Abstract
Prostaglandins of the E series, which have been proposed as therapeutic agents for the treatment of peptic ulcers and other gastrointestinal diseases, cause hyperplasia of the gastrointestinal mucosa in experimental animals. The changes are most evident in the stomach, especially the antrum, in which the wall is thickened by hyperplasia of surface mucous cells and/or submucosal edema. In rodents, the non-glandular forestomach becomes hyperplastic and hyperkeratotic. Affected stomachs are heavier and may have a larger surface area than control stomachs. Small intestines may be heavier and have a thicker mucosa, with elongation of villi and crypts. Colonic mucosa may exhibit mild hyperplasia at very high dosages. Conflicting data exist as to whether the gastrointestinal mucosal hyperplasia is more related to increased production or decreased loss of epithelial cells.