Intestinal Metaplasia In Patients Research Articles

Spatiotemporal genomic profiling of intestinal metaplasia reveals clonal dynamics of gastric cancer progression

Intestinal metaplasia (IM) is a pre-malignant condition of the gastric mucosa associated with increased gastric cancer (GC) risk. Analyzing 1,256 gastric samples (1,152 IMs) across 692 subjects from a prospective 10-year study, we identify 26 IM driver genes in diverse pathways including chromatin regulation (ARID1A) and intestinal homeostasis (SOX9). Single-cell and spatial profiles highlight changes in tissue ecology and IM lineage heterogeneity, including an intestinal stem-cell dominant cellular compartment linked to early malignancy. Expanded transcriptome profiling reveals expression-based molecular subtypes of IM associated with incomplete histology, antral/intestinal cell types, ARID1A mutations, inflammation, and microbial communities normally associated with the healthy oral tract. We demonstrate that combined clinical-genomic models outperform clinical-only models in predicting IMs likely to transform to GC. By highlighting strategies for accurately identifying IM patients at high GC risk and a role for microbial dysbiosis in IM progression, our results raise opportunities for GC precision prevention and interception.

S1886 Prevalence and Characteristics of Gastric Intestinal Metaplasia in Patients Undergoing Bariatric Surgery

S1886 Prevalence and Characteristics of Gastric Intestinal Metaplasia in Patients Undergoing Bariatric Surgery

Increased prevalence of gastric pathologies in patients with total hip and total knee prostheses: a retrospective endoscopic study

Aims: The objective of this retrospective study was to evaluate the prevalence of Helicobacter pylori (H. pylori) positivity, gastric atrophy, and intestinal metaplasia in patients with dyspeptic complaints who had undergone total hip and knee replacement surgeries, compared to a control group without prosthesis.
 Methods: The study group consisted of 51 patients with dyspeptic complaints and total knee and hip prosthesis, while the control group comprised 75 patients with similar complaints but without prosthesis. Endoscopic gastric biopsies were obtained from all participants, and the presence of H. pylori, gastric atrophy, and intestinal metaplasia were evaluated.
 Results: The prevalence of H. pylori positivity, gastric atrophy, and intestinal metaplasia were significantly higher in patients who underwent total knee and hip replacement compared to the control group without prosthesis.
 Conclusion: The results of this study suggest that patients who undergo total hip and knee replacement surgeries may be at higher risk for developing gastric pathologies, such as H. pylori infection, gastric atrophy, and intestinal metaplasia. Therefore, it is recommended that physicians who care for these patients monitor them closely for these conditions and consider endoscopic surveillance as part of their management plan.

Pancreatic acinar metaplasia at the gastroesophageal junction is associated with protective effect against intestinal metaplasia in patients with gastroesophageal reflux disease

Anecdotal evidence suggests that pancreatic acinar metaplasia (PAM) and intestinal metaplasia (IM) overlap infrequently at the gastroesophageal junction/distal esophagus (GEJ/DE). The goal of this study was to evaluate the significance of PAM at GEJ/DE in relation to IM in patients with gastroesophageal reflux disease (GERD). Group 1 comprised 230 consecutive patients with GEJ/DE biopsies (80.6% with GERD symptoms). Group 2 comprised 151 patients with established GERD and GEJ/DE biopsies taken before Nissen fundoplication. Group 3 comprised 540 consecutive patients used for a follow-up study of PAM. PAM was present in 15.7%-15.9% and IM in 24.8%-31.1% of patients in groups 1 and 2, respectively. PAM-IM overlap was present in 2.2%-3.3%, respectively. Patients with PAM were, on average, 6-12 years younger than patients with IM, and were predominantly female (72.2%-75%), in contrast to patients with IM (47.3%-32%). In the unadjusted logistic regression model, patients with PAM were 69%-65% less likely to also have IM, as compared to patients without PAM. In the fully adjusted model, patients with PAM were 35%-61% less likely to also have IM, although the P-value was not significant. Follow-up analysis of patients with PAM from group 3 (n=28) demonstrated the prevalence of IM and PAM in subsequent biopsies at 7.1% and 60.7%, respectively. No cases showed PAM-IM overlap on follow-up. The data suggests that PAM at the GEJ/DE is associated with protective effect against IM and thus could be useful as a marker of decreased susceptibility to IM.

