Incidence Of Metachronous Gastric Cancer Research Articles

Sa1545 The Incidence of Metachronous Gastric Cancer After Endoscopic Resection of Early Gastric Cancer According to the Degree of Differentiation of the Primary Gastric Cancer

Sa1545 The Incidence of Metachronous Gastric Cancer After Endoscopic Resection of Early Gastric Cancer According to the Degree of Differentiation of the Primary Gastric Cancer

Neutrophil infiltration and the distribution of intestinal metaplasia is associated with metachronous gastric cancer following endoscopic submucosal dissection.

Endoscopic submucosal dissection (ESD) of early gastric cancer is a minimally invasive procedure. However, the risk for metachronous cancers after successful cancer treatment remains high and the risk factors for metachronous cancers have not been elucidated. To evaluate the risk factors for metachronous gastric cancers after ESD with a long-term follow-up. A total of 155 consecutive patients (119 men, 36 women, mean age 68.9 years) were treated with ESD between September 2000 and September 2009. Biopsy specimens were obtained from the greater curvature of the antrum and middle corpus to evaluate gastric mucosal status, including Helicobacter pylori, intestinal metaplasia (IM) and neutrophil infiltration (NI) before ESD. Follow-up endoscopy after ESD was scheduled at two and six months, one year and annually thereafter. H pylori eradication was recommended when possible. The median follow-up period was 4.2 years. Metachronous gastric cancers were found in 23 of 155 patients (3.5% per year). No local recurrences were observed. The cumulative incidence of metachronous gastric cancer was significantly high in IM and NI in the corpus (P=0.0093 and P=0.0025, respectively [log-rank test]). The ORs for IM and NI in the corpus were 2.65 and 3.06, respectively, according to the Cox proportional hazards model (P=0.024 and P=0.0091, respectively). The presence of IM and NI in the corpus was closely related to the development of metachronous gastric cancer after ESD.

Failure of Helicobacter pylori eradication and age are independent risk factors for recurrent neoplasia after endoscopic resection of early gastric cancer in 283 patients

Whether the incidence of metachronous gastric dysplasia and cancer could be decreased by eradication of Helicobacter pylori after endoscopic submucosal dissection (ESD) for early gastric cancer (EGC). To compare the incidence of metachronous gastric lesion in the eradicated group and the persistent group. Second end point is to evaluate the risk factors for metachronous gastric lesions after ESD for EGC. In a single centre, between May 2007 and May 2010, the patients who had evidence of H. pylori infection at the time of ESD for EGC were included, and the follow-up data were analysed retrospectively. We enrolled 283 patients who have shown H. pylori infection at the time of ESD for EGC. Successful eradication was achieved for 214 patients (75.6%) (Eradicated group), and 69 patients (24.4%) showed persistent H. pylori infection (Persistent group). Metachronous gastric lesions developed in 13 (18.8%) in the persistent group and 18 (8.4%) in the eradicated group (P=0.016). In the ≥60-year-old group, the cumulative incidence of metachronous gastric cancer showed a significant increase (P=0.012). Cumulative hazard ratio of subsequent gastric metachronous lesions differed between the eradication group and the persistent infection group (OR=2.322, 95% CI=1.136-4.744, P=0.021), and ≥60 age at the time of endoscopic resection (OR=2.803, 95% CI=1.207-6.509, P=0.016). Both persistent H. pylori infection and old age (≥60) are independent risk factors for the increased incidence of metachronous gastric cancer.

Effect of Helicobacter pylori Eradication on Metachronous Recurrence After Endoscopic Resection of Gastric Neoplasm

