Anatomic Pathology: Gastrointestinal Pathology

• Autoimmune atrophic gastritis is associated with autoantibody against parietal cells and is characterized (in its late stages) by complete loss of oxyntic glands, mucosal atrophy, and presence of metaplastic epithelium, including intestinal metaplasia and pseudopyloric gland metaplasia.

• The massive destruction of parietal cells seen in autoimmune atrophic gastritis results in markedly decreased production of HCl, which in turn leads to compensatory hyperproduction of gastrin by antral G-cells.

• Enterochomaffin-life (ECL) cells in the gastric body and fundus, under chronic stimulation by increased gastrin levels, undergo hyperplasia, which can present in two patterns: (1) linear hyperplasia, whereby gastric glands are lined by a contiguous layer of endocrine cells, and (2) nodular hyperplasia, in which small nests of endocrine cells are seen.

• The entire spectrum of ECL-cell growth from hyperplasia to neoplasia has been observed in chronic atrophic gastritis and in MEN-1-associated with Zollinger–Ellison syndrome. When the nodules increase in size to greater than 0.5 mm or invade submucosa, the lesion is classified as a carcinoid.

• In the setting of chronic atrophic gastritis, carcinoids smaller than1 cm, and fewer than three to five in number can be endoscopically removed and have an excellent prognosis. If the carcinoid is larger than 1 cm or more than five lesions are present, antrectomy may be considered (to remove the source of gastrin) and local excision of the fundic lesions recommended.