The utility of cytokeratins 7 and 20 (CK7/20) immunohistochemistry in the distinction of short-segment Barrett esophagus from gastric intestinal metaplasia: is it reliable?
Interobserver variability in the diagnosis of crypt dysplasia in Barrett esophagus.
Immunohistochemical evaluation of a panel of tumor cell markers during malignant progression in Barrett esophagus.
Vascular and lymphatic properties of the superficial and deep lamina propria in Barrett esophagus.
Barrett esophagus is the most important risk factor for the development of esophageal adenocarcinoma.
Barrett esophagus is initiated by GERD, leading to reflux esophagitis with injury of the squamous epithelium.
The epidemiology of Barrett esophagus shows a male to female ratio of approximately 3:1.
Barrett esophagus cannot be detected on clinical grounds, as there are no specific symptoms of Barrett esophagus that distinguish this condition clinically from patients with GERD without Barrett esophagus.
In patients who have the findings of Barrett esophagus but no evidence of dysplasia, an upper endoscopy and biopsy should be repeated in one year to confirm negative dysplasia (Fig.
The treatment goals of patients with Barrett esophagus are to eliminate the symptoms of GERD and prevent GERD complications.
Biopsy samples from the squamocolumnar junction of patients with Barrett esophagus show neutral mucin-containing columnar (cardiac-type) epithelium (Figure 1, A) with interspersed goblet cells (Figure 1, B).
Tissue fragments containing fundic (oxyntic) mucosa reflect sampling of the proximal stomach, such as a hiatal hernia, rather than metaplasia within the esophagus and, thus, should not be considered to represent Barrett esophagus.
Glickman et al (8) evaluated multilayered epithelium in samples obtained from 17 patients and found that its glandular cells expressed neutral mucins, sialomucins, and sulfomucins at rates comparable to Barrett esophagus (88%, 100%, and 71% of cases, respectively, versus 100%, 100%, and 76%, respectively).
9-12) Nongoblet columnar epithelium in the distal esophagus also shows DNA content abnormalities at rates comparable to those of esophageal goblet cells, indicating that esophageal cardiac-type epithelium from patients with Barrett esophagus may already be "intestinalized," despite the absence of morphologic goblet cell differentiation.
Problems related to the evaluation and diagnosis of Barrett esophagus may be the purview of either gastro-enterologists or pathologists.