Predictive Factors for Metachronous Gastric Cancer in High-Risk Patients after Successful &lt;i&gt;Helicobacter pylori&lt;/i&gt; Eradication

Shiotani, Akiko; Uedo, Noriya; Iishi, Hiroyasu; Yamanaka, Yoshiaki; Ishii, Manabu; Manabe, Noriaki; Kamada, Takenobu; Kusunoki, Hiroaki; Hata, Jiro; Haruma, Ken

doi:10.1159/000173719

Cited by 63 publications

(72 citation statements)

References 41 publications

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“…Previously, a few studies suggested risk factors for metachronous cancer, such as H. pylori infection [17], chronic atrophic gastritis [13,14,16], and undifferentiated histologic appearance [15]. However, there have been many limitations in terms of relatively small numbers of patients, lack of evaluation for premalignant dysplastic lesions, and adjustment with multiple factors.…”

Section: Discussionmentioning

confidence: 99%

“…In one study, metachronous gastric cancer tended to develop in the same third of the stomach as the primary lesion with similar macroscopic and differentiated type [12]. Another two studies showed that atrophy in the background gastric mucosa was associated with the development of metachronous gastric cancer [13,14]. In another study, undifferentiated histologic appearance of the primary lesion was related to the occurrence of synchronous or metachronous gastric cancer [15].…”

Section: Introductionmentioning

confidence: 96%

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Risk factors for synchronous or metachronous tumor development after endoscopic resection of gastric neoplasms

et al. 2014

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Background Despite many advantages, the development of synchronous or metachronous neoplasm is one of the main concerns with endoscopic resection. We aimed to clarify the independent risk factors for synchronous or metachronous gastric neoplasm. Methods We retrospectively reviewed the medical records of all patients who had undergone endoscopic resection for gastric high-grade dysplasia or early gastric cancer between April 2001 and February 2011. Results Among 971 subjects, 56 synchronous neoplasms and 42 metachronous neoplasms developed during 12-131 months of follow-up. In univariate analysis, age over 65 years, male gender, absence of Helicobacter pylori infection, lower third location, mucosal atrophy, and intestinal metaplasia were related to multiple gastric neoplasms. In multivariate analysis, absence of H. pylori infection [odds ratio (OR) 1.610, 95 % confidence interval (CI) 1.038-2.497)], lower third location (OR 1.704, 95 % CI 1.070-2.713), and intestinal metaplasia (OR 4.461, 95 % CI 1.382-14.401) were independent risk factors for multiple gastric neoplasms. For synchronous neoplasm, primary tumor size less than 1 cm was the only independent risk factor. For metachronous neoplasm, absence of H. pylori infection (OR 2.416, 95 % CI 1.214-4.810) was found to be the only independent risk factor. H. pylori eradication was found to be unrelated to the development of metachronous gastric neoplasms. Conclusions For tumors located in the antrum and accompanied by intestinal metaplasia, meticulous endoscopic evaluation with close follow-up after endoscopic resection is recommended.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 96%

Risk factors for synchronous or metachronous tumor development after endoscopic resection of gastric neoplasms

et al. 2014

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“…However, the development of metachronous gastric cancer (MGC), owing to the preservation of the entire stomach after endoscopic resection, remains a possibility [8][9][10]. A previous multicenter prospective randomized study performed in Japan showed that eradication of Helicobacter pylori reduced the incidence of MGC after endoscopic resection for early gastric cancer [11].…”

Section: Introductionmentioning

confidence: 99%

“…A previous multicenter prospective randomized study performed in Japan showed that eradication of Helicobacter pylori reduced the incidence of MGC after endoscopic resection for early gastric cancer [11]. However, MGC sometimes develops even after successful H. pylori eradication, with an annual incidence of 0.8-4.1 % [9][10][11][12][13][14][15]. In most previous studies, only incidences of MGC within a 3-year median follow-up period were reported, and a study with a longer follow-up period is needed.…”

Section: Introductionmentioning

confidence: 99%

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Incidence of and risk factors for metachronous gastric cancer after endoscopic resection and successful Helicobacter pylori eradication: results of a large-scale, multicenter cohort study in Japan

