Surveillance and surgery for Barrett's esophagus: more results from Sweden. Oberg S, Johansson J, Wenner J, et al. Endoscopic Surveillance of Columnar-Lined Esophagus; Frequency of Intestinal Metaplasia Detection and Impact of Antireflux Surgery Ann Surg 2001;234:619-26
0
Citation
6
Reference
10
Related Paper
Abstract:
Abstract This study evaluated the prevalence of intestinal metaplasia (IM) in patients with varying lengths of columnar-lined esophagus (CLE) during long-term endoscopic and histopathologic surveillance. A total of 177 patients were followed for a median surveillance period of 5.1 yr and a median four endoscopies per patient. Fifty-two percent of the patients had IM at first surveillance endoscopy. The prevalence of IM increased with increasing number of endoscopies, and after six endoscopies the IM prevalence had increased from ≈30% to ≈64% in patients with a 1–2 cm CLE length, and from ≈45% to ≈89% in those with a 3–4 cm length. IM was found in longer CLE segments early in the surveillance period, whereas detection of IM was evenly spread out over the surveillance period in the short segment patients. A second aim of this study was to compare the effectiveness of antireflux surgery with acid suppressant therapy in preventing the development of IM. Studying patients without IM at the first two endoscopies, the investigators found that IM developed significantly less frequently among the 20 surgically treated patients compared with the 49 medically treated patients (PPI therapy in 45 out of 49). The time to development of IM was shorter in the medically treated group (p = 0.001, log-rank test) and in a multivariable logistic analysis, prior antireflux surgery was the only significant factor associated with a reduced risk of intestinalization (10.3-fold decreased risk).Keywords:
Intestinal metaplasia
Barrett's esophagus
Although the pathogenic role of gastroesophageal reflux in Barrett's esophagus is widely accepted, the pattern of gastric and esophageal pH profile of patients with Barrett's esophagus is not well documented. Moreover, the observation that a columnar-lined esophagus can also develop after gastrectomy implies that chronic irritation of the lower esophagus by duodenal juice can be as harmful as acid reflux. To test this hypothesis, we simultaneously monitored gastric and esophageal pH in 19 patients with endoscopically and histologically proven Barrett's esophagus, in 35 with slight-to-moderate esophagitis and in 10 healthy subjects. The gastroesophageal reflux pattern in both Barrett's esophagus and esophagitis was characterized by mainly acid refluxes. Esophageal acid exposure (% time pH < 4) was 39.4 in patients with Barrett's esophagus, 14.6 in patients with esophagitis (P < 0.05), and 3.1 in healthy subjects (P < 0.05). Seven of 19 patients with Barrett's esophagus and 7 of 35 with esophagitis had evidence of alkaline reflux too; but pure alkaline refluxes accounted for only 1.9% of total time in Barrett's esophagus and 0.3% in esophagitis patients. In conclusion, these results confirm the high prevalence and severity of acid reflux in patients with Barrett's esophagus and show that the reflux of pure alkaline material into the esophagus is a rare event in both Barrett's esophagus and esophagitis patients.
Reflux esophagitis
Barrett's esophagus
Esophagitis
Cite
Citations (10)
Chronic atrophic gastritis with intestinal metaplasia was considered as gastric precancerous lesions.Exploring effective drugs for its treatment is of great significance in reducing the morbidity and mortality of gastric cancer.Aims: To study the efficacy of gefarnate for the treatment of chronic atrophic gastritis with intestinal metaplasia.Methods: A total of 133 cases of chronic atrophic gastritis with intestinal metaplasia were enrolled and randomly assigned into gefarnate group and control group.Patients in gefarnate group were given gefarnate 100 mg tid for 3 months,and patients in control group were given Weifuchun 1400 mg tid for 3 months.Before and 3 months after treatment,subtyping of intestinal metaplasia was demonstrated by AB-PAS and HID-AB staining,and the inflammation degree of gastric mucosa was determined by HE staining.Results: The rate of chronic atrophic gastritis with intestinal metaplasia reversed to nonatrophic gastritis(reversal rate) in gefarnate group was significantly higher than that in control group(32.84% vs.15.15%,P = 0.017) 3 months after treatment.The reversal rate of incomplete-type small intestinal metaplasia in gefarnate group was significantly higher than that in control group(48.28% vs.16.67%,P = 0.016).The reversal rate of complete-type small intestinal metaplasia in gefarnate group was higher than that in control group but not reaching statistical significance(33.33% vs.16.67%,P = 0.375).The reversal rate of small intestinal metaplasia was significantly higher than the reversal rate of colon metaplasia in gefarnate group(44.74% vs.17.24%,P = 0.018).The inflammation degree of gastric mucosa in gefarnate group was significantly lower than that in control group(χ2= 11.061,P = 0.011).Conclusions: Gefarnate is effective for chronic atrophic gastritis,and it can reverse incomplete-type small intestinal metaplasia.