Type A, Type B, and Non-atrophic Gastritis

The gastric cancer risk varies based on the etiology and severity of gastritis, which depends on a history of Helicobacter pylori infection and the secretory capacity of the stomach. Type A gastritis is associated with reverse atrophy of the corpus and type B with progressive atrophy extending from the antrum to the corpus. Diffuse or spotty redness in the corpus together with high serum pepsinogen (PG) II levels and a low PG I/II ratio are observed in patients with H. pylori infection when secretory capacity of the stomach is intact. Diffuse-type gastric cancer may develop near the gastric folds, which is a rare site of atrophy. Low serum PG I levels are associated with progressive gastric corpus atrophy and intestinal metaplasia in patients with chronic and previous H. pylori infections. This clinical scenario predisposes patients to intestinal-type gastric cancer, which originates in the atrophic and metaplastic gastric mucosa. Conversely, a high PG I/II ratio is observed in patients without H. pylori infection. Serum PG I levels and the PG I/II ratio are high in patients with acute H. pylori-negative gastritis, including drug-induced gastritis but are significantly low in autoimmune gastritis. Gastric neuroendocrine tumors may develop in patients with autoimmune gastritis or in those with long-term acid suppressant use. Fasting serum gastrin levels and the risk of neuroendocrine tumors are high in both cases. In this review, types of gastritis are summarized along with evaluation performed to determine the secretory capacity of the background gastric mucosa.

Differences in gastric microbiota and mucosal function between patients with chronic superficial gastritis and intestinal metaplasia.

Chronic superficial gastritis (CSG) and intestinal metaplasia (IM) can further develop into gastric cancer, which seriously endangers the health of people all over the world. In this study, the differences in gastric microbiota between CSG patients and IM patients were detected by 16S rRNA gene sequencing. As the expression levels of mucin and CDX2 are closely related to IM, the expression differences of mucin (MUC2 and MUC5AC) and CDX2 in the gastric mucosa of CSG patients and IM patients were detected by Western blot and qRT-PCR. The results showed that both Faith_pd and Observed_species indexes of microbiota in the gastric juice of CSG patients were significantly higher than those of IM patients. At the genus level, Thermus and Anoxybacillus were dominant in the gastric juice of IM patients, and Helicobacter was dominant in the gastric juice of CSG patients. Non-metric multidimensional scaling (NMDS) demonstrated that the dispersion of samples in the CSG group is greater than that in the IM group, and some samples in the CSG group are clustered with samples in the IM group. The KEGG metabolic pathway difference analysis of gastric juice microbiota in CSG and IM patients revealed that the gastric juice microbiota in the CSG and IM patients were significantly enriched in the amino acid metabolism, carbohydrate metabolism, and metabolism of cofactors and vitamins, and the functional differences between the two groups were mainly concentrated in the bacterial secretion system (VirB1, VirB2, VirB3, VirD2, and VirD4). In conclusion, there are significant differences in gastric microbiota and mucosal function between the CSG and IM patients. Moreover, the results of this study may provide a new means for the detection of CSG and IM and a new direction for the prevention and treatment of CSG and IM.

Identification of anti-Helicobacter pylori antibody signatures in gastric intestinal metaplasia.