Although many epidemiologic studies have shown that Helicobacter pylori (H. pylori) eradication has prophylactic effects on gastric cancer, their results are less clear in high-risk populations. We conducted this study to examine whether H. pylori eradication would affect the occurrence of metachronous gastric cancer after endoscopic resection in patients with early gastric cancer. We retrospectively analyzed 2,089 adults who underwent endoscopic resection of gastric low-grade neoplasia, high-grade neoplasia, or differentiated invasive neoplasia from 2004 to 2008 at Asan Medical Center. Of these, a total of 1,007 patients with early gastric cancer were enrolled in this study. We evaluated the demographic data, the pathology, and the incidence of metachronous recurrence by dividing them into three groups: those without active H. pylori infection (Hp negative group, n=340), those who successfully underwent H. pylori eradication (eradicated group, n=485), and those who failed or did not undergo H. pylori eradication (noneradicated group, n=182). Metachronous recurrence was diagnosed in 75 patients, including 17 in the Hp, 34 in the eradicated, and 24 in the noneradicated groups. Median time to metachronous recurrence was 18 months (range, 7-75 months). The incidence of metachronous gastric cancer was 10.9 cases per 1,000 person-years in the Hp negative group, 14.7 cases per 1,000 person-years in the eradicated group, and 29.7 cases per 1,000 person-years in the noneradicated group. The hazard ratios in the noneradicated group compared with the Hp negative and eradicated groups were 2.5 (P<0.01) and 1.9 (P=0.02), respectively. H. pylori eradication reduced metachronous recurrence of gastric neoplasm, which was also shown in the secondary analysis of 1,487 patients with low-grade neoplasia and early gastric cancer. Successful H. pylori eradication may reduce the occurrence of metachronous gastric cancer after endoscopic resection in patients with early gastric cancer.

Sa1896 The Human Gastric Pathogen Helicobacter pylori Alters Intracellular Signaling by Inducing Truncated Forms of p53 Tumor Suppressor

patients (218 without current HP infection and 49 with successful eradication of HP infection) were HP negative status (HP-negative group), 107 patients (19 with failed eradication and 88 with no treatment of HP infection) were HP positive status (HP-positive group). The incidence of metachronous gastric cancer was compared in both groups, and the risk factors associated with the development of metachronous gastric cancer after ER was analyzed. Results: Median follow-up duration after ER was 4.1 years (range 1.0 10.5 years). During the follow-up period, metachronous gastric cancer developed in 16 patients (15.0% [16/ 107]) in the HP-positive group and in 15 patients (5.6% [15/267]) in the HP-negative group. The cumulative incidence of metachronous gastic cancer was significantly different between HP-negative and HP-positive groups (P= .003 by Log-rank test). In a multivariate Coxproportional hazard model, age . 65 years (hazard ratio [HR], 2.88; 95% confidential interval [CI], 1.28 6.49; P= .011), family history of gastric cancer (HR, 2.48; 95% CI, 1.11 5.53; P= .026), and HP-positive status (HR, 2.52; 95% CI, 1.24 5.14; P= .011) were associated with the development ofmetachronous gastric cancer. Conclusions: Persistent H. pylori infection after ER for EGC seems be associated with the development of metachronous gastric cancer during long-term follow-up period.

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

In the preoperative evaluation for gastric cancer, high-resolution endoscopic technologies allow us to detect small accessory lesions. However, it is not known if the gastric remnant after partial gastrectomy for synchronous multiple gastric cancers has a greater risk for metachronous cancer. The purpose of this study was to determine the incidence of metachronous cancer in this patient subset compared with that after solitary cancer surgery. Data on a consecutive series of 1,281 patients gastrectomized for early gastric cancer from 1991 to 2007 were analyzed retrospectively. The 715 gastric remnants after distal gastrectomy were periodically surveyed by endoscopic examination in Shikoku Cancer Center. Among those surveyed cases, 642 patients were pathologically diagnosed with solitary lesion (SO group) and 73 patients with synchronous multiple lesions (MU group) at the time of the initial surgery. In the follow-up period, 15 patients in the SO group and 3 patients in the MU group were diagnosed as having metachronous cancer in the gastric remnant. The cumulative 4-year incidence rate was 1.9 % in the SO group and 5.5 % in the MU group. The difference did not reach the significant level by the log-rank test. The incidence of metachronous cancer is higher after multiple cancer surgery; however, the difference is not statistically significant.

