Prevalence of Helicobacter pylori infection in gastric remnant after distal gastrectomy for primary gastric cancer

Abstract

therapy has improved, and a long postoperative life is usual in a majority of these patients with early-stage gastric carcinoma [1]. However, in these patients, the gastric remnant (GR) retains the mucosa that had been the background of the initial cancer, and the mucosa exists in nonphysiological circumstances. Thus, the possible development of a second primary cancer in the GR has been a problem. In practice, the incidence of a second primary cancer in the GR is considerably high. At our institute, second primary cancer in the GR was found in approximately 2% of the patients after curative resection of primary gastric carcinoma [2]. Thus, post-operative endoscopic surveillance has been emphasized to detect curable early-stage cancer in the GR [3].Our previous study demonstrated that the features of early-stage second primary cancer in the GR were somewhat different from those of ordinary primary gastric carcinoma; protruding lesions and intestinal type cancer were dominant, and the background mucosa of these lesions was often associated with atrophic gastritis or intestinal metaplasia [2,4]. Although the real cause of gastric carcinogenesis is not fully understood, several environmental factors, including infection with Helicobacter pylori, have been shown to be linked with gastric carcinogenesis [5]. Since Warren and Marshall [6] first isolated H. pylori from the stomachs of patients with gastritis, numerous studies have demonstrated the relationship between H. pylori infection and the development of gastric cancer [7][8][9][10]. Now, H. pylori is regarded as a definite carcinogen [11] and as a trigger for the sequence of carcinogenesis, because there is strong evidence for H. pylori infection as a cause of chronic atrophic gastritis and intestinal metaplasia, two possible precancerous lesions [9,10,[12][13][14]. Our previous observations on the background mucosa of early-stage carcinoma of the GR also indicated an intimate association between atrophic gastritis and intestinal-type gastric carcinoma [2]. Thus, involvement of H. pylori in carAbstract Background. The development of a second primary cancer in the gastric remnant after gastrectomy for early gastric carcinoma is a problem, and eradication of Helicobacter pylori after the operation has been recommended. However, to date, practical indications for H. pylori eradication after gastric cancer surgery have not yet been reported. Methods. We examined H. pylori infection in the gastric remnant after distal gastrectomy for primary gastric cancer. One hundred and nine patients who had had a gastrectomy were studied. Endoscopic findings and results from the urease test, bacteriologic assessment, serological test, and histopathological examination were analyzed. Results. Seventy-one patients (65.1%) were judged to be positive for H. pylori infection. The prevalence of H. pylori infection was found to be significantly decreased in older patients, patients in whom the operation had been performed a long time before examination, patients with symptoms, and pati...

Incidence of metachronous gastric cancer in the remnant stomach after synchronous multiple cancer surgery

“…It has been well known that Helicobacter pylori infection in the gastric remnant after gastrectomy is associated with metachronous gastric cancer [25][26][27]. Now, Helicobacter pylori eradication is considered preventative therapy for metachronous gastric cancer [25,28,29].…”

Analysis of the differences in structural chromosomal aberrations of the gastric mucosa between H. pylori positive and negative gastric cancer patients: Involvement of H. pylori in the onset of gastric cancer and examination of the mechanism in gastric carcinogenesis following H. pylori eradication

“…Hp infection has been regarded as an important factor associated with the onset of gastric cancer (9-13), and Hp eradication has been conducted to prevent the onset of gastric cancer (23,24). However, many cases of gastric cancer occurring after Hp eradication have been reported (14)(15)(16)24), and the extent to which Hp eradication can suppress the onset of gastric cancer and the site involved in Hp infection in gastric carcinogenesis are unknown. The onset mechanism of Hp-negative gastric cancer is also unknown.…”

“…Various studies have been ONCOLOGY REPORTS 16: 1333-1342, 2006 Analysis of the differences in structural chromosomal aberrations of the gastric mucosa between H. pylori positive and negative gastric cancer patients: Involvement of H. pylori in the onset of gastric cancer and examination of the mechanism in gastric carcinogenesis following H. pylori eradication conducted concerning the relationship between Hp infection and gastric cancer, demonstrating the high probability that Hp infection is involved in the onset of gastric cancer (9-13), however, the involving site of Hp infection in gastric carcinogenesis remains unknown. A number of cases of gastric cancer occurring after Hp eradication have been reported (14)(15)(16), and the evaluation of Hp eradication therapy for a prevention against gastric cancer onset is unknown. Factors responsible for carcinogenesis can be roughly divided into genetic and environmental (17)(18)(19).…”

Evaluation of the efficacy of triple therapy regimen for Helicobacter pylori eradication in gastrectomized patients with gastric adenocarcinoma

“…We believe that this congruity occurred because the control group was of the same socioeconomic status as the patients in the literature. The prevalence of H. pylori in gastrectomized patients varies according to several factors; such as the postoperative period, the technique employed, and the age of the patient [19][20][21][22]. The prevalence of H. pylori in Billroth I gastrectomized patients varies from 36.9% to 80.3% [5,19,20], while that in Billroth II gastrectomized patients varies from 0% to 58% [19,20,23].…”

“…The prevalence of H. pylori in gastrectomized patients varies according to several factors; such as the postoperative period, the technique employed, and the age of the patient [19][20][21][22]. The prevalence of H. pylori in Billroth I gastrectomized patients varies from 36.9% to 80.3% [5,19,20], while that in Billroth II gastrectomized patients varies from 0% to 58% [19,20,23]. There are few references in the literature concerning H. pylori and Roux-en-Y diversion; however, this technique could provide a high prevalence rate having in mind that biliary reflux is damaging to H. pylori [20][21][22][23].…”