Chronic atrophic gastritis is seen with glands showing goblet cell metaplasia. Low-grade dysplasia is seen near the top, characterized by epithelium which appear more cuboidal in shape rather than columnar, with a high nuclear:cytoplasmic ratio.
This gastric adenoma shows an areas with architectural complexity as well as marked cytological atypia (top); nthere is normal at the bottom,
This fundic gland polyp in a patient with FAP harbors a small focus of mild epithelial dysplasia.
Nuclear enlargement and elongation with crowding is seen along with pseudostratification. This is compatible with low grade dysplasia.
Intestinal gastric cancers usually are preceded by a sequence of histological events beginning with diffuse chronic gastritis and eventually leading to mucosal atrophy, intestinal metaplasia, and dysplasia. The extent and severity of atrophy, and the extent of intestinal metaplasia, are important indicators of increased cancer risk.
The prevalence of gastric dysplasia shows marked variation worldwide, from 9% to 20% in high-risk areas such as China, to 0.5% to 3.75% in Western countries, where gastric cancer is less common (Lauwers). The main causes of chronic atrophic gastritis are either pernicious anemia or chronic Helicobacter pylori infection. Those with familial adenomatosis polyposis, Menetrier's disease and Peutz-Jeuger are also at increased risk. Prevalence rates for gastric dysplasia of up to 40% have been reported in those with pernicious anemia.
Patients are usually in their 6th-7th decade. Most commonly affects the lesser curvature, particularly the antrum or the incisura angulus.
Given the low rate of malignant transformation of low-grade dysplasia, annual endoscopic surveillance with re-biopsy is recommended, and surgical resection is usually not necessary. Low-grade dysplasia occurring in a background of extensive intestinal metaplasia may be associated with a higher risk of malignancy. Patients with high-grade dysplasia should undergo definitive therapy.
The rate of malignant transformation for high-grade dysplasia ranges from 60% to 85% over a median interval of 4 to 48 months (Lauwers). By contrast, studies have demonstrates a relatively low risk of progression to cancer in patients with low-grade dysplasia (0% to 9%).
Lauwers GY, Srivastava A. Gastric preneoplastic lesions and epithelial dysplasia. Gastroenterol Clin North Am. 2007 Dec;36(4):813-29, vi.