Sa1892 The Association Between Helicobacter pylori Status and Incidence of Metachronous Gastric Cancer After Endoscopic Resection of Early Gastric Cancer

Sa1892 The Association Between Helicobacter pylori Status and Incidence of Metachronous Gastric Cancer After Endoscopic Resection of Early Gastric Cancer

Sa1893 Primary Genotypic Resistance of Helicobacter pylori and Its Relations With Virulence Factors - A Multicenter Surveillance Program in Taiwan

patients (218 without current HP infection and 49 with successful eradication of HP infection) were HP negative status (HP-negative group), 107 patients (19 with failed eradication and 88 with no treatment of HP infection) were HP positive status (HP-positive group). The incidence of metachronous gastric cancer was compared in both groups, and the risk factors associated with the development of metachronous gastric cancer after ER was analyzed. Results: Median follow-up duration after ER was 4.1 years (range 1.0 10.5 years). During the follow-up period, metachronous gastric cancer developed in 16 patients (15.0% [16/ 107]) in the HP-positive group and in 15 patients (5.6% [15/267]) in the HP-negative group. The cumulative incidence of metachronous gastic cancer was significantly different between HP-negative and HP-positive groups (P= .003 by Log-rank test). In a multivariate Coxproportional hazard model, age . 65 years (hazard ratio [HR], 2.88; 95% confidential interval [CI], 1.28 6.49; P= .011), family history of gastric cancer (HR, 2.48; 95% CI, 1.11 5.53; P= .026), and HP-positive status (HR, 2.52; 95% CI, 1.24 5.14; P= .011) were associated with the development ofmetachronous gastric cancer. Conclusions: Persistent H. pylori infection after ER for EGC seems be associated with the development of metachronous gastric cancer during long-term follow-up period.

Recent Development of Gastric Cancer Prevention

A mass screening program using photofluorography has been used as a secondary prophylaxis of gastric cancer in Japan. However, we are at a turning point for reconsidering the strategy of gastric cancer prevention because of various problems with photofluorography. The shift from current secondary prophylaxis to primary prophylaxis is now required. After a Japanese multicenter randomized controlled trial showed that Helicobacter pylori eradication reduced the incidence of metachronous gastric cancer after endoscopic resection of early gastric cancer, primary prophylaxis of gastric cancer has gained greater attention. The combination of H. pylori eradication as a primary prophylaxis and screening as a secondary prophylaxis is necessary for the elimination of gastric cancer in Japan. The strategy of test, treat and screening for H. pylori infection is effective in reducing the incidence and mortality of gastric cancer in communities with a high incidence of gastric cancer. We have proposed a program of risk stratification based on the presence of H. pylori infection with or without atrophic gastritis followed by targeted interventions.

9 Long-Term Follow-up Study About Preventive Effect of H. pylori Eradication for the Incidence of Metachronous Gastric Cancer After Endoscopic Resection of Primary Early Gastric Cancer

Background:It has been proved thatH. pylori eradication prevents the incidence of metachronous gastric cancer after endoscopic resection (ER) of primary early gastric cancer during short-term follow-up. However, it has not been clarified whether preventive effect of H. pylori eradication for gastric cancer continues in the long term. To determine the long-term effect of H. pylori eradication on the development of gastric cancer, a follow-up study of a JGSG trial (Lancet 2008; 372: 392-7) was conducted. Methods: In this multi-center, openlabel, randomized controlled trial, 544 patients who received ER of early gastric cancer were randomly assigned to the H pylori eradication group (n=272) or to the control group (n= 272). Endoscopy was performed every year after randomization to evaluate metachronous cancer. Diagnosis of a new gastric cancer at another site of the stomach was defined as primary endpoint. Metachronous cancers were confirmed through histological examination. The frequency of metachronous cancer in the eradication group was compared to that in the control group. Results: There were no significant differences between eradication and control groups in baseline characteristics. The follow-up period was 10 years at maximum. After three years of follow-up, metachronous gastric cancer was detected in 32 participants. In the end, metachronous gastric carcinoma had developed in 22 patients in the eradication group and 43 in the control group. In the modified intention-to-treat population, including patients with at least one post-randomization assessment of tumor status and adjusting for loss to follow-up (255 patients in the eradication group, 250 in the control group), the hazard ratio for metachronous gastric carcinoma was 0.497 (95% CI 0.2970.831; p=0.008). The eradication group and the control group showed no difference in characteristics of metachronous cancer. Conclusions: This study showed that H. pylori eradication prevented the development of metachronous gastric cancers after ER during long-term follow-up.

