Levin S
Pathology Department, G. D. Searle & Company, Skokie, Illinois 60062.
Toxicol Pathol. 1988;16(2):237-44. doi: 10.1177/019262338801600216.
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.
E系列前列腺素已被提议作为治疗消化性溃疡和其他胃肠道疾病的治疗药物，可导致实验动物胃肠道黏膜增生。这些变化在胃中最为明显，尤其是胃窦，其壁因表面黏液细胞增生和/或黏膜下水肿而增厚。在啮齿动物中，非腺性前胃会增生并角化过度。受影响的胃比对照胃更重，表面积可能更大。小肠可能更重，黏膜更厚，绒毛和隐窝延长。在非常高的剂量下，结肠黏膜可能会出现轻度增生。关于胃肠道黏膜增生与上皮细胞产生增加还是丢失减少的关系，存在相互矛盾的数据。
