Distal squamous mucosa is replaced by metaplastic specialized (intestinalized columnar) epithelium,

e.g. goblet cells, as a response to chronic injury; may regress after treatment

Also called columnar lined esophagus

Terminology

Long segment: Barrett mucosa extends 3 cm or more

Short segment: Barrett mucosa extends less than 3 cm

Ultra short segment: Barrett mucosa extends less than 1 cm

Pathophysiology

May be preceded by a distinctive type of multilayered epithelium at the squamocolumnar junction

with features of both squamous and columnar epithelium (Am J Surg Pathol 2001;25:569, Hum
Pathol 2001;32:1157); superficial aspects are similar to specialized columnar epithelium in Barrett
esophagus; similar changes have also been observed in columnar epithelium in metaplastic mucosa
(morphology, mucin types, cytokeratin expression, CDX2 expression, genetic changes)

Cell of origin: unknown; basal layer of squamous epithelium, submucosal or mucosal glands or ducts
and mesenchyme are possibilities

Etiology

Usually due to chronic gastroesophageal reflux (odds ratio 12.0, World J Gastroenterol 2007;13:1585;
Barrett is present in 3 - 12% of GERD patients who are biopsied)

Columnar epithelium of Barrett may be more resistant to acid, pepsin and bile

Often associated with sliding hiatal hernia; also bile / pancreatic juice reflux, chemotherapy,
decreased resting pressure of lower esophageal sphincter, esophageal stricture, lye ingestion, peptic
ulceration

Clinical features

Overwhelming majority are acquired (World J Gastroenterol 2006;12:1521), rare cases may be
congenital (Arch Pathol Lab Med 1981;105:546)

Incidence higher in whites, males, obese (especially with central adiposity); also with hiatal hernia
and high degree of duodenal gastric reflux

Mean age at diagnosis is 63 years; usually white men, rarely children with cystic fibrosis (causes
reflux) or after chemotherapy (Nat Rev 2003;3:676, CA Cancer J Clin 2005;55:334, N Engl J Med
2011;365:1375)

Symptoms: long history of heartburn and other reflux symptoms; more massive reflux with more
numerous and longer episodes than most reflux patients

Major risk factor for esophageal adenocarcinoma; however, relative risk varies from 11 - 100x; the
absolute annual risk is 0.12 to 0.5

Other types of carcinoma are uncommon

Barrett patients have similar mortality rate as general population and death from esophageal
adenocarcinoma is rare (Gut 2003;52:1081); of note, 95% with adenocarcinoma did NOT have Barrett
(Gastroenterology 2002;122:633, Gastroenterology 2002;122:26, Clin Gastroenterol Hepatol
2010;8:235)

Both long segment and short segment Barrett esophagus have similar staining patterns to each other
and to intestinal metaplasia of GE junction but different from intestinal metaplasia associated with H.
pylori gastritis (Am J Surg Pathol 2001;25:87)

Barrett should be differentiated from intestinal metaplasia at GE junction or in gastric cardia; H.

pylori infection is major cause of intestinal metaplasia of gastric cardia but risk of progression of
cardia intestinal metaplasia to dysplasia and adenocarcinoma is significantly lower than in Barrett

Diagnosis

Characteristic endoscopic appearance plus characteristic histologic findings; 8 random biopsies

recommended (Am J Gastroenterol 2007;102:1154); routine use of Alcian blue staining to detect
goblet cells (pH 2.5, detects acid mucins) is not recommended as pseudogoblet cells may be reactive
(Odze: Surgical Pathology of the GI Tract, Liver, Biliary Tract and Pancreas, 2nd Edition, 2009); report
should include type of epithelium present and presence / absence of dysplasia, grade of dysplasia
and extent of dysplasia

In children, endoscopic Barrett esophagus may have only cardiac type epithelium without intestinal
metaplasia

Recommended to take biopsies beginning in stomach, then every 1 - 2 cm until obvious squamous
epithelium is reached

In some locations outside of North America (e.g. Great Britain), presence of goblet cells is not
necessary (Gut 2006;55:442)

Laboratory

Specimen processing: obtain 4 levels of step sections to document goblet cell metaplasia; may want
additional levels in patients with known Barrett to evaluate dysplasia (Am J Clin Pathol 2005;123:886)

Treatment

Antireflux therapy (medical or surgical, Curr Opin Gastroenterol 2007;23:452), endoscopy every 1 - 2
years to detect dysplasia or early adenocarcinoma with 4 quadrant biopsies using jumbo forceps at
intervals of 2 cm or less throughout the length of the Barrett segment plus any suspicious lesions

Nota: nu exista o dovada clara asupra faptulu ca ar creste sansele de supravietuire sau ca evita
aparitia adenocarcinomului