Answer: Autoimmune metaplastic atrophic gastritis

Histology: The biopsy of body mucosa shows intestinal metaplasia and loss of oxyntic glands (chief cells and parietal cells) in a background of extensive low-lying chronic inflammation of the lamina propria. A negative gastrin stain confirms that the biopsy was indeed taken from the gastric corpus and not the antrum. A chromogranin stain highlights both linear and nodular enterochromaffin-like (ECL) cell hyperplasia.

Discussion: Autoimmune metaplastic atrophic gastritis (AMAG) is an immune-mediated chronic gastritis where the antibodies are directed against gastric parietal cells and intrinsic factor, resulting in loss of oxyntic cells, hypochlorhydria, achlorhydria, vitamin B12 deficiency and anemia.

Chemical gastropathy changes related to nonsteroidal anti-inflammatory drugs (NSAIDs) and bile reflux are frequently seen in antral biopsies which show cork-screwing of the glands, epithelial mucin loss, and smooth muscle strands in the lamina propria.

Helicobacter gastritis has a prominent superficial plasmacytic infiltrate, often accompanied by acute inflammatory cells. The chronic inflammation seen in AMAG is predominantly lymphoid and has a deeper, low-lying distribution close to the muscularis mucosae.

While patients with AMAG are predisposed to carcinoid tumors (type 1 carcinoid), and may have multiple carcinoid tumors in the body, these lesions are indolent and behave well in comparison to the more aggressive sporadic gastric carcinoids (type 3 carcinoid). The chromogranin stain in the biopsy shows linear and nodular hyperplasia (defined as 5 or more cells grouped together in a linear or nodular fashion) of ECL cells that are stimulated by increased gastrin levels. The low acid state created by the loss of parietal cells stimulates gastrin secretion.