Kinetic changes and experimental carcinogenesis after Billroth I and II gastrectomy

Abstract

To determine the risk of gastric remnant cancer according to the type of surgical reconstruction, the distal two-thirds of the glandular stomach was resected in male Wistar rats, followed by gastroduodenostomy (Billroth I anastomosis) or gastrojejunostomy (Billroth II anastomosis). No carcinogens were given and the animals were killed 50 weeks after operation. No cancers developed in 22 rats undergoing Billroth I gastrectomy, but five of 24 with Billroth II anastomosis had adenocarcinoma (P < 0.05). All carcinomas were confined to the stoma. Animals with Billroth II anastomosis had a more advanced grade of mucosal atrophy at the stoma, with a higher incidence of cystic dilatation, submucosal adenocystic proliferation and pseudopyloric metaplasia (P < 0.05). Cell kinetics in the stomal mucosa after Billroth II gastrectomy showed an increased cell count in the proliferative zone, longer duration of S phase and increased cell cycle time (P < 0.05). These results suggest that Billroth II gastrectomy carries a greater risk of cancer than the Billroth I procedure.

Microsatellite instability in patients with gastric remnant cancer

“…Many reports have studied the pathogenesis and causes of gastric remnant cancer [5][6][7][8][9][10], but there is little information available on molecular biological analyses to identify individuals susceptible to gastric remnant cancer.…”

Carbon-14 urea breath test: does it work in patients with partial gastric resection?

“…or malignant causes [9][10][11]. The incidence of gastric stump cancer reached up to 2 % in this group [12].…”

“…As in non-operated patients, atrophic gastritis, intestinal metaplasia, dysplasia, and finally gastric cancer are closely related with the H. pylori infection in PGR patients [1]. Therefore, these high-risk cases should be screened for H. pylori, and eradication therapy should be given when the infection is detected [9][10][11].…”

Duodenogastric Reflux Increases the Penetration of N‐3H‐Methyl‐N‐nitro‐N‐nitrosoguanidine into the Antral Mucosa of Rats: A Possible Role for Mucosal Erosions and Increased Cell Proliferation in Gastric Carcinogenesis

“…15,16) Moreover, duodenogastric reflux increases the cell proliferation, and elongates the cell cycle time and the S-phase in the corpus mucosa. 17) Similar results are not available for the antrum.…”