The Effect of Eradicating Helicobacter Pylori on the Development of Gastric Cancer in Patients with Peptic Ulcer Disease

Take, Sachiko; Mizuno, Motowo; Ishiki, Kuniharu; Nagahara, Yasuhiro; Yoshida, Tomowo; Yokota, Kenji; Oguma, Keiji; Okada, Hiroyuki; Shiratori, Yasushi

doi:10.1111/j.1572-0241.2005.41384.x

Cited by 198 publications

(204 citation statements)

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“…However, many of these included cases whose cancer lesions developed relatively soon after eradication, namely within 2 years after the treatment (Take et al 2005;Kamada et al 2005;Takenaka et al 2007;Fukase et al 2008;Ogura et al 2008).…”

Section: Discussionmentioning

confidence: 99%

“…There have been several reports that showed the incidence and characteristic features of gastric cancer after H. pylori eradication (Take et al 2005;Kamada et al 2005;Takenaka et al 2007;Fukase et al 2008;Ogura et al 2008;Yanaoka et al 2009;de Vries et al 2009). However, many of these included cases whose cancer lesions developed relatively soon after eradication, namely within 2 years after the treatment (Take et al 2005;Kamada et al 2005;Takenaka et al 2007;Fukase et al 2008;Ogura et al 2008).…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies consistently reported that H. pylori eradication had some inhibitory effects on the subsequent development of gastric cancer, at least in certain conditions (Take et al 2005;Takenaka et al 2007;Fukase et al 2008;Ogura et al 2008). However, it also has been revealed that there are sporadic cases of gastric cancer even after successful eradication (Kamada et al 2005;Yanaoka et al 2009;de Vries et al 2009).…”

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confidence: 99%

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Gastric Cancers Emerging after H. pylori Eradication Arise Exclusively from Non-Acid-Secreting Areas

Iijima

Abe

Koike

et al. 2012

Tohoku J. Exp. Med.

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Although Helicobacter pylori (H. pylori) eradication has some inhibitory effects on the subsequent development of gastric cancer, there are sporadic cases of gastric cancer even after successful eradication. The pathogenesis of gastric cancer emerging after H. pylori eradication remains to be clarified. In this study, employing Congo-red chromoendoscopy, which is capable of visualizing the acid-secreting fundic mucosa, we investigated the topographic relationship of the acid secretion pattern to the occurrence site of gastric cancers emerging after eradication. Fourteen consecutive patients who suffered from new gastric cancer after eradication, defined as lesions that were discovered at least 2 years after the eradication, were prospectively enrolled. Whether the neoplasias arose from acid-secreting or nonacid-secreting areas was evaluated with Congo-red chromoendoscopy. Biopsy specimens taken from the two areas were subjected to histologic evaluation and immunohistochemistry for Ki-67 and p53. The mean period from the eradication to the subsequent occurrence of gastric cancer was 74 (44) months. There were two cancer lesions in 5 cases, and thus there was a total 19 lesions from 14 cases. Congo-red chromoendoscopy revealed that all 19 lesions arose exclusively from non-acid-secreting areas. Histological examination revealed sustained hyperproliferation and accumulation of p53 protein was frequently detectable in non-acid-secreting areas. Genetic alteration such as p53 mutation seems to be already present in the residual non-acid-secreting areas after eradication, areas that could be the origin of gastric carcinogenesis after eradication. Identification of such high-risk areas should be a promising approach for estimating the individual cancer risk after eradication.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Gastric Cancers Emerging after H. pylori Eradication Arise Exclusively from Non-Acid-Secreting Areas

Iijima

Abe

Koike

et al. 2012

Tohoku J. Exp. Med.

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“…Graham [4] and Uemura et al [6] reported that approximately 20% of H. pylori-infected individuals develop clinically significant diseases, and the frequency of duodenal ulcers in individuals with H. pylori infection is thought to be approximately 16% [4]. Although Fischer et al [7] found 48 cases of concomitant gastric cancer while reviewing 45000 patients with duodenal ulcer (0.1%), Miwa et al [8] stated that six patients with gastric cancer among their 356 patients (1.7%) also showed duodenal ulcers, and Take et al [9] and Kamada et al [10] reported that gastric cancer did not develop in patients with duodenal ulcer. Uemura et al [6] conducted a 5-year follow-up of many Japanese subjects with H. pylori infections and found that all those with duodenal ulcers were also infected with H. pylori; however, none of the patients with duodenal ulcer developed gastric cancer, although 3.4% of the patients with gastric ulcer did, and gastric cancer subsequently appeared in 5% of the patients with H. pylori infections.…”

