Short segments of Barrett’s epithelium and intestinal metaplasia in normal appearing oesophagogastric junctions: the same or two different entities?

Pereira, António Dias; Suspiro, Alexandra; Chaves, Paula; Saraiva, Ageu de Oliveira; Glória, L; Almeida, Jorge; Leitão, C. Nobre; Soares, Jorge; Mira, F. Costa

doi:10.1136/gut.42.5.659

Cited by 80 publications

(51 citation statements)

References 24 publications

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“…In this study, IM was found in 55% of patients with segments of esophageal columnar lining measuring 2 cm or less. This is similar to studies of other investigators 2,20,21 who found IM in 48% to 61% ofpatientssuspectedofhavingshort-segmentBarrettesophagus. Furthermore, our results suggest that the duration of GERD and the presence of duodenoesophageal reflux are important factors in the pathogenesis of IM.…”

Section: Commentsupporting

confidence: 80%

Determinants of Intestinal Metaplasia Within the Columnar-Lined Esophagus

Öberg

Peters²,

DeMeester³

et al. 2000

Arch Surg

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Section: Commentsupporting

confidence: 80%

Determinants of Intestinal Metaplasia Within the Columnar-Lined Esophagus

Öberg

Peters²,

DeMeester³

et al. 2000

Arch Surg

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“…It is difficult to determine differences in the prevalence rate of IM in the true gastric cardia compared to metaplastic columnar epithelium in the distal esophagus because the protocols used in most studies are not able to distinguish these two regions accurately (42,53). However, the results of several studies have shown that the prevalence of IM is higher in patients who have longer lengths of mucosa composed of pure cardia-type mucous glands (8,9,17).…”

Section: Intestinal Metaplasia Of the Gastroesophageal Junction Regionmentioning

confidence: 86%

“…Up to one-third of patients without endoscopic evidence of BE who present for upper GI endoscopy show IM in the GEJ region (2,39,42,43,(51)(52)(53)(54). The wide variation in reported prevalence rates between various studies is due to a variety of factors, such as differences in endoscopic techniques with and without magnification endoscopy; with and without the application of acetic acid, with and without the application of vital dye biopsy protocols, and patient populations utilized, the precise location and number of biopsies (i.e., true gastric cardia vs metaplastic columnar epithelium in the distal esophagus) and differences in histologic detection methods.…”

Section: Intestinal Metaplasia Of the Gastroesophageal Junction Regionmentioning

confidence: 99%

Unraveling the Mystery of the Gastroesophageal Junction: A Pathologist's Perspective

Odze

2005

Am J Gastroenterology

158

100

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The gastroesophageal junction (GEJ), which is defined as the point where the distal esophagus joins the proximal stomach (cardia), is a short anatomic area that is commonly exposed to the injurious effects of GERD and/or Helicobacter pylori infection. These disorders often lead to inflammation and intestinal metaplasia (IM) of this anatomic region. The true gastric cardia is an extremely short segment (<0.4 mm) of mucosa that is typically composed of pure mucous glands, or mixed mucous/oxyntic glands that are histologically indistinguishable from metaplastic mucinous columnar epithelium of the distal esophagus. In patients with GERD, whether physiologic or pathologic, the length of cardia-type epithelium increases and extends proximally above the level of the anatomic GEJ into the distal esophagus. Columnar metaplasia of the distal esophagus represents a squamous to columnar metaplastic reaction that develops from an esophageal stem cell and may pass through an intermediate phase characterized by the presence of a type of epithelium that possesses a mixture of squamous and columnar features, termed multilayered epithelium. In contrast, IM of the gastric cardia represents a columnar to columnar cell metaplastic reaction that develops from a gastric stem cell located in the deep foveolar compartment of the gastric mucosa. Intestinal metaplasia, particularly the incomplete type, is widely believed to represent the precursor lesion upon which dysplasia and cancer arises. The frequency of IM is probably greater in metaplastic columnar epithelium in the esophagus secondary to GERD, than in cases of true gastric carditis secondary to H. pylori, and may be a reason why there is a higher risk of carcinoma in the former compared to the latter. A variety of clinical, endoscopic, histologic, and histochemical methods can be used to distinguish GERD-induced columnar metaplasia of the distal esophagus from H. pylori-induced inflammation of true gastric cardia, and these are outlined in this review, but further controlled studies are needed to critically evaluate these techniques. Further prospective trials are needed to adequately evaluate the different etiologic and pathogenetic mechanisms and, most importantly, the risk of malignancy in these two conditions.

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“…In studies carried out by Spechler et al 24 and Nandurkar et al, 25 a relation between SSBE and GER was not found. On the contrary, studies by Johnston et al 23 Pereira et al 26 showed a significant relation between SSBE and GER. Although we did not find a relation between the presence of esophagitis and BE, nonerosive GER disease that cannot be detected during endoscopic examination may be an important factor in the development of BE.…”

Section: Discussionmentioning

confidence: 85%

Utility of Endoscopy for Diagnosis of Barrett in a Non-Western Society: Endoscopic and Histopathologic Correlation

Ege¹,

Dinç

Yildiz

et al. 2015

International Surgery

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Barrett esophagus is metaplastic transformation of esophageal squamous epithelium to columnar cells. A total of 1370 patients who had undergone upper endoscopy because of dyspeptic complaints were enrolled in the study. Age, sex, alcohol and smoking habits, body mass index, type and duration of symptoms (heartburn, epigastric pain, nausea, vomiting), and use of proton pump inhibitors were evaluated in all patients and recorded on standardized forms. Patients were grouped as normal esophagogastric junction, long-segment Barrett esophagus, and short-segment Barrett. Biopsies were taken from at least 6 points and examined histopathologically. Of the 1370 patients involved in the study, 748 (54.6%) were female and 622 (45.4%) were male. Mean age was 47.2 6 15.30 years. Short-segment Barrett esophagus was detected in 16 patients, and long-segment Barrett was detected in 11 patients. Although Barrett esophagus was detected in 11 cases that were suspected to have Barrett during endoscopy, histopathology was negative in all cases that were not suspected to have Barrett. Barrett esophagus prevalence was significantly higher in people who used alcohol and tobacco and who had hiatal hernia. Although Barrett esophagus was detected in 40% of cases that were suspected to have Barrett during endoscopy, histopathology was negative in all cases that were not suspected to have Barrett. Barrett was detected in 40.7% of cases that were suspected to have Barrett during endoscopy; histopathology was negative in all cases that were not suspected to have Barrett. Senstivity of endoscopy is questionable in detection of short-segment Barrett.

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Short segments of Barrett’s epithelium and intestinal metaplasia in normal appearing oesophagogastric junctions: the same or two different entities?

Cited by 80 publications

References 24 publications

Determinants of Intestinal Metaplasia Within the Columnar-Lined Esophagus

Determinants of Intestinal Metaplasia Within the Columnar-Lined Esophagus

Unraveling the Mystery of the Gastroesophageal Junction: A Pathologist's Perspective

Utility of Endoscopy for Diagnosis of Barrett in a Non-Western Society: Endoscopic and Histopathologic Correlation

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