BackgroundChronic Helicobacter pylori infection may induce gastric intestinal metaplasia (IM). We compared anti-H. pylori antibody profiles between IM cases and non-atrophic gastritis (NAG) controls. MethodsWe evaluated humoral responses to 1528 H. pylori proteins among a discovery set of 50 IM and 50 NAG using H. pylori protein arrays. Antibodies with ≥ 20% sensitivity at 90% specificity for either group were selected and further validated in an independent set of 100 IM and 100 NAG using odds ratios (OR). A validated multi-signature was evaluated using the area under the receiver operating characteristics curve (AUC) and net reclassification improvement (NRI). ResultsSixty-two immunoglobulin (Ig) G and 11 IgA antibodies were detected in > 10%. Among them, 22 IgG and 6 IgA antibodies were different between IM and NAG in the discovery set. Validated antibodies included 11 IgG (anti-HP1177/Omp27/HopQ [OR = 8.1, p < 0.001], anti-HP0547/CagA [4.6, p < 0.001], anti-HP0596/Tipα [4.0, p = 0.002], anti-HP0103/TlpB [3.8, p = 0.001], anti-HP1125/PalA/Omp18 [3.1, p = 0.001], anti-HP0153/RecA [0.48, p = 0.03], anti-HP0385 [0.41, p = 0.006], anti-HP0243/TlpB [0.39, p = 0.016], anti-HP0371/FabE [0.37, p = 0.017], anti-HP0900/HypB/AccB [0.35, p = 0.048], and anti-HP0709 [0.30, p = 0.003]), and 2 IgA (anti-HP1125/PalA/Omp18 [2.7, p = 0.03] and anti-HP0596/Tipα [2.5, p = 0.027]). A model including all 11 IgG antibodies (AUC = 0.81) had better discriminated IM and NAG compared with an anti-CagA only (AUC = 0.77) model (NRI = 0.44; p = 0.001).ConclusionsOur study represents the most comprehensive assessment of anti-H. pylori antibody profiles in IM. The target antigens for these novel antibodies may act together with CagA in the progression to IM. Along with other biomarkers, specific H. pylori antibodies may identify IM patients, who would benefit from surveillance.Supplementary Information The online version contains supplementary material available at 10.1007/s00535-022-01933-0.

Multicenter Randomized Controlled Trial of Surveillance Versus Endoscopic Therapy for Barrett’s Esophagus With Low-grade Dysplasia: The SURVENT Trial: Study Rationale, Methodology, Innovation, and Implications

Multicenter Randomized Controlled Trial of Surveillance Versus Endoscopic Therapy for Barrett’s Esophagus With Low-grade Dysplasia: The SURVENT Trial: Study Rationale, Methodology, Innovation, and Implications

Endoscopic diagnosis of gastric intestinal metaplasia in patients with autoimmune gastritis using narrow-band imaging: does pseudopyloric metaplasia muddy the waters?

Background and study aims In autoimmune atrophic gastritis (AAG), associated with intestinal (IM) and/or pseudopyloric metaplasia (PPM), endoscopic surveillance is recommended for gastric cancer risk mainly linked to IM. Endoscopic Grading of Gastric Intestinal Metaplasia (EGGIM) reliably identifies IM, but has not been assessed in AAG. We aimed to assess the performance of EGGIM (index test) versus histology (reference test) of corpus IM in AAG. Patients and methods This was a cross-sectional study of 210 AAG patients undergoing surveillance gastroscopy with narrow-band imaging (NBI): corpus IM scored according to EGGIM, histology according to updated Sydney system, and morphological criteria. Results NBI identified corpus IM in 88.6 % of AAG patients: EGGIM were 0, 1, 2, 3, 4 in 11.4 %, 0.5 %, 33.3 %, 1.9 %, and 52.9 %, respectively. Histology identified corpus IM in 78.1 % and PPM in 79.5 % of patients. PPM was present with IM in 57.6 % and without IM in 21.9 % patients, 20.5 % had IM without PPM. EGGIM, compared to histology, correctly classified 76.2 % of patients, showing high sensitivity (91.5 %, 95 %CI 86.1–95.3). EGGIM correctly classified 93 % of patients with IM without PPM, 90.9 % with both metaplasias, and 21.7 % with PPM without IM yielding low specificity (21.7 %, 95 %CI 10.9–36.4). Conclusions In AAG, EGGIM showed high accuracy and sensitivity identifying > 90 % of patients with histological corpus IM. EGGIM overestimated IM when PPM without IM was present, yielding low specificity. These findings raise the question of whether in AAG, PPM and IM may display similar endoscopic features on NBI.

