Barrett syndrome

(redirected from Barrett metaplasia)

Bar·rett syn·drome

(bar'ĕt),
chronic peptic ulceration of the lower esophagus, which is lined by columnar epithelium, resembling the mucosa of the gastric cardia, acquired as a result of long-standing chronic esophagitis; esophageal stricture with reflux, and adenocarcinoma, also have been reported. Associated with a 30-to-40 fold increased risk of adenocarcinoma.

Bar·rett syn·drome

, Barrett esophagus , Barrett metaplasia (bar'ĕt sin'drōm, ĕ-sof'ă-gŭs, met'ă-plā'zē-ă)
Chronic peptic ulceration of the lower esophagus, which is lined by columnar epithelium, resembling the mucosa of the gastric cardia, acquired as a result of long-standing chronic esophagitis; esophageal stricture with reflux, and adenocarcinoma, also have been reported.

Barrett,

Norman Rupert, English surgeon, 1903-1979.
adenocarcinoma in Barrett esophagus - an adenocarcinoma arising in the lower third of the esophagus that has become columnar cell lined (Barrett mucosa) due to gastroesophageal reflux.
Barrett epithelium - columnar esophageal epithelium seen in Barrett syndrome.
Barrett esophagus - chronic peptic ulceration of the lower esophagus acquired as a result of long-standing chronic esophagitis. Synonym(s): Barrett syndrome; Barrett ulcer
Barrett syndrome - Synonym(s): Barrett esophagus
Barrett ulcer - Synonym(s): Barrett esophagus
Eagle-Barrett syndrome - Synonym(s): prune belly syndrome

Bar·rett syn·drome

, Barrett esophagus , Barrett metaplasia (bar'ĕt sin'drōm, ĕ-sof'ă-gŭs, met'ă-plā'zē-ă)
Chronic peptic ulceration of the lower esophagus, which is lined by columnar epithelium, resembling the mucosa of the gastric cardia, acquired as a result of long-standing chronic esophagitis.
References in periodicals archive ?
Although a cervical inlet patch is not considered a premalignant lesion like Barrett metaplasia, it may be symptomatic and should be looked for during esophagoscopy.
To the Editor.--The article titled "The Significance of 'Indefinite for Dysplasia' Grading in Barrett Metaplasia" by Mamoun Younes et al (1) reports that esophageal mucosa diagnosed as indefinite for dysplasia (IND), when present in samples from at least 2 levels of the esophagus (INDM), is as likely as low-grade dysplasia (LGD) to progress to high-grade dysplasia or carcinoma.
The significance of "indefinite for dysplasia" grading in Barrett metaplasia. Arch Pathol Lab Med.
An interesting finding was that a small island of normal pink squamous mucosa was present in the sea of Barrett metaplasia (figure).
Hematoxylin-eosin-stained sections of formalin-fixed and paraffin-embedded tissue from initial and follow-up biopsies from 276 patients with histologically confirmed Barrett metaplasia, without high-grade dysplasia (HGD) or EAC on the initial biopsy and with a mean follow-up of 41 months (median, 35), were evaluated for dysplasia using standard criteria.
Using the established criteria for grading dysplasia in mucosal biopsies of the esophagus from patients with Barrett metaplasia, we could not reach a confident grading of dysplasia in 20% of the initial biopsies in this series.
The patient exhibited no evidence of esophagitis or Barrett metaplasia. The LES is typically closed at rest.
* Context.--Identification of intestinal-type goblet cells (ITGCs) in hematoxylin-eosin-stained sections of esophageal biopsies is essential for the diagnosis of Barrett metaplasia. However, we have seen cases diagnosed as Barrett metaplasia based solely on cells that pose morphologic similarity to ITGCs on hematoxylin-eosin staining or stain positive with Alcian blue.
Design.--Initial biopsies from 78 patients with original diagnosis of Barrett metaplasia negative for dysplasia and a mean follow-up of 72 months were reviewed and reclassified into 3 categories: (1) ITGCs, (2) goblet cell mimickers, or (3) neither.
There was no significant association between PAM and patient gender (24 male, 47 female versus 166 male, 207 female; P = .12), the mean number of biopsy pieces taken at endoscopy (3.5 versus 3.6, P = .75), the presence of active inflammation (9 of 70 versus 66 of 377, P = .39), Barrett metaplasia (21 of 71 versus 103 of 373, P = .58), the presence of pseudogoblet cells (9 of 71 versus 57 of 373, P = .72), or multilayered epithelium (6 of 71 versus 20 of 373, P = .28).
They demonstrated that Notch inhibition could induce goblet cell differentiation and reduce cell proliferation, while cellular proliferation and progression of BE could be promoted by Notch activation, suggesting that Notch signaling might play binary roles in regulating Barrett metaplasia and its progression [4].
"And my answer to that at this moment in time is indefatigably, no, you should not, unless you have a secondary risk factor," such as Barrett metaplasia or colon polyps (or a secondary cardiovascular risk factor).