Squamous Epithelium In Patients Research Articles

FA02.07: BARRIER STRUCTURE AND FUNCTION OF THE NEO-SQUAMOUS EPITHELIUM FOLLOWING SUCCESSFUL BARRETT’S ENDOTHERAPY IS IMPAIRED

Abstract Background The neo-squamous epithelium that replaces columnar epithelium after successful endoscopic ablation of Barrett's esophagus (BE) has not been fully characterized in regard to its structural and functional integrity. Intercellular space is a surrogate marker for epithelial structural integrity and mucosal impedance (MI) is a surrogate for transepithelial resistance and thus epithelial functional integrity. Impairment of the structural and functional integrity may influence recurrence following successful ablation. We aimed to measure the esophageal epithelial intercellular space diameter and MI in the neo-squamous and normal squamous epithelium of patients who underwent successful radiofrequency ablation for dysplastic BE. Methods Forty patients with complete remission of intestinal metaplasia (CRIM) (defined as two negative surveillance endoscopies for intestinal metaplasia) were prospectively recruited. Patients were excluded if they had endoscopic evidence of esophagitis. MI measurements were taken at 1 cm above the GE junction and 2 cm above the prior BE segment (targeting uninvolved squamous epithelium), using a novel through the scope MI probe. Endoscopic biopsies were also taken at these corresponding sites to assess intercellular space diameter using transmission electron microscopy (TEM) using standard techniques. Results 80% of patients were male with a mean age of 69 years. Mean follow since achieving CRIM was 30 months. 39 patients underwent RFA for dysplasia. The mean intercellular space diameter was higher in the neo-squamous epithelium (1.01 μm) when compared to the untreated native squamous epithelium (0.96 μm) [Difference of 0.056 μm, 95% CI of -0.036 to 0.148, P = 0.228]. The mean MI was significantly lower in the neosquamous epithelium (4001.3 Ω) when compared to the untreated native epithelium (5168.1 Ω) [Difference of 1166.7 Ω, 95% CI 418.8 to 1914.6, P = 0.003]. Conclusion Neo-squamous epithelium that replaces BE epithelium following successful endoscopic therapy for BE appears to be functionally and likely structurally deficient with regards to acid reflux barrier function, when compared to native squamous esophageal epithelium. This impairment may be associated with recurrence following successful ablation. Disclosure All authors have declared no conflicts of interest.

Signatures of field cancerization: a step towards earlier detection of esophageal adenocarcinoma.

In the March 2017 issue of Neoplasia Reed et al . report on a metabolic signature in the normal esophageal squamous tissue in patients with esophageal adenocarcinoma (EAC) arising in a background of Barrett’s esophagus (BE). The study utilized 1 H-nuclear magnetic resonance ( 1 H-NMR) to assess complex metabolic mixtures within tissue samples from normal squamous, BE- and EAC-affected areas of the esophagus to identify individual metabolites and metabolic signatures associated with each state. A metabolic signature was identified that distinguished normal squamous epithelium from BE patients with EAC (n=30) from normal squamous epithelium from patients with dyspeptic symptoms but no detectable BE or EAC (n=68). The signature produced by a partial least squares discriminant analysis (PLS-DA) model included the metabolites 3-hydroxybutyrate, succinate, formate, acetate, glycerophosphocholine, ADP and lactate. The authors discussed potential rationale for the observed differences in these metabolites in the squamous epithelium of patients with EAC, including the possibility that the elevated levels of formate may be related to ATP and NAD(P)H synthesis as cells adapt to changes in energy requirements in the cancer-bearing state. Additional studies will be required to understand why these particular metabolites are altered in the normal squamous mucosa adjacent to EAC.

Hyperplasia of the submucosal glands of the columnar-lined oesophagus.

To evaluate the presence of multi-layered epithelium (ME) and to compare the distribution, size and morphology of the oesophageal submucosal glands (SMG) beneath reflux exposed metaplastic columnar mucosa with those of normal squamous epithelium in patients with columnar-lined oesophagus (CLO). In eight oesophageal resection specimens, the SMG of the metaplastic segments were significantly larger than those in the squamous segments of patients with CLO (0.81 versus 0.56mm(2) , P=<0.001). There was an accumulation of SMG close to the neosquamocolumnar junction (NSCJ), as indicated by a higher median frequency of SMG (0.080 SMG/mm) compared with that of the squamous (0.013 SMG/mm) and metaplastic segments (0.031 SMG/mm) (P=0.022). The frequency of ME was significantly higher in the metaplastic compared with the normal squamous segments (1/158mm and 1/341mm, respectively, P=0.028) and ME was found almost exclusively (96%) in direct connection with the excretory ducts of SMG. Hyperplasia of SMG in the metaplastic segment, accumulation of SMG near the NSCJ, the presence of ME in connection with the excretory ducts of SMG and metaplasia are all reflux-induced morphological changes, possibly induced by stimulation of progenitors in the excretory ducts of the SMG.