Mori

Nakajima

Asada³

et al. 2015

Gastric Cancer

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Background A previous multicenter prospective randomized study from Japan showed that Helicobacter pylori eradication reduced the development of metachronous gastric cancer (MGC) after endoscopic resection for early gastric cancer. MGC risk, however, is not eliminated; yet few studies have evaluated its long-term incidence and risk factors. In this study, we investigated the incidence of and risk factors for MGC in patients who underwent endoscopic resection for early gastric cancer with successful H. pylori eradication. Methods A total of 594 patients who underwent endoscopic resection for early gastric cancer and successful H. pylori eradication at three institutions (National Cancer Center Hospital, University of Tokyo Hospital, and Wakayama Medical University Hospital) were analyzed retrospectively. Annual endoscopic surveillance was performed after initial endoscopic resection. MGC was defined as a gastric cancer newly detected at least 1 year after successful H. pylori eradication. Results Ninety-four MGCs were detected in 79 patients during the 4.5-year median follow-up period. KaplanMeier analysis showed the cumulative incidence of MGC 5 years after successful H. pylori eradication was 15.0 %; the incidence of MGC calculated by use of the person-year method was 29.9 cases per 1000 person-years. Multivariate analysis using the Cox proportional hazards model revealed that male sex, severe gastric mucosal atrophy, and multiple gastric cancers before successful H. pylori eradication were independent risk factors for MGC. Eleven percent of MGCs (10 of 94) were detected more than 5 years after successful H. pylori eradication. Conclusion Surveillance endoscopy for MGC in patients who have undergone endoscopic resection for early gastric cancer should be performed even after successful H. pylori eradication.

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Serum pepsinogen levels can quantify the risk of development of metachronous gastric cancer after endoscopic resection

Iguchi

Kato

Yoshida

et al. 2016

Intl Journal of Cancer

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We have previously reported that serum pepsinogen (PG) can quantify the level of gastric mucosal atrophy, and that H. pylori eradication reduces cancer development in subjects with mild atrophy identified by serum PG levels. The aim of this study was to elucidate the predictive ability of serum PG levels for the development of metachronous gastric cancer (MGC) after endoscopic resection (ER) of primary cancer in association with H. pylori eradication. A retrospective chart review was performed, and 330 patients who underwent ER for initial early gastric cancer were enrolled. Presence or absence of H. pylori, serum PG levels, and endoscopic atrophy at ER were evaluated. H. pylori eradication was performed at the patient's request after ER. The incidence of MGC in these patients was analyzed. Of 330 patients, 47 developed MGC. Endoscopic extensive atrophy was observed more frequently in patients with MGC (p 5 0.001). Although PG I or PG II alone did not significantly differ according to development of MGC, the proportion of PG I/II 3.0, which is one of the criteria of PG test-positive, was significantly higher in patients with MGC (83 vs. 69%, p 5 0.04). H. pylori eradication after ER did not affect MGC development (p 5 0.2). On multivariate analysis, serum PG I/II ratio 3.3 was significantly associated with the development of MGC (hazard ratio: 3.66, 95% confidence interval: 1.47-12.25, p 5 0.004). The risk of MGC after ER could be quantitatively predicted by the PG I/II ratio regardless of H. pylori status.The International Agency for Research on Cancer (IARC) GLOBOCAN indicated that an estimated 1 million new cases of gastric cancer occurred worldwide in 2012, and it was the third most common cause of cancer death, accounting for 723,000 deaths. 1,2 In Japan, gastric cancer is the second most common cause of cancer death, accounting for 49,000 deaths per year.Accompanied by improvements in and increased use of endoscopy, detection of early stage gastric cancer has become more frequent. With improvement in endoscopic resection (ER) technique, represented by endoscopic submucosal dissection (ESD), ER has been widely accepted for local tumor resection. One of the merits of ER is that it can preserve the entire stomach. However, the procedure inevitably leaves stomach encompassing atrophic gastric mucosa, which is considered to be a hazardous region for cancer development. Hence, follow-up endoscopy for detecting metachronous gastric cancer (MGC) after ER is important.H. pylori infection causes chronic gastritis, which results in gastric atrophy, intestinal metaplasia, dysplasia and cancer. [3][4][5] In 1994, the IARC categorized H. pylori as a Group 1 carcinogen for gastric cancer. Recently, several meta-analyses reported the preventive effect of H. pylori eradication on gastric cancer development, [6][7][8][9] and the effect appears to be influenced by the background gastric mucosal status to some extent. Chen et al. reported that H. pylori eradication reduced the risk of gastric cancer in patients with non-atrop...

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Predictive Factors for Metachronous Gastric Cancer in High-Risk Patients after Successful <i>Helicobacter pylori</i> Eradication

Cited by 63 publications

References 41 publications

Risk factors for synchronous or metachronous tumor development after endoscopic resection of gastric neoplasms

Risk factors for synchronous or metachronous tumor development after endoscopic resection of gastric neoplasms

Incidence of and risk factors for metachronous gastric cancer after endoscopic resection and successful Helicobacter pylori eradication: results of a large-scale, multicenter cohort study in Japan

Serum pepsinogen levels can quantify the risk of development of metachronous gastric cancer after endoscopic resection

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