Helicobacter pylori infection following partial gastrectomy for gastric cancer

Table 1 Differences in the characteristics and manifestations of different gastric resections recently presented

Manifestations	Distal gastrectomy	Proximal gastrectomy
Bile reflux	↑	↓
Polymorphonuclear infiltration (i.e., rate of inflammation)	↑ (60.5%)	↓ (12.9%)
H. pylori infection rate	↑	↓
Chronic and active inflammation	↑	↓
Intestinal metaplasia	↓	↑

It is suggested that the presence of a gastric stump after proximal gastrectomy promotes the progression of intestinal metaplasia and hampers the colonization of Helicobacter pylori (H. pylori). However, this notion is contrary to results from previous studies showing a relatively low H. pylori prevalence in the gastric stump.

Table 2 Some issues disputed among researchers regarding Helicobacter pylori infection in the gastric remnant after partial gastrectomy

Issues	Prospective	Consequence
H. pylori infection decreases after partial gastrectomy, depending upon surgery and anastomosis type	Distal gastrectomy leads to bile reflux and resultant elevated intra-gastric pH, hampering H. pylori inhabitation; this was also shown in an in vitro study[19] Billroth type II anastomosis has higher bile reflux compared with Billroth type I or vagotomy, with concordant lower H. pylori infection prevalence[6,8] Bile refluxate is toxic to H. pylori, leading to spontaneous eradication[23]	Subjects with proximal gastrectomy are prone to intestinal metaplasia, which is a difficult environment for H. pylori survival[25] Duodenogastric reflux “facilitates” the survival of H. pylori[27]
H. pylori is a risk factor of carcinogenesis in the gastric stump	Some academic gastroenterological societies recognize H. pylori as a risk factor equivalent to the intact organ[1,2]	Showing a rather low H. pylori infection rate suggests a different pathogenesis of gastric cancer from the remnant stomach[3]
H. pylori eradication is required	H. pylori-positive subjects with a remnant stomach after gastrectomy for cancer showed a higher prevalence for premalignant lesions compared to H. pylori-negative subjects H. pylori eradication is strongly recommended[1]	Eradication therapy improved intestinal metaplasia, preventing premalignant changes[30] Some academic gastroenterological societies do not advocate H. pylori eradication in the gastric stump
Bile reflux inhibits H. pylori inhabitation in the gastric stump	Spontaneous eradication by the reflux of bile contents is suggested[23]	There was no apparent inverse relationship between the quantity of bile refluxate and H. pylori infection[11] Pylorus-preserving gastrectomy led to the spontaneous clearance of H. pylori[28]

H. pylori: Helicobacter pylori.