Clinical Outcomes of Patients with Barrettʼs Esophagus Treated with Radiofrequency Ablation Using Only the Focal Device

Purpose: Endoscopic eradication therapy with radiofrequency ablation (RFA) is an effective method to achieve reversion of metaplastic epithelium to normal-appearing squamous epithelium in patients with Barrett's esophagus (BE). The HALO 90 focal ablation device is attached to the distal end of an endoscope, and is generally used in follow-up treatments for focal residual Barrett's after prior treatment with the circumferential ablation balloon device (HALO 360). However, outcomes of patients with BE who were treated solely with the focal ablation device have rarely been reported. Methods: We analyzed the data from a cohort of patients with BE who were treated with RFA from June, 2004 to April, 2011 at a single referral center. Fifty-eight patients (46 men, 12 women: mean age 64.6±9.9 years) who had their RFA treatments using only HALO 90 were enrolled in the study. Complete response (CR) was defined as complete eradiation of all dysplasia and intestinal metaplasia. Recurrence was defined as any biopsy from the esophagus showing intestinal metaplasia. Results: Baseline histology prior to RFA: non-dysplastic BE, n=24 (41.4%), low grade dysplasia, n=14 (24.1%), high grade dysplasia and intramucosal carcinoma, n=20 (34.5%). Mean length of Barrett's mucosa was 2.5±2.0 cm. Mean size of hiatal hernia was 1.9±1.3 cm. Endoscopic mucosal resection (EMR) was performed in 11 cases (19.0%) prior to RFA. Fundoplication was performed in three cases (5.2%) prior to RFA. Mean ablations per session was 48.7±18.2. CR was achieved in 56 cases (96.6%). Median number of RFA sessions to CR was two (range 1-5). CR within three RFA sessions (CR3) was achieved in 53 cases (91.4%): CR3 was 97.2% in BE ≤ 2 cm, 89.5% in BE > 2 cm and ≤ 4 cm, and 33.3% in BE > 4 cm. Patients were followed up for mean 25±15 months. One case (1.7%) recurred as low grade dysplasia and was successfully treated with EMR. Symptomatic stricture requiring dilation occurred in two cases (3.4%). There were no buried glands detected. Conclusion: RFA therapy in patients with BE using only the HALO 90 focal device is effective and safe, even in longer segments. CR within three RFA sessions was achieved in 94.5% (52/55) of patient with BE ≤ 4 cm. Disclosure - Dr. Chang: Barrx Covidien - Consultant, Olympus Japan - Consultant, Cook Medical - Consultant Dr. Lee: Cook Medical - speaker's bureau - honorarium Dr. Samarasena: Barrx Covidien - honorarium.

Nanoscale markers of esophageal field carcinogenesis: potential implications for esophageal cancer screening

Esophageal adenocarcinoma (EAC) has a dismal prognosis unless treated early or prevented at the precursor stage of Barrett's esophagus-associated dysplasia. However, some patients with cancer or dysplastic Barrett's esophagus (DBE) may not be captured by current screening and surveillance programs. Additional screening techniques are needed to determine who would benefit from endoscopic screening or surveillance. Partial wave spectroscopy (PWS) microscopy (also known as nanocytology) measures the disorder strength (Ld ), a statistic that characterizes the spatial distribution of the intracellular mass at the nanoscale level and thus provides insights into the cell nanoscale architecture beyond that which is revealed by conventional microscopy. The aim of the present study was to compare the disorder strength measured by PWS in normal squamous epithelium in the proximal esophagus to determine whether nanoscale architectural differences are detectable in the field area of EAC and Barrett's esophagus. During endoscopy, proximal esophageal squamous cells were obtained by brushings and were fixed in alcohol and stained with standard hematoxylin and Cyto-Stain. The disorder strength of these sampled squamous cells was determined by PWS. A total of 75 patient samples were analyzed, 15 of which were pathologically confirmed as EAC, 13 were DBE, and 15 were non-dysplastic Barrett's esophagus; 32 of the patients, most of whom had reflux symptoms, acted as controls. The mean disorder strength per patient in cytologically normal squamous cells in the proximal esophagus of patients with EAC was 1.79-times higher than that of controls (P<0.01). Patients with DBE also had a disorder strength 1.63-times higher than controls (P<0.01). Intracellular nanoarchitectural changes were found in the proximal squamous epithelium in patients harboring distal EAC and DBE using PWS. Advances in this technology and the biological phenomenon of the field effect of carcinogenesis revealed in this study may lead to a useful tool in non-invasive screening practices in DBE and EAC.