Intestinal metaplasia
Atrophic gastritis
Metaplasia
Chronic gastritis
Cite
Citations (0)
Objective To compare the differences in mucin-histochemistry and etiology of Barrett's esophagus (BE) intestinal metaplasia (IM) , cardiac intestinal metaplasia (CIM) and gastric antrum intestinal metaplasia (GA-IM). Methods Alcian blue /periodic acid-schiff (AB/PAS) and high iron diamine / alcian blue (HID/AB) histochemical methods were used to classify IM in BE, cardia and gastric antrum, and IM were classified into three subtypes: complete small intestinal type (type Ⅰ ) , incomplete small intestinal type (type Ⅱ) and incomplete colonic type (type Ⅲ). Compared the prevalence of different subtypes of IM in above-mentioned sites, and investigated their relationships among the symptoms of gastroesophageal reflux disease (GERD) and Helicobacter pylori (Hp) infection. Results The prevalence of type Ⅲ IM in long-segment BE (LSBE) and short-segment BE (SSBE) is 75. 0% and 63. 3% respectively, it is significantly higher than that in CIM (23. 1% ) and GA-IM ( 17. 7% ) (P 0. 01 ). The positive rates of the symptoms of GERD in LSBE, SSBE, CIM and GA-IM are 78. 6% , 76. 7% , 42. 3% and 17. 7% respectively , and the former three are significantly higher than the latter one (P 0. 01). The positive rates of Hp infection in LSBE (17. 9% ) and SSBE (20. 0% ) are significantly lower than those in CIM (46. 2% ) and GA-IM (64. 7% ) (P 0. 01). Conclusion The subtypes of IM in LSBE and SSBE are type 1 predominantly , but there are low incidence of type 3333 in CIM and GA-IM. LSBE and SSBE are significantly associated with GERD, and aren't with Hp infection. However, CIM and GA-IM are mainly related to Hp infection, while GERD probably participates to the pathogenesis of CIM.
Intestinal metaplasia
Barrett's esophagus
Bile reflux
Cite
Citations (0)
Barrett's esophagus is the only known esophageal precursor for the development of esophageal adenocarcinoma. However, screening for Barrett's esophagus remains controversial. Although screening is advocated in selected populations, it is unclear how it should be implemented. In this review, the current definition of Barrett's esophagus will be discussed. There will be a review of the emerging evidence supporting the cost-effectiveness of screening and surveillance for Barrett's esophagus in preventing esophageal adenocarcinoma. The known risk factors for Barrett's esophagus and the development of esophageal adenocarcinoma, currently utilized to determine the appropriate populations to screen, will be reviewed. Finally we will review the standard techniques utilized to screen for Barrett's esophagus and examine new technologies that might improve the efficacy and availability of Barrett's esophagus screening.