Epigenteic Alteration of DOK7 Gene CpG Island in Blood Leukocyte of Patients with Gastric Cancer and Intestinal Methaplasia.

Intestinal metaplasia (IM) is a benign lesion with no serious concern for patients' health. On the other hand, gastric cancer (GC) is a malignant lesion that has to be differentially diagnosed from benign intestinal metaplasia. Epigenetic modifications have been suggested to play an important role in cancer initiation and development, and they have been investigated as a reliable biomarker tool even for early cancer diagnosis. Whole blood leucocytes (WBC) are potentially the most accessible tissue for cancer early diagnosis, especially for GC, which is hard to diagnose in the early stage. This study aims to investigate the methylation status of DOK7 gene CpG island in blood leukocytes of patients with IM and GC compared to normal control groups. DNA was extracted from the whole blood of 30 IM patients, 30 GC patients, and 34 normal controls samples, and MSRE-PCR was utilized to evaluate the loci methylation status. Significant hypermethylation of DOK7 gene CpG has been observed in GC 88.1 % (p < 0.001) and IM 66.0 % (p = 0.03) in comparison to the normal control group 56.8%. A cutoff upper than 84.5 % of hypermethylation is considered as a presence of gastric cancer malignant lesions. This is the first reported on hypermethylation in DOK7 CPG in blood leukocytes of patients with GC and IM and establishing a laboratory blood based test that may be useful as a novel biomarker test in the early diagnosis and screaning of GC and IM.

Lamb’s tripe extract and vitamin B12 capsule plus celecoxib reverses intestinal metaplasia and atrophy: A retrospective cohort study

BACKGROUNDChronic atrophic gastritis (AG) with intestinal metaplasia (IM) significantly increases the risk of gastric cancer. Some medicines have showed definite therapeutic effects in AG and IM regression. AIMTo validate the efficacy of Lamb’s tripe extract and vitamin B12 capsule (LTEVB12) initial therapy and celecoxib rescue therapy for IM and AG.METHODSA total of 255 patients were included to receive LTEVB12 initial therapy (2 capsules each time, three times daily for 6 mo) in hospital in this study. The patients with failure of IM regression continued to receive celecoxib rescue therapy (200 mg, once daily for 6 mo). After each therapy finished, the patients underwent endoscopy and biopsy examination. The regression efficiency was assessed by the operative link on gastritis assessment (OLGA) and the operative link on the gastric intestinal metaplasia assessment (OLGIM) staging system. Logistic regression analysis was applied to identify factors associated with the curative effect.RESULTSFor LTEVB12 initial therapy, the reversal rates of IM and AG were 52.95% and 48.24%, respectively. Analogously, for celecoxib rescue therapy, the effective rates for IM and AG were 56.25% and 51.56%, respectively. The IM regression rate of complete therapy was up to 85.03%. In different OLGA and OLGIM stages of IM patients, therapeutic efficiency showed a significant difference in each group (P < 0.05). For both therapies, patients with high stages (III or IV) of both the OLGA and OLGIM evaluation systems showed a higher IM or AG regression rate than those with low stages (I or II). Among patients with high stages (OLGIM III and IV), the IM regression rate was above 70% for each therapy. Eating habits, fresh vegetable intake, and high-salt diet were identified as independent factors for the IM reversal effect of LTEVB12 therapy, especially high-salt diet (odds ratio = 1.852, P < 0.05).CONCLUSIONMonotherapy could reverse IM and AG. LTEVB12 initial therapy and celecoxib rescue therapy significantly increase the regression effect. IM may not be the point of no return among gastric precancerous lesions.

Is intestinal metaplasia the point of no return in the progression of gastric carcinogenesis?

Is intestinal metaplasia the point of no return in the progression of gastric carcinogenesis?

