The role of duodenogastric reflux in formation of precarcinogenic gastric lesions: An experimental study

Abstract

Duodenogastric reflux, commonly encountered as an aftermath of gastroenteroanastomosis, with or without gastric resection (Billroth I, Billroth II), vagotomy and pyloroplastic surgery, is known to cause inflammatory-dystrophic-metaplastic lesions of gastric mucosa. Our objective was to determine the effects of surgery-induced duodenogastric reflux on the development of precarcinogenic lesions or carcinoma in correlation with the reflux duration. The experiment was performed on three groups of Wistar rats with 1) Billroth II-induced reflux surgery, 2) resection of the Rouxr-en-Y type reconstruction, and 3) control group with no resection. The aim of the experiment was to study the effects ofduodenogastric reflux on the rat gastric mucosa in correlation with two different types of gastroenteroanastomosis 8, 16 and 24 weeks after the surgery. In Billroth II group, hyperplastic changes were observed as early as in week 16. Statistically significant results were recorded in week 24, with 6.7% of metaplastic alterations, including dysplasia of all three degrees, dominantly severe dysplasia in 66.67%, early carcinoma in 20% and gastric carcinoma in 6.67%. In the Roux-en-Y group, gastric mucosa remained predominantly normal (60%), with somewhat increased frequency ofgastritis and dysplasia in week 24. In the control group, the finding of normal gastric mucosa was constant. The experiment confirms that direct contact of duodenal juice with gastric mucosa associated with Billroth II resection causes precarcinogenic lesions. Development of adenocarcinoma caused solely by duodenogastric reflux, excluding a carcinogenic agent is possible 20 weeks after the experiment--earlier than suggested by previous researchers.