11 The Rising Incidence of Esophageal Adenocarcinoma is Not Accompanied With an Increase in Mortality: Results of a Population-Based Cohort Study

Background:It has been proved thatH. pylori eradication prevents the incidence of metachronous gastric cancer after endoscopic resection (ER) of primary early gastric cancer during short-term follow-up. However, it has not been clarified whether preventive effect of H. pylori eradication for gastric cancer continues in the long term. To determine the long-term effect of H. pylori eradication on the development of gastric cancer, a follow-up study of a JGSG trial (Lancet 2008; 372: 392-7) was conducted. Methods: In this multi-center, openlabel, randomized controlled trial, 544 patients who received ER of early gastric cancer were randomly assigned to the H pylori eradication group (n=272) or to the control group (n= 272). Endoscopy was performed every year after randomization to evaluate metachronous cancer. Diagnosis of a new gastric cancer at another site of the stomach was defined as primary endpoint. Metachronous cancers were confirmed through histological examination. The frequency of metachronous cancer in the eradication group was compared to that in the control group. Results: There were no significant differences between eradication and control groups in baseline characteristics. The follow-up period was 10 years at maximum. After three years of follow-up, metachronous gastric cancer was detected in 32 participants. In the end, metachronous gastric carcinoma had developed in 22 patients in the eradication group and 43 in the control group. In the modified intention-to-treat population, including patients with at least one post-randomization assessment of tumor status and adjusting for loss to follow-up (255 patients in the eradication group, 250 in the control group), the hazard ratio for metachronous gastric carcinoma was 0.497 (95% CI 0.2970.831; p=0.008). The eradication group and the control group showed no difference in characteristics of metachronous cancer. Conclusions: This study showed that H. pylori eradication prevented the development of metachronous gastric cancers after ER during long-term follow-up.

10 PA32540, a Tablet Containing Enteric-Coated (EC) Aspirin 325 mg and Unbuffered Immediate-Release Omeprazole 40 mg, Provides Percent Time Gastric pH >4 Significantly Less Than EC Omeprazole 40 mg, but With Faster Onset and Less Exposure to Omeprazole

Background:It has been proved thatH. pylori eradication prevents the incidence of metachronous gastric cancer after endoscopic resection (ER) of primary early gastric cancer during short-term follow-up. However, it has not been clarified whether preventive effect of H. pylori eradication for gastric cancer continues in the long term. To determine the long-term effect of H. pylori eradication on the development of gastric cancer, a follow-up study of a JGSG trial (Lancet 2008; 372: 392-7) was conducted. Methods: In this multi-center, openlabel, randomized controlled trial, 544 patients who received ER of early gastric cancer were randomly assigned to the H pylori eradication group (n=272) or to the control group (n= 272). Endoscopy was performed every year after randomization to evaluate metachronous cancer. Diagnosis of a new gastric cancer at another site of the stomach was defined as primary endpoint. Metachronous cancers were confirmed through histological examination. The frequency of metachronous cancer in the eradication group was compared to that in the control group. Results: There were no significant differences between eradication and control groups in baseline characteristics. The follow-up period was 10 years at maximum. After three years of follow-up, metachronous gastric cancer was detected in 32 participants. In the end, metachronous gastric carcinoma had developed in 22 patients in the eradication group and 43 in the control group. In the modified intention-to-treat population, including patients with at least one post-randomization assessment of tumor status and adjusting for loss to follow-up (255 patients in the eradication group, 250 in the control group), the hazard ratio for metachronous gastric carcinoma was 0.497 (95% CI 0.2970.831; p=0.008). The eradication group and the control group showed no difference in characteristics of metachronous cancer. Conclusions: This study showed that H. pylori eradication prevented the development of metachronous gastric cancers after ER during long-term follow-up.

