Barrett esophagus and dysplasia appear to be precursors or markers of adenocarcinoma development
10% of patients with gastroesophageal reflux will have Barrett esophagus
10% of patients with Barrett esophagus will have dysplasia
10% of patients with Barrett esophagus will have adenocarcinoma at the time of initial diagnosis
Longterm followup of patients with low grade dysplasia in Barrett esophagus (Sharma 2004)
10% progress to high grade dysplasia
3% progress to carcinoma
Followup of patients with high grade dysplasia in Barrett esophagus (Konda 2008)
40% develop carcinoma
87% of these are intramucosal
Only 13% are invasive into submucosa or beyond
Notes on the diagnosis of dysplasia in Barrett esophagus
Dysplasia is best evaluated in areas without significant acute inflammation (see indefinite for dysplasia below)
Dysplastic features should be present on the lumenal surface
Reactive atypia rarely extends to the lumenal surface
Dysplasia may be focal, requiring adequate sampling
A diagnosis of dysplasia should be confirmed by an experienced gastrointestinal pathologist
Criteria for dysplasia
Negative for dysplasia
Orderly glandular architecture
Regenerative basal glands may have cytologic atypia
Hyperchromasia
Pleomorphism
Nuclear stratification
Nucleus:cytoplasm ratio usually normal or only slightly increased
Atypia tends to be more uniform than in dysplasia
The cells mature at the surface where these features are lost
Most dysplasia is of intestinal type, resembling the changes seen in colonic adenomas
Low grade intestinal type dysplasia
Architecture preserved or minimally abnormal
Nuclei elongated and crowded at base but not at apex of cells
Pseudostratification may be extensive
Nuclear enlargement
Mild to moderate nuclear hyperchromasia and irregularity
Mitotic figures may be present at surface
Cytologic atypia extends to cells on the bowel lumenal surface
Surface villous transformation may be present
High grade intestinal type dysplasia demonstrates markedly atypical features
Marked cytologic atypia
Nuclear stratification to surface of cell with loss of polarity
Nuclei no longer radially oriented
Abnormal architecture
Lateral budding
Branching
Intraglandular bridging
Villus formation
Dilated glands containing necrotic debris
No single cell or small cluster infiltration (intramucosal carcinoma)
Gastric foveolar type dysplasia has been reported in up to 20% of cases
Single layer of basally oriented round to oval nuclei
Lacks pseudo- and real stratification of intestinal type
Frequently mixed with intestinal type
Has also been called "nonadenomatous dysplasia"
Grading criteria have only recently been proposed by Mahajan
Primarily based on nuclear size
Low grade foveolar type dysplasia
Nuclei enlarged to 2-3x size of lymphocytes
Variably prominent nucleoli
Pleomorphism absent to mild
Full thickness population of uncrowded glands
Cytoplasm is usually mucinous
High grade foveolar dysplasia
Nuclei enlarged to 3-4x size of lymphocytes
Prominent nucleoli
Pleomorphism mild to moderate
Glandular crowding
Cytoplasm frequently eosinophilic/oncocytic
Variable features
Villiform growth
Cribriform glands
Dilated glands with lumenal debris
Indefinite for dysplasia should be used if the lesion is suggestive of but not diagnostic of dysplasia
Significant atypia with lack of surface maturation in the context of inflammation
Significant atypia with surface maturation in the absence of inflammation
Significant atypia with partial surface maturation
If acute inflammation is present, dysplasia should be diagnosed with caution and then only if the dysplastic findings are clearly disproportionate to the degree of inflammation