Intercellular Space Volume Is Mainly Increased in the Basal Layer of Esophageal Squamous Epithelium in Patients with GERD

At present, the dilation of esophageal intercellular spaces (ICS) is considered an early morphologic marker of acid damage in patients with GERD. Nevertheless, previous electron microscopic (EM) studies had focused only on the suprabasal layer of squamous epithelium or did not nearly specify which layer of squamous epithelium was studied. Therefore, we aimed to assess the volumetric amount of the ICS in all layers of SE in patients with GERD. In this study, 48 patients were prospectively included (NERD = 18, ERD = 17; Barrett's esophagus = 5, controls = 8). All patients with ERD and NERD had typical reflux symptoms, as assessed by a valid GERD questionnaire. ICS volume was assessed by electron microscopy in the superficial, prickle cell, and basal layers of esophageal squamous epithelium using the method of Weibel. ERD was associated with increased ICS volume in the basal layer (LA-A, p = 0.038; LA-B, p = 0.005) and prickle cell layer (LA-A, p = 0.006; LA-B, p = 0.007) as compared to controls. Comparisons between NERD and ERD patients revealed more dilated ICS in the basal layer (LA-B, p = 0.007), prickle cell layer (LA-A, p = 0.008; LA-B, p = 0.001) and superficial layer (LA-B, p = 0.018) in patients with ERD. Not only the diameter but also the volume of the ICS is increased in patients with GERD. Furthermore, the dilation of ICS is present in all three layers of the SE, being more pronounced in the basal layer. These findings support the concept that the impairment of the esophagus begins in the deeper parts of the esophageal epithelium.

Histopathologic Variability in Children With Eosinophilic Esophagitis

The diagnosis of eosinophilic esophagitis (EoE) is based on histologic findings of eosinophilia in the esophageal squamous epithelium in patients presenting with esophageal symptoms. Variability in the degree of squamous epithelial eosinophil infiltration presents a challenge to diagnostic accuracy. We examined the histopathologic features in a well-defined cohort of children with EoE to derive an optimal number of biopsies needed for diagnosis. A total of 30 patients diagnosed with EoE based on>15 eosinophils per high-power field (eos/HPF) were evaluated. The diagnosis of EoE was based on persistent esophageal eosinophilia following acid suppression therapy. All patients had mid and distal biopsy specimens that were analyzed along with 24-h pH probe studies. A total of 221 biopsy specimens were reviewed with a median of 7.8 (range, 5-8) specimens per patient. Eight patients demonstrated abnormal pH studies. The median eos/HPF was 41 (range, 0-288 eos/HPF). Using a criterion of>15 eos/HPF, the diagnostic sensitivity of a single biopsy was 73%, which increased to 84%, 97% and 100% for two, three and six biopsies, respectively. Five patients (17%) would not have met the criteria for diagnosis if biopsies were only taken from the mid esophagus whereas one patient (3%) would have been missed if only distal biopsies were analyzed. Significant histologic variability exists among biopsy specimens from pediatric patients with EoE. Using the criterion of>15 eos/HPF, three biopsy specimens achieved a diagnosis of EoE in 97% of patients. Histopathologic changes consistent with EoE can persist following proton pump inhibitor therapy in patients with EoE and gastroesophageal reflux disease when the latter is defined by increased distal esophageal acid exposure.

