scholarly journals Risk of gastric cancer in the second decade of follow-up after Helicobacter pylori eradication

2019 ◽  
Vol 55 (3) ◽  
pp. 281-288 ◽  
Author(s):  
Susumu Take ◽  
Motowo Mizuno ◽  
Kuniharu Ishiki ◽  
Chiaki Kusumoto ◽  
Takayuki Imada ◽  
...  

Abstract Background and aims Eradication of Helicobacter pylori reduces the risk of gastric cancer. In this study, we investigated the risk beyond 10 years after eradication of H. pylori. Methods We conducted a retrospective cohort study of 2737 patients who had yearly endoscopic follow-up after cure of H. pylori infection. For comparison of gastric cancer risk in the second decade of follow-up with that in the first decade, we calculated standardized incidence ratios (SIRs) by dividing the number of observed cases of gastric cancer in the second decade of follow-up by that of expected cases which was estimated using the incidence rate ratio of age in the first decade. Results During the follow-up for as long as 21.4 years (mean 7.1 years), gastric cancer developed in 68 patients (0.35% per year). The SIRs for diffuse-type gastric cancer was infinity (0 expected case and 4 observed cases) in patients with mild gastric mucosal atrophy and 10.9 (95% confidence interval 4.53–26.1) with moderate atrophy, whereas no significant increase of SIRs was observed in intestinal-type cancer regardless of the grade of baseline gastric atrophy or in diffuse-type cancer in patients with severe atrophy even though who had the highest risk. Conclusions The longer the follow-up, the greater the risk of developing diffuse-type gastric cancer becomes in patients with mild-to-moderate gastric atrophy at baseline. Endoscopic surveillance should be continued beyond 10 years after cure of H. pylori irrespective of the severity of gastric atrophy.

Author(s):  
Youn I Choi ◽  
Jun-Won Chung

The role of <i>Helicobacter pylori</i> (<i>H. pylori</i>) eradication in patients undergoing gastrectomy for gastric cancer is unclear. Although European and Asian guidelines strongly recommend <i>H. pylori</i> eradication in patients who undergo endoscopic resection for early gastric cancer, these guidelines do not specify the tests useful for diagnosing <i>H. pylori</i> infection, the optimal timing and appropriate eradication regimens, and follow-up strategies in patients undergoing gastrectomy for gastric cancer. This review aims to update the guidelines for the diagnosis and management of <i>H. pylori</i> infection in patients undergoing gastrectomy for gastric cancer. We have focused on the following issues: 1) diagnostic tests for <i>H. pylori</i> infection in the remnant stomach, 2) optimal timing and regimen for <i>H. pylori</i> eradication, and 3) role of <i>H. pylori</i> eradication in reducing the risk of metachronous gastric cancer in the remnant stomach.


2003 ◽  
Vol 11 (4) ◽  
pp. 233-237 ◽  
Author(s):  
Marica Otasevic ◽  
Aleksandar Nagorni ◽  
Dobrila Stankovic-Djordjevic ◽  
Marina Dinic ◽  
Ljiljana Otasevic

BACKGROUND: Helicobacter pylori (H. pylori) is classified as a Group 1 carcinogen, because H. pylori infection considerably increases the risk of gastric cancer development. METHODS: The study involved a total of 191 patients divided into two groups. The first group comprised 117 patients who underwent endoscopy. A total of 203 biopsy specimens of the gastric mucosa were taken and analyzed using microbiological and histopathological methods. The second group comprised 74 patients with gastric cancer, who were examined for the gastric cancer type, the presence of H. pylori infection and the cancer localization. The presence of H. pylori infection in the tissue was con?firmed by staining pathohistological sections according to the method of Warthin-Starry. The microbilogical diagnosis involved the staining of direct tissue smears according to the method of Gram, as well as the cultivation of the specimens. To test the hypothesis for possible differences in H. pylori positive findings between the treatment groups, x2 test with Yates correction or Fisher exact test were used. RESULTS: The first treatment group comprised 117 patients with various clinical diagnoses. Gastric cancer was diagnosed in 8 patients, and of these 87.50% were found to have H. pylori. No statistically significant difference in H. pylori positive tests was detected between the patients with gastric ulcer and the patients with gastric cancer (Fisher exact test: p=1.00; p>0.05) nor was it established between the patients with duodenal ulcer and those with gastric cancer (Fisher exact test: p= 1.00; p>0.05). The second treatment group comprised 74 patients, of whom 52 (70.27%) had intestinal-type gastric cancer and 22 (29.72%) had diffuse-type gastric cancer. No statistically significant difference in the positive tests for H. pylori was registered between the patients with intestinal-type and those with diffuse-type gastric cancer (x2=0.07; p=0.798; p>0.05). The most frequent localization of the cancer was the antrum. CONCLUSION: The results are supportive of the hypothesis on a correlation between H. pylori infection and gastric adenocarcinoma development, but no differences between the intestinal and diffuse type of adenocarcinoma have been revealed with respect to the malignant process.