Long-term effect of Helicobacter pylori eradication on the development of metachronous gastric cancer after endoscopic resection of early gastric cancer

A prospective, randomized trial proved that Helicobacter pylori eradication significantly reduces the incidence of metachronous gastric cancer during a 3-year follow-up. To investigate the long-term effect of H pylori eradication on the incidence of metachronous gastric cancer after endoscopic resection of early gastric cancer. Retrospective, multicenter study. Kyushu University Hospital and 6 other hospitals in Fukuoka Prefecture, Japan. Follow-up data for 268 H pylori-positive patients who had undergone endoscopic resection of early gastric cancer were retrospectively investigated. A total of 177 patients underwent successful H pylori eradication (eradicated group), whereas 91 had persistent H pylori infection (persistent group). The incidence of metachronous gastric cancer was compared in these 2 groups. When the follow-up period was censored at 5 years, the incidence rate in the eradicated group was lower than that observed in the persistent group (P = .007). During the overall follow-up period ranging from 1.1 to 11.1 years (median 3.0 years), metachronous gastric cancer developed in 13 patients (14.3%) in the persistent group and in 15 patients (8.5%) in the eradicated group (P = .262, log-rank test). Based on a multivariate logistic regression analysis, baseline severe mucosal atrophy and a follow-up of more than 5 years were found to be independent risk factors for the development of metachronous gastric cancer. Retrospective study. H pylori eradication does not reduce the incidence of metachronous gastric cancer. H pylori eradication should be performed before the progression of gastric mucosal atrophy.

Autofluorescence imaging for predicting development of metachronous gastric cancer after Helicobacter pylori eradication

Although Helicobacter pylori eradication decreases the incidence of metachronous gastric cancer after endoscopic treatment for early gastric cancer (EGC), metachronous cancer still develops after successful eradication, particularly in patients with severe corpus gastritis. We investigated whether the extent of atrophic fundic gastritis diagnosed by autofluorescence imaging (AFI) videoendoscopy is predictive of development of metachronous gastric cancer after H. pylori eradication in patients treated with endoscopic submucosal dissection (ESD) for EGC. A total of 82 patients who underwent ESD for EGC from 2003 to 2006, who received eradication therapy participated in this study. The extent of chronic atrophic fundic gastritis was evaluated by AFI and categorized into closed and open type. The main outcome was the incidence of metachronous gastric cancer detected by annual surveillance endoscopy. During a median observation period of 55 months, metachronous gastric cancer developed in 12 of 82 patients (14.6%). Multivariate Cox's proportional hazard analysis revealed that open-type, atrophic fundic gastritis diagnosed by AFI was significantly associated with development of metachronous gastric cancer (hazard ratio: 4.88, 95% confidence interval [CI]: 1.32-18.2, P = 0.018) after adjustment for age, sex, histological intestinal metaplasia, serum pepsinogen level, and H. pylori status. Metachronous EGC developed after successful H. pylori eradication, and extensive atrophic fundic gastritis diagnosed by AFI was a significant predictor, thus it could identify patients undergoing ESD for EGC who still required intensive surveillance after eradication.

Long‐term treatment of localized gastric marginal zone B‐cell mucosa associated lymphoid tissue lymphoma including incidence of metachronous gastric cancer

According to a few recent reports on the long-term clinical outcome of gastric marginal zone B-cell mucosa associated lymphoid tissue lymphoma (MALT lymphoma); localized gastric MALT lymphoma generally has a favorable prognosis. However, the risk of metachronous gastric cancer has not been evaluated. In this study, we analyzed long-term outcomes of localized gastric MALT lymphoma including the incidence of metachronous gastric cancer. Between April 1996 and May 2008, 60 patients (31 men and 29 women; mean age 58.1 years) with localized gastric MALT lymphoma (stage I and II(1) according to Lugano classification) were analyzed retrospectively. Forty-eight patients (82.6%) achieved complete remission by eradication therapy. Radiation therapy was conducted on eight patients as second-line treatment, and all of them achieved remission. The median follow-up period was 76 months (range, 12-157 months). One patient had local relapse after remission for 5 years and three patients developed early gastric cancer without recurrence of lymphoma (5%). All of the three gastric cancers appeared in the same areas where MALT lymphoma had been eradicated. Eradication therapy and radiation therapy for localized gastric MALT lymphoma have a favorable long-term outcome, though regular follow-up endoscopy should be performed for detecting metachronous early gastric cancer.

Management of Helicobacter pylori.

Meta-analysis has shown that successful Helicobacter pylori eradication therapy improved atrophic gastritis and intestinal metaplasia. Moreover, successful eradication therapy against atrophic gastritis has led to the suppression of the incidence of metachronous gastric cancer. Thus, the Japanese Society for Helicobacter Research concluded that all ‘H. pylori-infected persons’ should be considered for eradication therapy, irrespective of any background diseases. Successful eradication can prevent transmission of this bacterium, and recent publications show that curing H. pylori infection seems to reduce the risk of gastric cancer.