Effectiveness of esophagogastroduodenoscopy in changing treatment outcome in refractory gastro-esophageal reflux disease

Background/aims The effectiveness of screening esophagogastroduodenoscopy (EGD) for refractory gastroesophageal reflux disease (GERD) symptoms alone has not been validated. Methods We performed an observational study of patients with refractory GERD who underwent EGD from 2013 to 2016 at a tertiary hospital. Among 928 patients with GERD, we excluded patients with other alarm features, other indications for EGD, history of gastroesophageal surgery, or EGD done for other diagnostic procedures, and identified 301 patients who underwent EGD solely for persistent reflux symptoms such as heartburn or regurgitation. Results Among 301 patients with refractory GERD, 81.4% of patients were taking PPIs. 49.8% of patients had completely normal EGD findings and 33.6% of patients had benign or incidental findings. Two patients (0.6%) had LA grade C or D esophagitis, and 16.3% of patients had irregular Z line or salmon-colored mucosa. 91.0% (122/134) who had a biopsy had normal or benign findings. 4.0% (12/301) of patients had biopsy-proven intestinal metaplasia which is similar to the previously known prevalence of intestinal metaplasia in patients without heartburn (5.6%) and none had dysplasia or malignancy. Male sex was associated with endoscopic intestinal metaplasia suspected lesions in multivariate analysis (OR: 1.96, 95% CI: 1.04–3.70, p = .036) but not biopsy-proven intestinal metaplasia. Elderly age, obesity, alcohol or cigarette consumption, PPI use, GERD duration >3–5 years did not predict endoscopically suspected or biopsy-proven intestinal metaplasia. Only 5% of patients had a pH-impedance study for refractory reflux symptoms. Conclusions Most patients who underwent EGD for refractory GERD symptoms alone did not have pathological findings requiring a change in management. Screening EGD for patients only with persistent reflux symptoms should not be routinely recommended.

Management of gastric intestinal metaplasia in patients undergoing routine endoscopy before bariatric surgery.

Routine preoperative endoscopic evaluation for bariatric surgery is controversial; however, for patients undergoing endoscopy, some findings may alter surgical management. Gastric intestinal metaplasia (GIM) is found in up to 11.7% of the general population. When associated with determined risk factors, GIM has a risk of progressing to gastric cancer. The aim of our study was to assess the prevalence of GIM and possible associated factors in those undergoing bariatric surgery. We performed a retrospective chart review of patients who underwent primary sleeve gastrectomy or Roux-en-Y gastric bypass at our institution between January 1, 2016 and June 30, 2020. Baseline characteristics and preoperative endoscopic findings were obtained from all patients. Histopathologic analysis of sleeve gastrectomy specimens was reviewed. We identified 753 patients. Mean (SD) age and body mass index were 49.0 (13.1) years and 43.9 (7.1) kg/m2, respectively. Procedures consisted of 411 (54.6%) gastric bypasses and 342 (45.4%) sleeve gastrectomies. Esophagitis and Barrett esophagus were found in 18.1% and 5.0% of patients, respectively. Preoperative gastric biopsy identified Helicobacter pylori in 6.4% and GIM in 2.7%. Regression analysis found an association of Barrett esophagus (odds ratio 4.60; 95% CI 1.25-16.82) and age ≥ 60years (odds ratio 2.67; 95% CI 1.04-6.90) with preoperative findings of GIM. Histopathologic analysis of sleeve gastrectomy specimens identified H. pylori in 1.8% and GIM in 0.9%. Older age and Barrett esophagus were associated with GIM in preoperative gastric biopsy. This association emphasizes the importance of a diligent examination during preoperative endoscopy.

Circular RNA hsa_circ_0007507 May Serve as a Biomarker for the Diagnosis and Prognosis of Gastric Cancer.

