Postgastrectomy gastritis is gastric inflammation developing after partial or subtotal gastrectomy (except in cases of gastrinoma). Chronic inflammation may lead to atrophy.
Metaplasia of the remaining corpus mucosa is common. The degree of gastritis is usually greatest at the lines of anastomosis.
Several mechanisms are responsible:
Bile reflux, which is common after such surgery, damages the gastric mucosa.
Loss of antral gastrin decreases stimulation of parietal and peptic cells, causing atrophy.
Vagotomy may result in a loss of vagal trophic action.
There are no specific symptoms of gastritis. Postgastrectomy gastritis often progresses to severe atrophy and achlorhydria. Production of intrinsic factor may cease with resultant vitamin B12 deficiency (which may be worsened by bacterial overgrowth in the afferent loop). The relative risk of gastric adenocarcinoma seems to increase 15 to 20 years after partial gastrectomy; however, given the low absolute incidence of postgastrectomy cancer, routine endoscopic surveillance is probably not cost effective, but upper gastrointestinal symptoms or anemia in such patients should prompt endoscopy.