Prevention of Gastric Cancer by Helicobacter pylori Eradication

Attention was focused on whether the incidence of gastric cancer could be decreased by eradication of Helicobacter pylori (H. pylori) infection after H. pylori infection was found to be an important risk factor for gastric cancer,. The Japan Gast Study Group (JGSG) planned a randomized study, with the primary endpoint being the development of gastric cancer after H. pylori eradication. To design a study with a fairly small sample size and short follow-up period, the conclusion was reached that the study should be conducted in patients who had undergone endoscopic mucosal resection (EMR) for early gastric cancer because they have the highest incidence of recurrent gastric cancer. There were no differences of age, gender, tumor site, histology, tumor depth, and tumor size between the two groups. The incidence of metachronous gastric cancer in eradication group was significantly lower than in control group in the analysis ignoring observation period (Odds ratio: 0.353, 95% CI: 0.161-0.775, p=0.009). Kaplan-Meier analysis revealed that the cumulative incidence of gastric cancer was different between the two groups. The Japanese Society for Helicobacter Research has published a guideline recommending that H. pylori infection should be treated by eradication therapy following this study. New evidence obtained from our study in Japan may be helpful for the prevention and eventually elimination of gastric cancer worldwide.

989 Eradication of Helicobacter pylori for the Incidence of Metachronous Gastric Cancer After Endoscopic Resection

989 Eradication of Helicobacter pylori for the Incidence of Metachronous Gastric Cancer After Endoscopic Resection

Helicobacter pylori eradication and metachronous gastric cancer after endoscopic mucosal resection of early gastric cancer

SummaryAimTo conduct a retrospective multicentre study at 31 medical centres in Japan, to investigate the association between the eradication of Helicobacter pylori and the development of new gastric cancer after endoscopic mucosal resection (EMR) for early gastric cancer.MethodsPatients included those in whom early gastric cancer had been removed by EMR, and who had received follow‐up endoscopic treatment. All patients underwent follow‐up endoscopic treatment at least once a year after the initial EMR. The rate of new gastric cancer development was compared among those patients for whom H. pylori had been successfully eradicated and those with persistent H. pylori infection.ResultsThe study included 2835 patients with a median follow‐up period of 2 years (range 0.5–12 years). Helicobacter pylori was eradicated in 356 patients (13%). Metachronous gastric cancers developed in eight (2%) patients among those who had been successfully treated for H. pylori, compared with 129 patients (5%) among those with persistent H. pylori infection (P = 0.021; OR = 0.42; 95% CI = 0.20–0.86).ConclusionAlthough longer term, prospective randomized controlled trials are needed to better estimate the extent and sustainability of possible benefits, this study suggests that the eradication of H. pylori may help reduce the incidence of metachronous gastric cancer.

Helicobacter pylori eradication and metachronous gastric cancer after endoscopic mucosal resection of early gastric cancer

SummaryAimTo conduct a retrospective multicentre study at 31 medical centres in Japan, to investigate the association between the eradication of Helicobacter pylori and the development of new gastric cancer after endoscopic mucosal resection (EMR) for early gastric cancer.MethodsPatients included those in whom early gastric cancer had been removed by EMR, and who had received follow‐up endoscopic treatment. All patients underwent follow‐up endoscopic treatment at least once a year after the initial EMR. The rate of new gastric cancer development was compared among those patients for whom H. pylori had been successfully eradicated and those with persistent H. pylori infection.ResultsThe study included 2835 patients with a median follow‐up period of 2 years (range 0.5–12 years). Helicobacter pylori was eradicated in 356 patients (13%). Metachronous gastric cancers developed in eight (2%) patients among those who had been successfully treated for H. pylori, compared with 129 patients (5%) among those with persistent H. pylori infection (P = 0.021; OR = 0.42; 95% CI = 0.20–0.86).ConclusionAlthough longer term, prospective randomized controlled trials are needed to better estimate the extent and sustainability of possible benefits, this study suggests that the eradication of H. pylori may help reduce the incidence of metachronous gastric cancer.