PurposeThe morbidity and mortality of gastric cancer (GC) remain high worldwide. In recent years, circular RNAs (circRNAs) have attracted widespread attention among cancer researchers due to the stable ring structure. The present work aims to find serum circRNA biomarkers that can be used in clinical applications and effective diagnosis.MethodsHsa_circ_0007507 was extracted through circRNA sequencing. Exonuclease digestion assay, actinomycin D, agarose gel electrophoresis (AGE), and Sanger sequencing verified the potential of hsa_circ_0007507 as a biomarker. Besides, a real-time fluorescent quantitative polymerase chain reaction (RT-qPCR) was established to detect the level of expression of hsa_circ_0007507. Twenty cases of GC and the paired adjacent tissues were collected to verify its overexpression. Then, serum samples from 30 cases of colorectal cancer, 30 cases of thyroid cancer, and 30 cases of breast cancer were collected to verify their organ specificity. Additionally, serum samples from 80 healthy people, 62 gastritis patients, 31 intestinal metaplasia patients, and 100 GC patients were collected, and the diagnostic efficacy was evaluated through analysis of the receiver operating characteristic (ROC) curve. Furthermore, 16 post-operative GC samples, samples of 65 relapsed patients and 36 non-relapsed patients were collected to evaluate the prognosis of GC.ResultsThe level of expression of hsa_circ_0007507 in GC tissues was up-regulated (p = 0.0121), which was consistent with the results of circRNA sequencing. Exonuclease digestion assay and actinomycin D confirmed that hsa_circ_0007507 had a stable structure and a longer half-life. In the analysis of organ specificity experiments, serum hsa_circ_0007507 did not have specificity for patients with colorectal cancer (p = 0.5319), thyroid cancer (p = 0.5422), or breast cancer (p = 0.5178). Analysis of diagnostic efficacy indicated that the expression of hsa_circ_0007507 was significantly higher than that of normal people (p <0.0001); the area under the ROC (AUC) was 0.832 (95% CI: 0.771-0.892); the diagnostic power of hsa_circ_0007507 was higher than that of CEA (AUC = 0.765, 95% CI: 0.697-0.833) and CA199 (AUC = 0.587, 95% CI: 0.504-0.67). Through diagnosis using a combination of the three, GC patients could be distinguished from normal people (AUC = 0.849), and higher diagnostic efficiency could be achieved. The expression of serum hsa_circ_0007507 in GC patients significantly decreased after surgery (p = 0.001). Besides, the expression of serum hsa_circ_0007507 in patients with post-operative recurrence was significantly up-regulated again (p = 0.0139).ConclusionsSerum hsa_circ_0007507 is differentially expressed in GC patients, post-operative GC patients, gastritis patients, intestinal metaplasia patients and relapsed patients, suggesting that serum hsa_circ_0007507 can be used as a new diagnostic and dynamic monitoring biomarker for GC.

The Transition from Gastric Intestinal Metaplasia to Gastric Cancer Involves POPDC1 and POPDC3 Downregulation.

Intestinal metaplasia (IM) is an intermediate step in the progression from premalignant to malignant stages of gastric cancer (GC). The Popeye domain containing (POPDC) gene family encodes three transmembrane proteins, POPDC1, POPDC2, and POPDC3, initially described in muscles and later in epithelial and other cells, where they function in cell–cell interaction, and cell migration. POPDC1 and POPDC3 downregulation was described in several tumors, including colon and gastric cancers. We questioned whether IM-to-GC transition involves POPDC gene dysregulation. Gastric endoscopic biopsies of normal, IM, and GC patients were examined for expression levels of POPDC1-3 and several suggested IM biomarkers, using immunohistochemistry and qPCR. Immunostaining indicated lower POPDC1 and POPDC3 labeling in IM compared with normal tissues. Significantly lower POPDC1 and POPDC3 mRNA levels were measured in IM and GC biopsies and in GC-derived cell lines. The reduction in focal IM was smaller than in extensive IM that resembled GC tissues. POPDC1 and POPDC3 transcript levels were highly correlated with each other and inversely correlated with LGR5, OLFM4, CDX2, and several mucin transcripts. The association of POPDC1 and POPDC3 downregulation with IM-to-GC transition implicates a role in tumor suppression and highlights them as potential biomarkers for GC progression and prospective treatment targets.