MicroRNA-143 and -205 Expression in Neosquamous Esophageal Epithelium Following Argon Plasma Ablation of Barrett’s Esophagus

IntroductionAblation of Barrett’s esophagus using Argon plasma coagulation (APC) is usually followed by the formation of a neosquamous epithelium. Investigating simple columnar or stratified squamous epithelium associated cytokeratin and microRNA (miRNA) expression in neo-squamous epithelium could help determine the identity and stability of the neosquamous epithelium. MethodsNine patients underwent ablation of Barrett’s esophagus with APC. Biopsies were collected from Barrett’s esophagus mucosa and proximal normal squamous epithelium before ablation, and from neosquamous and normal squamous epithelium after ablation. Additional esophageal mucosal biopsies from ten nonrefluxing subjects were used as a reference. RNA was extracted and real-time polymerase chain reaction was used to measure the expression of the cytokeratins CK-8 and CK-14 and the microRNAs miR-143 and miR-205. ResultsCK-8 and miR-143 expression were significantly higher in Barrett’s esophagus mucosa, compared to neosquamous and normal squamous epithelium before and after APC, whereas miRNA-205 and CK-14 expression was significantly lower in Barrett’s esophagus mucosa compared to all categories of squamous mucosa. The expression of CK-8, CK-14, miR-205, and miR-143 was similar between neosquamous epithelium compared to normal squamous epithelium in patients with Barrett’s esophagus. Only miR-143 expression was significantly higher in neosquamous and normal squamous epithelium before and after APC compared to normal squamous epithelium from control subjects (p < 0.004). ConclusionsThe expression levels of cytokeratins and miRNAs studied in post-ablation neosquamous epithelium and normal squamous epithelium in patients with Barrett’s esophagus are similar. In patients with Barrett’s esophagus, miR-143 expression is still elevated in both neosquamous mucosa, and the squamous mucosa above the metaplastic segment, suggesting that this mucosa may not be normal; i.e., it is different to that seen in subjects without Barrett’s esophagus. miR-143 could promote a Barrett’s epithelium gene expression pattern, and this could have a role in development of Barrett’s esophagus.

Lectin UEA-I-Binding Proteins Are Specifically Increased in the Squamous Epithelium of Patients with Barrett’s Esophagus

Background: Chronic gastritis and esophagitis are associated with changes in mucosal glycosylation patterns. Lectins represent a group of specific carbohydrate binding proteins that can be used as sensitive tools for the analysis of glycosylation patterns. Aim: To investigate the binding patterns of lectins Ulex europaeus agglutinin-I (UEA-I), Dolichos biflorus agglutinin (DBA), Helix pomatia agglutinin (HPA) and peanut agglutinin (PNA) at the gastroesophageal junction in nonerosive (NERD), erosive reflux disease (ERD) and Barrett’s esophagus (BE). Methods: One hundred and twenty-two patients (female n = 53; male n = 69; controls n = 28; NERD n = 36; ERD n = 24 and BE n = 34) were included in this study. The binding patterns of lectins were examined immunohistochemically at the squamocolumnar junction, in squamous epithelium and columnar-lined epithelium. Staining patterns of lectins were semiquantitatively evaluated using an immunohistochemical score and the data were analyzed using non-parametric tests. Results: BE, as compared to the controls, was associated with specific lectin-binding patterns: lectin binding of UEA-I and DBA were significantly decreased at the superficial (p = 0.012; p = 0.00036, respectively) and at the deep glandular body (p = 0.045; p = 0.055, respectively). Comparisons of lectin-staining scores between GERD and BE revealed significant increases of UEA-I in both the stratum superficiale (p = 0.0155) and stratum spinosum (p = 0.0048) of SE in patients with BE. Notable, this change was specific for patients with BE, while no difference was observed between patients with GERD and controls. Conclusion: We found two major types of lectin-binding patterns. First, lectin-binding characteristics associated with GERD in general, and second, lectin-binding patterns which were specific for BE. Lectin UEA-I-binding proteins were specifically increased in the squamous epithelium of patients with BE. Thus, UEA-I may serve as a potential marker for BE, especially in patients with short segment BE.

Differences in activity and phosphorylation of MAPK enzymes in esophageal squamous cells of GERD patients with and without Barrett's esophagus

