Gastric carcinoma after treatment of ulcer

Intragastric Bile Acids in Patients with Gastric Ulcer and with Gastric Cancer

“…It has been proposed that the existence of DGR plays an important role in the development of gastric lesions in two circumstances: in the nonoperated stomach by causing atrophic chronic gastritis, and in the stomach operated for peptic ulcer due to the combination of hypochlorhydria and DGR that follow surgery [3,6,7,22]. Evidence exists indicating that a chronic increase of DGR induces inflammatory lesions in the gastric mu cosa [4,22], and several studies have shown a relation between the existence of chronic gastritis and the devel opment of cancer [13][14][15][16][17], However, the results of the present study indicate that nonoperated patients with type I gastric ulcer or with gastric cancer in an advanced stage do not have a significant increase in the amount of BA refluxed into the stomach, in agreement with other recent studies [23][24][25].…”

“…Patients who undergo partial gastrectomy for benign disease appear to have an increased risk of developing gastric cancer, particularly if ulcer disease was located in the stomach [1][2][3]. Partial gastrectomy causes reflux of the duodenal content into the stomach, which in turn leads to alkaline reflux gastritis [4], atrophic gastritis and mucosal metaplasia [1,5], It has been suggested that duodenogastric reflux (DGR) is an important factor in the origin of chronic gastritis that accompanies and often precedes cancer [6,7], However, DGR may also occur through the intact pyloric channel, physiologically in small proportions [8], and in higher amounts in nonoperated ulcer patients [9][10][11][12], Therefore, if atrophic chronic gastritis and metaplasia are indeed cancer precursors [13][14][15][16][17], nonoperated persons with high levels of DGR should be prone to gastric cancer.…”

An experimental study of gastric mucosal proliferation due to regurgitation of duodenal contents.

“…Berenblum (1854) proposed a hypothetical mechanism which indicated that chemical carcinogenesis is produced through two different steps; an initiating action followed by a promotive action. In several clinical studies, the development of carcinomas was observed with a higher incidence in the resected stomach than that found in the nonoperated general population (Liavaag, 1962;Hilbe et al 1968;Kobayashi, 1970;Stalsberg and taksdal, 1971;Saegesser and jamws, 1972;Morgenstern et al 1973;Papachriston et al 1976;Peitsch and Burkhardt, 1976;Helsingen and Hillestad, 1976;Domellof and Januger, 1977). Further experimental studies have revealed that duodenogastric reflux subsequent to gastrectomy was one of the most important factors for carcinoma development in the remnant stomach (Schonlenben et al 1976;Dahm et al 1976;Meister and Schlag, 1979;Wieman et al 1980;Langhans et al 1981;Nishidoi, 1983 …”

On the possibility of an increased risk of breast cancer in patients who underwent breast surgeries for benign diseases

“…В частности, в ряде исследований оценивали частоту развития рака желудка у пациентов, перенёсших оперативное вмешательство по поводу язвенной болезни данного органа или двенадцатиперстной кишки [4]. В результате было показано, что любое оперативное вмешательство на желудке или двенадцатиперстной кишке (резекция желудка по Бильрот I и Бильрот II, ваготомия, пилоропластика) статистически значимо повышает частоту развития рака желудка через 5 лет и более, прошедших с момента операции [3]. Средний интервал времени с момента операции по поводу язвенной болезни до момента постановки диагноза рака желудка составлял 10-15 лет, причём риск развития рака желудка оказался прямо пропорционален длительности этого интервала.…”