S0405 Wide Area Transepithelial Sampling in Adjunct to Forceps Biopsy in Post Treatment Barret’s Esophagus: Increasing Diagnostic Yield

INTRODUCTION: Previous studies have shown that WATS-3D as an adjunct to both targeted and random FB increases the diagnostic yield for the detection of dysplasia. However, till date, there have been no published studies that assess the use of WATS-3D after endoscopic ablation or endoscopic mucosal resection (EMR). The aim of this study is to evaluate whether the addition of WATS-3D to standard FB would improve the yield of detecting intestinal metaplasia, dysplasia or carcinoma in patients undergoing post-ablation/EMR surveillance endoscopy and if this changes the medical management. METHODS: A single center, retrospective cohort study was conducted. Consecutive patients undergoing WATS-3D procedure after post-ablation between 2018 and 2019 with a known prior history of BE with low-grade dysplasia (LGD), high-grade dysplasia (HGD), and/or intramucosal adenocarcinoma (IMCA) were included. Data was collected on endoscopic information, pathologic evaluation of slides, and other demographic variables. RESULTS: A total of 37 subjects with a confirmed history of BE with a prior endoscopic intervention underwent EGD with FB and WATS-3D sampling. Biopsies from FB and WATS-3D were compared: negative for dysplasia or positive for metaplasia/dysplasia (Table 2). The readings were concordant on both FB and WATS-3D in 28/37 subjects or 75.6% of the samples. One additional case was detected only by FB showing LGD, representing a yield of FB alone of 2.7%. Eight additional cases were detected only by WATS-3D. Seven of them showed intestinal metaplasia and one showed indefinite for dysplasia. This increment represents an increased yield of detected metaplasia of 350% (=7/2) with WATS-3D. The absolute increase of 7 cases of metaplasia, results in a number needed to treat (NNT) of 37/7 = 5.2. Three of those additional 8 cases detected by WATS-3D, had an increase in the interval of follow-up (Table 3). The former constitutes a change in management of 37.5% of those additional 8 cases. CONCLUSION: Our study shows that WATS-3D as an adjunct to FB increases the diagnostic yield for the detection of intestinal metaplasia in patients undergoing post-ablation/resection surveillance endoscopy by 350% (=7/2) (NNT: 5.2). In addition, WATS-3D had a direct impact of change in the medical management with closer follow up in 37.5% of those additional 8 cases. Further multicenter prospective studies are needed to evaluate the diagnostic benefit of WATS-3D in surveillance endoscopies.Table 1.: Clinical and demographic characteristics of subjects with BE (n = 37)Table 2.: Forceps biopsy and WATS-3D biopsy reads: negative for dysplasia, positive for metaplasia or dysplasiaTable 3.: Interval of follow-up and change in management

Feasibility of Plasma-Methylated SFRP2 for Early Detection of Gastric Cancer.

Gastric cancer (GC) is fifth most frequently diagnosed cancer and second leading cause of cancer in China. More than 80% of GC are diagnosed at an advanced stage due to low uptake rate of invasive screening method. The performance of methylated SFRP2 test was evaluated in 236 plasma samples, including 92 patients with GC, 16 intestinal metaplasia patients, 26 gastric fundic gland polyp patients, 13 small adenoma patients, 39 hyperplastic polyp patients, and 50 control patients. The sensitivity of plasma methylated SFRP2 was compared to serum CEA, CA72-4, CA19-9, and CA242 results in 79 patients with GC. The sensitivities for detecting GC and gastric intestinal metaplasia by methylated SFRP2 test were 60.9% and 56.3% with a specificity of 86.0%. Methylated SFRP2 test had significantly higher positive detection rate for patients with GC than gastric fundic gland polyp, small adenoma, and hyperplastic polyp patients. In 79 patients with GC, the sensitivities of CEA, CA72-4, CA19-9, and CA242 for detecting GC were 22.8%, 16.5%, 12.7%, and 11.4%. In comparison, the sensitivity of methylated SFRP2 test for detecting GC was 58.2%. Plasma methylated SFRP2 test may become a valuable tool for the noninvasive detection of GC and precursor lesions and showed higher sensitivity than serum tumor markers.

Association between interleukin-21 gene rs907715 polymorphism and gastric precancerous lesions in a Chinese population.