Section: Frequencies Of Duodenal Ulcer and Gastric Cancermentioning

confidence: 99%

Why is the coexistence of gastric cancer and duodenal ulcer rare? Examination of factors related to both gastric cancer and duodenal ulcer

et al. 2011

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The coexistence of gastric cancer with duodenal ulcer has been found empirically to be rare, but why it is rare is difficult to explain satisfactorily. To elucidate this question, we carried out a literature review of the subject. The frequency with which the two diseases coexist is 0.1-1.7%, and the main factor associated with both gastric cancer and duodenal ulcer is Helicobacter pylori infection. However, there are marked differences between the disorders of hyperchlorhydria in duodenal ulcer, and hypochlorhydria in gastric cancer. The most acceptable view of the reason for the difference may be that the acquisition of H. pylori infection occurs mainly in childhood, so that the time of acquisition of atrophic gastritis may be the most important, and if atrophic gastritis is not acquired early, high levels of gastric acid may occur, and consequently acute antral gastritis and duodenal ulcer may occur in youth, whereas, in elderly individuals, persistent H. pylori infections and the early appearance of atrophic gastritis may be the causes of low gastric acid, and consequently gastric cancer may occur. In patients with duodenal ulcer, factors such as nonsteroidal anti-inflammatory drugs (NSAIDs) and dupA-H. pylori strains may contribute to preventing the early acquisition of atrophic gastritis, while acid-suppressive therapy and vascular endothelial growth factor and other entities may inhibit atrophic gastritis. In contrast, in gastric cancer, factors such as excessive salt intake, acid-suppressive therapy, polymorphisms of inflammatory cytokines, and the homB-H. pylori strain may contribute to the early acquisition of atrophic gastritis, while factors such as NSAIDs; fruits and vegetables; vitamins A, C, and E; and good nutrition may inhibit it.

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“…Intervention studies conducted in Latin America and Asia and meta-analysis have shown that H pylori eradication is an effective step in preventing gastric cancer, particularly if treatment is performed on patients prior to development of precancerous conditions (atrophic gastritis and intestinal metaplasia) (65,139,193,206,210) . Studies using animal models have also confirmed that gastric cancer development can be prevented by early eradication of the microorganism (14,151) .…”

Section: Statement 17mentioning

confidence: 99%

3rd BRAZILIAN CONSENSUS ON Helicobacter pylori

Coelho

Maguinilk

Zaterka³

et al. 2013

Arq. Gastroenterol.

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Significant progress has been obtained since the Second Brazilian Consensus Conference on Helicobacter pylori Infection held in 2004, in São Paulo, SP, Brazil, and justify a third meeting to establish updated guidelines on the current management of H. pylori infection. The Third Brazilian Consensus Conference on H pylori Infection was organized by the Brazilian Nucleus for the Study of Helicobacter, a Department of the Brazilian Federation of Gastroenterology and took place on April 12-15, 2011, in Bento Gonçalves, RS, Brazil. Thirty-one delegates coming from the five Brazilian regions and one international guest, including gastroenterologists, pathologists, epidemiologists, and pediatricians undertook the meeting. The participants were allocated in one of the five main topics of the meeting: H pylori, functional dyspepsia and diagnosis; H pylori and gastric cancer; H pylori and other associated disorders; H pylori treatment and retreatment; and, epidemiology of H pylori infection in Brazil. The results of each subgroup were submitted to a final consensus voting to all participants. Relevant data were presented, and the quality of evidence, strength of recommendation, and level of consensus were graded. Seventy per cent and more votes were considered as acceptance for the final statement. This article presents the main recommendations and conclusions to guide Brazilian doctors involved in the management of H pylori infection.

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The Effect of Eradicating Helicobacter Pylori on the Development of Gastric Cancer in Patients with Peptic Ulcer Disease

Abstract: H. pylori eradication may reduce their risk of developing gastric cancer in patients with gastric ulcer. Large-scale studies in additional populations of this important international public-health issue are warranted.

Cited by 198 publications

References 19 publications

Gastric Cancers Emerging after H. pylori Eradication Arise Exclusively from Non-Acid-Secreting Areas

Gastric Cancers Emerging after H. pylori Eradication Arise Exclusively from Non-Acid-Secreting Areas

Why is the coexistence of gastric cancer and duodenal ulcer rare? Examination of factors related to both gastric cancer and duodenal ulcer

3rd BRAZILIAN CONSENSUS ON Helicobacter pylori

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