Barrett's esophagus
Esophageal adenocarcinoma
Cite
Citations (5)
Confocal laser endomicroscopy (CLE) can provide real-time, microscopic visualization of the gastrointestinal mucosa, allowing an endoscopic approach to the histologic evaluation of Barrett's esophagus and Barrett's esophagus-associated neoplasia.Both endoscope-based (eCLE) and probe-based (pCLE) CLE systems have been used to evaluate Barrett's esophagus and Barrett's esophagus-associated neoplasia. Criteria for distinguishing Barrett's esophagus with neoplasia from nondysplastic Barrett's esophagus have been developed and validated for both eCLE and pCLE. Several studies have shown excellent detection of Barrett's esophagus neoplasia by CLE, and the technique may be used to guide endoscopic therapy. Advanced endomicroscopy systems and peptides and antibodies that target neoplasia are in development.CLE has provided a new way of evaluating Barrett's esophagus and Barrett's esophagus-associated neoplasia and is being used to improve detection and management of neoplasia in Barrett's esophagus.
Endomicroscopy
Barrett's esophagus
Cite
Citations (9)
Background/aim: To compare the frequency of intestinal metaplasia and dysplasia in H. pylori-positive and negative dyspeptic patients referred for routine upper gastrointestinal endoscopy. Materials and methods: One hundred and forty-one dyspeptic patients were studied (average age 44.7+16 years, range 16-87 years, 62 males and 79 females). Antrum and corpus biopsies were taken for detection of H. pylori, intestinal metaplasia and dysplasia histologically. Results: There were 96 H. pylori-positive patients in 141 patients (68.1%). Intestinal metaplasia and dysplasia were found in 42.7% (41/96) and 5.2% (5/96) among the H. pylori-positive patients and in 37.7% (17/45) and 4.4% (2/45) among the H. pylori-negative patients, respectively (P>0.05). 70.7% (41/58) of the patients with intestinal metaplasia and 71.4% (5/7) of the patients with dysplasia were H. pylori- positive, respectively (P>0.05). Conclusions: There was no statistically significant difference in the frequency of intestinal metaplasia and dysplasia between the patients who were H. pylori-positive and –negative, but the high ratio of H. pylori among the patients with intestinal metaplasia and dysplasia warrants attention.
Intestinal metaplasia
Metaplasia
Cite
Citations (0)
There is an unmet need for identifying novel biomarkers in Barrett's esophagus that could stratify patients with regards to neoplastic progression. We investigate the expression patterns of extracellular matrix (ECM) molecules in Barrett's esophagus and Barrett's esophagus-related neoplasia, and assess their value as biomarkers for the diagnosis of Barrett's esophagus-related neoplasia and to predict neoplastic progression. Gene-expression analyses of ECM matrisome gene sets were performed using publicly available data on human Barrett's esophagus, Barrett's esophagus-related dysplasia, esophageal adenocarcinoma (ADCA) and normal esophagus. Immunohistochemical expression of basement membrane (BM) marker agrin (AGRN) and p53 was analyzed in biopsies of Barrett's esophagus-related neoplasia from 321 patients in three independent cohorts. Differential gene-expression analysis revealed significant enrichment of ECM matrisome gene sets in dysplastic Barrett's esophagus and ADCA compared with controls. Loss of BM AGRN expression was observed in both Barrett's esophagus-related dysplasia and ADCA. The mean AGRN loss in Barrett's esophagus glands was significantly higher in Barrett's esophagus-related dysplasia and ADCA compared with non-dysplastic Barrett's esophagus (NDBE; P < 0.001; specificity = 82.2% and sensitivity = 96.4%). Loss of AGRN was significantly higher in NDBE samples from progressors compared with non-progressors (P < 0.001) and identified patients who progressed to advanced neoplasia with a specificity of 80.2% and sensitivity of 54.8%. Moreover, the combination of AGRN loss and abnormal p53 staining identified progression to Barrett's esophagus-related advanced neoplasia with a specificity and sensitivity of 86.5% and 58.7%. We highlight ECM changes during Barrett's esophagus progression to neoplasia. BM AGRN loss is a novel diagnostic biomarker that can identify patients with NDBE at increased risk of developing advanced neoplasia.
