The epithelium is altered by hyperchromatic, enlarged nuclei and depletion of cytoplasmic mucin which involves the surface mucosa. The process involves to the epithelial surface with architectural changes that include budding of glands, and pseudostratification.
Low grade dyplasia typically resembles a tubular adenoma of the colon.
Villous architectural change may occur.
Neoplastic progression from Barrett esophagus to esophageal adenocarcinoma is a multistep dysplasia-carcinoma process associated with increasing genetic abnormalities, which are accompanied by morphological changes including atypia, loss of cellular differentiation, distributed loss of tissue architecture, and ultimately invasion.
75% of patients diagnosed with LGD in general practice have been downgraded to negative for dysplasia upon expert review of the pathology.
The transition from LGD to HGD includes increasing architectural distortion (branching, budding, irregular glands), nuclear pleomorphism, increased N/C ratio, nuclear hyperchromatism and increased mitotic activity. These alterations extend at least focally to the top of the glands (Rosai). Loss of nuclear polarity and markedly enlarged hyperchromatic cells are not features of LGD, but rather HGD (Iacobuzio).
If LG dysplasia is diagnosed, gastroenterological societies recommend increasing the frequency of endoscopic surveillance from every 3 years to every 6–12 months.
There remains considerable controversy regarding the natural history of LG dysplasia. Some studies reported that in 66–75% of patients initially diagnosed with LGD, subsequent endoscopic biopsies fail to confirm LGD. Other studies have shown that in patients in whom the diagnosis of LGD is confirmed by multiple pathologists, the risk for progression to high-grade dysplasia or carcinoma may be as high as 40% within 2 years. These conflicting findings may be explained at least in part by the variability of the endoscopic work-up in earlier studies and the reliability of the baseline histological diagnosis.
LG dysplasia is frequently overdiagnosed in community practice.
A diagnosis of LG dysplasia confirmed by mutliple experts carries about a 40% chance of disease progression.
Iacobuzio-Donahue CA, Montgomery EA. Gastrointestinal and Liver Pathology: Foundations in Diagnostic Pathology. Philadelphia, PA: Elsevier; 2005: 46-8.
Rosai, J. Rosai and Ackerman's Surgical Pathology. 9th Ed. Philadelphia, PA: Elsevier; 2004: 622-3.