoids originate from MIST1+ cells, indicating their gastric chief cell lineage. Functional analyses show that activation of the RAS signaling pathway drives MNNG-induced metaplasia in 3D organoids, mirroring the characteristics observed in human GIM. Consequently, modeling intestinal metaplasia using 3D organoids offers valuable insights into the molecular mechanisms and spatiotemporal dynamics of the gastric epithelial lineage during the development of intestinal metaplasia within the gastric mucosa. We conclude that the MNNG-induced metaplasia model utilizing 3D organoids provides a robust platform for developing preventive and therapeutic strategies to mitigate the risk of gastric cancer before precancerous lesions occur.
| S-EPMC11744189 | biostudies-literature