We hypothesized that, in esophageal squamous epithelial cells, there are differences among individuals in the signal transduction pathways activated by acid reflux that might underlie the development of Barrett's esophagus. To explore that hypothesis, we immortalized nonneoplastic, esophageal squamous cells from patients with gastroesophageal reflux disease (GERD) with (NES-B3T) and without (NES-G2T) Barrett's esophagus and used those cells to study acid effects on MAPK proteins. During endoscopy in patients with GERD with and without Barrett's esophagus, we took biopsy specimens from the distal squamous esophagus to study MAPK proteins before and after esophageal perfusion with 0.1 N HCl. We used immunoblotting and Western blotting to study MEK1/2 phosphorylation at two activating sites (serines 217/221), MEK1 phosphorylation at an inhibitory site (threonine 286), and MEK1/2 activity. After acid exposure, both cell lines exhibited increased MEK1/2 phosphorylation at the activating sites; the NES-B3T cells had higher levels of MEK1 phosphorylation at the inhibitory site, however, and only the NES-G2T cells showed an acid-induced increase in MEK1/2 activity. Similarly, in the squamous epithelium of patients with GERD with and without Barrett's esophagus, acid perfusion increased MEK1/2 phosphorylation at the activating sites in both patient groups; the Barrett's patients had higher levels of MEK1 phosphorylation at the inhibitory site, however, and only the patients without Barrett's demonstrated an acid-induced increase in ERK1/2 phosphorylation. In esophageal squamous cell lines and biopsies from patients with GERD with and without Barrett's esophagus, we have found differences in MAPK pathways activated by acid exposure. We speculate that these differences might underlie the development of Barrett's metaplasia.

M1943 Specific Increase of Lectin UEA-I Binding Proteins in the Squamous Epithelium of Patients with Barretts Esophagus

M1943 Specific Increase of Lectin UEA-I Binding Proteins in the Squamous Epithelium of Patients with Barretts Esophagus

Circumferential and axial distribution of esophageal mucosal damage in reflux disease

The aim of this study was to evaluate the axial and radial distribution of histological markers including hyperplasia of the basal cell layer, elongation of the papillae and dilatation of the intercellular spaces of the squamous epithelium in patients with nonerosive reflux disease compared to controls and to relate this to the macroscopic topography in erosive reflux disease. Two different study populations were included in this report. Endoscopic esophageal biopsies were taken from 21 healthy control subjects and 21 nonerosive reflux disease patients before and after 4 weeks of esomeprazole therapy. Endoscopic still images from 50 erosive reflux disease patients were reviewed for the radial orientation of LA grade A and/or B esophagitis (Los Angeles criteria for grading of reflux esophagitis). The 3 o'clock position of the squamocolumnar junction showed significantly thicker basal cell layer (P=0.011) and more intercellular space dilatation (P=0.01) in nonerosive reflux disease patients compared to the 9 o'clock position. Only a significant difference in dilatation of the intercellular spaces (P=0.018) between nonerosive reflux disease patients and controls were observed in the 3 o'clock region at the squamocolumnar junction, whereas 1-2 cm orally, all three histological criteria differed significantly (P<or=0.01). After treatment, on the contrary, papillary length was significantly less pronounced at the squamocolumnar junction (P<0.01). Endoscopically, erosions were predominantly visualized in the 3 o'clock region (P<0.05). Histological mucosal changes in nonerosive reflux disease patients and visible mucosal erosions in erosive reflux disease patients occur most frequently at the same position, namely in the 3 o'clock quadrant in the distal esophagus. The histological difference between nonerosive reflux disease patients and controls are more distinct 1-2 cm oral to rather than at the squamocolumnar junction. However the effect of therapy is most pronounced at the squamocolumnar junction.

Radial Distribution of Dilated Intercellular Spaces of the Esophageal Squamous Epithelium in Patients with Reflux Disease Exhibiting Discrete Endoscopic Lesions

Introduction: Dilatation of intercellular spaces of the esophageal squamous epithelium has been suggested as a marker of early acid reflux-induced damage. This change is a potentially useful addition to histomorphological changes that represent so called minimal endoscopic lesions. We have assessed dilatation of intercellular spaces with regard to: (1) interobserver variability, and (2) whether the incidence of this varies between ‘red streaks’ and the adjacent normal looking squamous epithelium. Methods: Esophageal biopsies from 44 patients with chronic gastro-esophageal reflux (GERD) were evaluated. At endoscopy, these patients had one or more red streaks on the tops of the mucosal folds in the distal esophagus. Biopsies were taken from the red streaks and from the normal-appearing mucosa 1 cm lateral to the red streaks. Biopsies were assessed in a blinded fashion by two independent pathologists (MV & RF). Criteria for assessing intercellular space dilatation were evaluated and agreed on prior to the study. Results: Good interobserver agreement was recorded (kappa = 0.82 at the streaks and 0.77 for the control tissues) for absence/presence of intercellular space dilatation. Red streak and control biopsies differed significantly (p = 0.0001), with respect to presence of dilated intercellular spaces, with 90.5 % of the former demonstrating this as present compared to 56.1% in the controls. Conclusion: This study supports the concept that esophageal mucosal minimal changes due to reflux is localised and that dilatation of intercellular spaces is an early sign of reflux-induced epithelial damage. The low interobserver variability in the assessment of intercellular space dilatation suggests that this may be a useful variable for assessment of early signs of acid-reflux induced damage to the squamous epithelium of the esophagus by use of light microscopy.