Barrett's esophagus
Esophageal disease
Cite
Citations (3)
<div>AbstractPurpose:<p>There is an unmet need for identifying novel biomarkers in Barrett's esophagus that could stratify patients with regards to neoplastic progression. We investigate the expression patterns of extracellular matrix (ECM) molecules in Barrett's esophagus and Barrett's esophagus–related neoplasia, and assess their value as biomarkers for the diagnosis of Barrett's esophagus–related neoplasia and to predict neoplastic progression.</p>Experimental Design:<p>Gene-expression analyses of ECM matrisome gene sets were performed using publicly available data on human Barrett's esophagus, Barrett's esophagus–related dysplasia, esophageal adenocarcinoma (ADCA) and normal esophagus. Immunohistochemical expression of basement membrane (BM) marker agrin (AGRN) and p53 was analyzed in biopsies of Barrett's esophagus–related neoplasia from 321 patients in three independent cohorts.</p>Results:<p>Differential gene-expression analysis revealed significant enrichment of ECM matrisome gene sets in dysplastic Barrett's esophagus and ADCA compared with controls. Loss of BM AGRN expression was observed in both Barrett's esophagus–related dysplasia and ADCA. The mean AGRN loss in Barrett's esophagus glands was significantly higher in Barrett's esophagus–related dysplasia and ADCA compared with non-dysplastic Barrett's esophagus (NDBE; <i>P</i> < 0.001; specificity = 82.2% and sensitivity = 96.4%). Loss of AGRN was significantly higher in NDBE samples from progressors compared with non-progressors (<i>P</i> < 0.001) and identified patients who progressed to advanced neoplasia with a specificity of 80.2% and sensitivity of 54.8%. Moreover, the combination of AGRN loss and abnormal p53 staining identified progression to Barrett's esophagus–related advanced neoplasia with a specificity and sensitivity of 86.5% and 58.7%.</p>Conclusions:<p>We highlight ECM changes during Barrett's esophagus progression to neoplasia. BM AGRN loss is a novel diagnostic biomarker that can identify patients with NDBE at increased risk of developing advanced neoplasia.</p></div>
Barrett's esophagus
Esophageal disease
Cite
Citations (0)
<div>AbstractPurpose:<p>There is an unmet need for identifying novel biomarkers in Barrett's esophagus that could stratify patients with regards to neoplastic progression. We investigate the expression patterns of extracellular matrix (ECM) molecules in Barrett's esophagus and Barrett's esophagus–related neoplasia, and assess their value as biomarkers for the diagnosis of Barrett's esophagus–related neoplasia and to predict neoplastic progression.</p>Experimental Design:<p>Gene-expression analyses of ECM matrisome gene sets were performed using publicly available data on human Barrett's esophagus, Barrett's esophagus–related dysplasia, esophageal adenocarcinoma (ADCA) and normal esophagus. Immunohistochemical expression of basement membrane (BM) marker agrin (AGRN) and p53 was analyzed in biopsies of Barrett's esophagus–related neoplasia from 321 patients in three independent cohorts.</p>Results:<p>Differential gene-expression analysis revealed significant enrichment of ECM matrisome gene sets in dysplastic Barrett's esophagus and ADCA compared with controls. Loss of BM AGRN expression was observed in both Barrett's esophagus–related dysplasia and ADCA. The mean AGRN loss in Barrett's esophagus glands was significantly higher in Barrett's esophagus–related dysplasia and ADCA compared with non-dysplastic Barrett's esophagus (NDBE; <i>P</i> < 0.001; specificity = 82.2% and sensitivity = 96.4%). Loss of AGRN was significantly higher in NDBE samples from progressors compared with non-progressors (<i>P</i> < 0.001) and identified patients who progressed to advanced neoplasia with a specificity of 80.2% and sensitivity of 54.8%. Moreover, the combination of AGRN loss and abnormal p53 staining identified progression to Barrett's esophagus–related advanced neoplasia with a specificity and sensitivity of 86.5% and 58.7%.</p>Conclusions:<p>We highlight ECM changes during Barrett's esophagus progression to neoplasia. BM AGRN loss is a novel diagnostic biomarker that can identify patients with NDBE at increased risk of developing advanced neoplasia.</p></div>
Barrett's esophagus
Esophageal disease
Cite
Citations (0)