PATHOGENESIS OF CHRONIC GASTRIC ULCER EXTRA-ORDINARY COMPLICATION OF HYDATID CYSTS OF ΤΗΕ LIVER ADJACENT TO ΤΗΕ STOMACH AND PROJECTING ΙΝΤΟ ΤΗE GASTRIC LUMEN

Abstract

Purpose of this retrospective clinicopathologic study is the determination of the immediate causative agents and the elucidation of the (till now unknown) pathogenesis of chronic gastric ulcer. Data from 33 intramural solid benign gastric tumors (19 leiomyomas & 14 neurilemomas) and 37 cases of hydatid cysts of the liver (3 of which were adjacent and projecting into the gastric lumen) are presented. The finding of enormous ulcerative crater in almost all of the 33 above intramural gastric tumors and especially ulceration on the more prominent apex of hydatid cysts, which impress gastric wall, is discussed. Our data (according to Schwarz's dictum "no acid-no ulcer" & next to Dragsted regards-1970) add further support to the belief that a relationship is existing between ulcer-promoting factors and factors protecting the stomach's mucosal lining. The fact that the gastric ulcers occur usually on the lesser curgature (gastric luminal road of Sclavunos or sulcus of Waldeyer), on the angulus or the antrum near the angulus (gastric & channel ulcers) as well as the cardiac, stomal & jejunal ulcers provides evidence of long-continued process and supports the above aspect. There are at least two mechanisms whereby both (protective and damaging) factors might cause mucosal damage. First, alteration of protective mucous layer overlying epithelial cells, malcing it easier for acid and pepsin to reach the cells, or Secondf, absence of mucus because of continuous mechanical replacement or/and inhibited reproduction. Thus the reduced mucus protection is the primary or precipitating event that precedes ulceration or the initial lesion with acid and pepsin supervening secondarily after the "gastric mucosal barrier disruption". We hope the question of whether gastric ulcers are caused by decreased mucus protection has been finally answered.