Prevention of adenocarcinoma by reversing Barrett's esophagus with mucosal ablation.

The ultimate goal of therapy in patients with Barrett's esophagus (BE) is to reduce the risk of developing adenocarcinoma of the esophagus. Neither pharmacologic nor surgical therapy has been documented to reduce this risk. There is preliminary evidence that many forms of mucosal ablation combined with acid reduction therapy result in restitution of normal squamous epithelium in patients with BE. Acid reduction can be accomplished with high-dose proton pump inhibitor therapy or antireflux surgery. Endoscopic ablation can be accomplished with photodynamic therapy, laser, multipolar electrocoagulation, a heater probe, and argon plasma coagulation. These techniques require further study so the complication rates can be compared. The success of reversing BE must be evaluated in a standard way utilizing large-capacity biopsy forceps through a therapeutic endoscope. Ideally, patients at high risk of developing adenocarcinoma of the esophagus can be treated with ablation therapy and followed to document a reduction in the development of adenocarcinoma of the esophagus. A validated biomarker would help select high risk patients appropriate for reversal therapy. Currently, patients who are at prohibitive risk for surgery or who refuse surgery are candidates for combination therapy including mucosal ablation to reverse their BE. This therapy offers the promise of less morbidity and greater quality of life than resection.

Effect of multipolar electrocoagulation on EUS findings in Barrett's esophagus

Background: Restoration of squamous epithelium in patients with Barrett's epithelium may be achieved by treatment with a proton pump inhibitor plus selective electrocoagulation of the metaplastic epithelium. The effect of such treatment on esophageal wall thickness and morphology, as determined by EUS, is unknown. Methods: Patients with Barrett's esophagus were treated with omeprazole (40 mg by mouth, twice daily) and underwent selective multipolar electrocoagulation of the metaplastic segment monthly until complete squamous re-epithelialization or a maximum of 6 treatments was achieved. EUS was performed before and 6 months after the end of treatment. Four-quadrant large-forceps biopsy specimens were taken every 2 cm at the 6-month follow-up. Results: Twenty-five patients with Barrett's epithelium (mean length 3.1 cm, range 2-6 cm) were included. Complete endoscopic reversal was achieved in 24 patients. Residual intestinal metaplasia beneath squamous epithelium was observed in 1 patient. In 4 patients there was intestinalized mucosa at the neosquamocolunmar junction. The thickness of the treated distal esophageal wall decreased from 4.0 ± 0.1 mm to 3.7 ± 0.1 mm (mean ± SEM; p < 0.05, 2-tailed paired t test). Untreated (control) esophageal wall thickness at the level of the aortic arch (2.1 ± 0.1 mm vs. 2.2 ± 0.1 mm) and the mid-body gastric wall thickness (2.9 ± 0.1 mm vs. 3.1 ± 0.1 mm) did not change. Among the 6 patients with residual intestinal metaplasia there was no change in mean wall thickness (3.7 ± 0.2 mm vs. 3.8 ± 0.2 mm); among the 19 without metaplasia, thickness decreased from 4.1 ± 0.2 mm to 3.6 ± 0.2 mm; p < 0.01. Of 11 patients with a decrease in wall thickness, only 1 had residual intestinal metaplasia. No changes in the 5-layer sonographic pattern of the esophageal wall were observed. Conclusions: Multipolar electrocoagulation of Barrett's esophagus results in a slight decrease in thickness of the treated esophageal wall. A decrease in wall thickness by EUS was associated with the absence of intestinal metaplasia in follow-up biopsy specimens. (Gastrointest Endosc 2002;55:23-6.)

Acid perfusion activates a proliferative response in the squamous epithelium of patients with erosive esophagitis, but not of patients with Barrett's esophagus

Acid perfusion activates a proliferative response in the squamous epithelium of patients with erosive esophagitis, but not of patients with Barrett's esophagus

Acid perfusion activates a proliferative response in the squamous epithelium of patients with erosive esophagitis, but not of patients with Barrett's esophagus

Acid perfusion activates a proliferative response in the squamous epithelium of patients with erosive esophagitis, but not of patients with Barrett's esophagus