Humpath.com - Human pathology

Home > E. Pathology by systems > Digestive system > Stomach > alkaline reflux gastritis

alkaline reflux gastritis

Sunday 4 March 2012

Alkaline reflux gastritis develops in patients with abnormalpyloric sphincter function, often resulting from previous surgical interventions, chronic alcohol ingestion, or aging.

Both alkaline duodenal secretions and bile damage the gastricmucosa. Bile salts increase mucosal permeability to hydrogenions, resulting in H+
back-diffusion.

The most severe injury occurs in the antrum. The amount of reflux often correlates with symptom severity, but the endoscopic and histologic features rarely correlate with one another.

The histologic features of alkaline reflux gastritis are quite subtle and often overlooked. They include:
- glandular elongation,
- tortuosity and hypercellularity ofthe gastric pits;
- foveolar hyperplasia;
- mucosal villiform transformation.

Some patients develop prominent villiform transformation of the surface with foveolar hyperplasia that can be quite pronounced. The hyperplastic epithelium almost appears adenomatous.

At first glance, the mucosa does not appear to be abnormal, although there might be a slight increase in the number of chronic inflammatory cells within the mucosa. Higher magnification of a different area of the same biopsy demonstrates the presence of an irregular gland con-taining bile crystals.

The glandular epithelium appears regenerative both within the mucous neckregion and at the free surface. The lamina propria contains a very mild increase in the number of mononuclear cells.

The regenerative glands may appear more angular thanusual. The foveolar cells show mild mucin depletion and vacuolization.

Other changes include capillary congestion and vasodilation in the superficial lamina propria, edema, and increased numbers of smooth muscle fibers that sometimes extend quite high in the lamina propria.

The number ofchronic inflammatory cells and neutrophils is generally sparse.

The lack ofinflammation is in striking contrast to the degree of epithelial hyperplasia.

Bile may be present onthe luminal surface or within glands.

Glandular atrophy develops in patients who have had an antrectomy, due to loss ofthe gastrin-producing G cells in the antral mucosa.

The output of gastric acid, however, remains unchanged.

Intestinal metaplasia and/or atrophy maydevelop in longstanding disease.