In H. pylori-associated gastritis, which histologic features are typical, and what may accompany intestinal metaplasia?

In H. pylori-associated gastritis, which histologic features are typical, and what may accompany intestinal metaplasia?

• A. Chronic active gastritis with lymphoid aggregates and H. pylori organisms; glandular atrophy and intestinal metaplasia may accompany.
• B. Acute gastritis with neutrophils only; no metaplasia.
• C. Normal mucosa with H. pylori without inflammation.
• D. Predominant eosinophilic infiltration without H. pylori.

Answer: (A)

H. pylori causes a chronic active gastritis pattern. The mucosa shows a mix of chronic inflammatory cells in the lamina propria with neutrophils actively infiltrating the surface epithelium and glands, reflecting ongoing inflammation driven by the infection. A characteristic feature is the presence of lymphoid aggregates in the mucosa, often with germinal centers, due to immune stimulation from the bacteria. Over time, this chronic inflammatory milieu can lead to glandular atrophy of the stomach lining, and intestinal metaplasia may develop, where gastric epithelium is replaced by intestinal-type epithelium with goblet cells. This sequence—chronic active gastritis with H. pylori colonization and lymphoid aggregates, potentially accompanied by glandular atrophy and intestinal metaplasia—fits the typical histologic pattern seen with H. pylori infection. Other patterns, like acute gastritis with neutrophils only, normal mucosa, or eosinophilic-dominant infiltration without H. pylori, do not reflect the usual histology of this infection.

H. pylori causes a chronic active gastritis pattern. The mucosa shows a mix of chronic inflammatory cells in the lamina propria with neutrophils actively infiltrating the surface epithelium and glands, reflecting ongoing inflammation driven by the infection. A characteristic feature is the presence of lymphoid aggregates in the mucosa, often with germinal centers, due to immune stimulation from the bacteria. Over time, this chronic inflammatory milieu can lead to glandular atrophy of the stomach lining, and intestinal metaplasia may develop, where gastric epithelium is replaced by intestinal-type epithelium with goblet cells. This sequence—chronic active gastritis with H. pylori colonization and lymphoid aggregates, potentially accompanied by glandular atrophy and intestinal metaplasia—fits the typical histologic pattern seen with H. pylori infection. Other patterns, like acute gastritis with neutrophils only, normal mucosa, or eosinophilic-dominant infiltration without H. pylori, do not reflect the usual histology of this infection.