BACKGROUNDThe single nucleotide polymorphisms of interleukin-21 (IL-21) gene were confirmed to be related to various diseases, but no studies have examined the possible role of IL-21 single nucleotide polymorphisms (SNPs) (rs907715, rs2221903, and rs12508721) in gastric precancerous lesions.AIMTo explore the associations between SNPs of IL-21 gene (rs907715, rs2221903, and rs12508721) and gastric precancerous lesions in a Chinese population.METHODSThree SNPs of IL-21 were genotyped using polymerase chain reaction–ligase detection reaction in 588 cases and 290 healthy controls from May 2013 to December 2016 in northwestern China. Gastric precancerous lesions were confirmed by endoscopic examination and categorized as non-atrophic gastritis, atrophic gastritis, and intestinal metaplasia. Descriptive statistic and logistic regression were used for data analyses.RESULTSIL-21 rs907715 genotype CC and C frequencies were higher in in patients with gastric precancerous lesions than in the controls (OR = 1.59, 95%CI: 1.06-2.38, P = 0.013; OR = 1.28, 95%CI: 1.01-2.22, P = 0.044, respectively) after adjusting for confounding factors. For SNP rs907715 in intestinal metaplasia patients, significant differences between cases and controls were observed in the frequencies of genotype CC and C (OR = 1.92, 95%CI: 1.24-2.98, P = 0.004; OR = 1.53, 95%CI: 1.04-2.24, P = 0.028, respectively); for non-atrophic gastritis and atrophic gastritis patients, the CC and C genotypes showed no significant association with risk in all models. No association between either rs2221903 or rs12508721 and gastric precancerous lesions was found in the present study. In the haplotype analysis, the TC haplotype (rs907715 and rs12508721) and TT haplotype (rs2221903 and rs907715) were more frequent in the case group than control group (P < 0.05).CONCLUSIONOur findings indicate that SNP rs907715 of IL-21 gene is associated with gastric precancerous lesions. The TC haplotype (rs907715 and rs12508721) and TT haplotype (rs2221903 and rs907715) increased the risk of gastric precancerous lesions. If confirmed, these findings will shed light on the etiology of precancerous lesions.

Recurrence Is Rare Following Complete Eradication of Intestinal Metaplasia in Patients With Barrett’s Esophagus and Peaks at 18 Months

There have been few studies describing the long-term durability of complete eradication of intestinal metaplasia (CE-IM) in patients with Barrett's esophagus (BE)-related neoplasia who received endoscopic eradication therapy (EET). Data are needed to guide surveillance interval protocols and identify patients at risk for recurrence. We assessed the rate of recurrence of intestinal metaplasia and dysplasia, histologic features, and outcomes after recurrence of CE-IM, and identified factors associated with recurrence. We performed a prospective study of 807 patients with BE who underwent EET, which produced CE-IM, at 4 tertiary-care referral centers, from January 2013 to October 2018. Kaplan-Meier estimates of cumulative incidence rates (IR) of recurrence were calculated for up to 5 years following CE-IM and were stratified by baseline level of histology. Density estimates of recurrence were used to determine the change in the rate of recurrence over time. We conducted logistic regression analysis to identify factors associated with recurrence. Intestinal metaplasia recurred in 121 patients (15%; IR, 5.2/100 person-years), and dysplasia recurred in 41 patients (5.1%; IR, 1.8/100 person-years), after a median follow-up time of 2317 person-years. The rate of recurrence was not constant and the time to any recurrence converged to a normal distribution; recurrences peaked at 1.6 y after patients had CE-IM. Baseline high-grade dysplasia or intramucosal cancer (adjusted odds ratio [aOR], 4.19), presence of reflux symptoms (aOR, 12.1) or hiatal hernia (aOR, 13.8), and number of sessions required to achieve CE-IM (aOR, 1.8) were associated with recurrence. In a prospective study of a large cohort of patients with BE undergoing EET, we found a low rate of recurrence after CE-IM. The rate of recurrence peaked at 1-2 y after CE-IM. These findings indicate that aggressive surveillance might not be necessary more than 1 y after CE-IM and should be considered in surveillance guidelines. Clinicaltrials.gov no: NCT02634645.