2021 ◽  
Author(s):  
Hideki Ishibashi ◽  
Hidetoshi Takedatsu ◽  
Taro Tanabe ◽  
So Imakiire ◽  
Hiroki Matsuoka ◽  
...  

Abstract Background. Helicobacter pylori (H. pylori) infection is an important risk factor for developing gastric cancer. However, even after H. pylori eradication, early gastric cancer (EGC) can develop. We elucidated the characteristics of EGCs diagnosed after H. pylori eradication. Methods. Thirty-six EGCs in 32 patients diagnosed after H. pylori eradication were defined as the eradication group (H. pylori-EG). The clinicopathological and endoscopic features were compared with those of 156 EGCs in 140 patients in the H. pylori-positive group (H. pylori-PG). Twenty-nine EGC lesions in the H. pylori-EG were further divided into two subgroups: the first included six lesions of none to mild atrophic mucosa around the EGC, and the second included 23 lesions of moderate to severe atrophic mucosa around the EGC. We compared them between the two subgroups. Results. Endoscopic features of EGCs in the H. pylori-EG were characterized as small (P = 0.049) and of the depressed type (P = 0.022) compared with those in the H. pylori-PG. EGCs in the H. pylori-EG were detected on the upper region of the stomach more frequently than those in the H. pylori-PG (P = 0.002). As for submucosal ECGs in the H. pylori-EG, it was more likely to be seen in the none to mild atrophic mucosa subgroup compared to the moderate to severe atrophic gastric mucosa subgroup (P = 0.003). Conclusions. EGCs after H. pylori eradication were characterized as small and of the depressed type. Submucosal invasive EGCs developed more frequently in the none to mild atrophic mucosa after H. pylori eradication. Therefore, careful patient follow-up is important after H. pylori eradication.


2020 ◽  
Author(s):  
Hideki Ishibashi ◽  
Hidetoshi Takedatsu ◽  
Taro Tanabe ◽  
So Imakiire ◽  
Hiroki Matsuoka ◽  
...  

Abstract Background: Helicobacter pylori (H. pylori) infection is an important risk factor for developing gastric cancer. However, even after H. pylori eradication, early gastric cancer (EGC) can develop. We elucidated the characteristics of EGCs diagnosed after H. pylori eradication. Methods: Thirty-six EGCs in 32 patients diagnosed after H. pylori eradication were defined as the eradication group (H. pylori-EG). The clinicopathological and endoscopic features were compared with those of 156 EGCs in 140 patients in the H. pylori-positive group (H. pylori-PG). Twenty-nine EGC lesions in the H. pylori-EG were further divided into two subgroups: the first included six lesions of none to mild atrophic mucosa around the EGC, and the second included 23 lesions of moderate to severe atrophic mucosa around the EGC. We compared them between the two subgroups. Results: Endoscopic features of EGCs in the H. pylori-EG were characterized as small (P = 0.049) and of the depressed type (P = 0.022) compared with those in the H. pylori-PG. EGCs in the H. pylori-EG were detected on the upper region of the stomach more frequently than those in the H. pylori-PG (P = 0.002). As for submucosal ECGs in the H. pylori-EG, it was more likely to be seen in the mild atrophic mucosa subgroup (4/6, 67%) compared to the moderate to severe atrophic gastric mucosa subgroup (1/23, 4%) (P = 0.003).Conclusions: EGCs after H. pylori eradication were characterized as small and of the depressed type. Submucosal invasive EGCs developed more frequently in the none to mild atrophic mucosa after H. pylori eradication. Therefore, careful patient follow-up is important after H. pylori eradication.


2020 ◽  
Author(s):  
Hideki Ishibashi ◽  
Hidetoshi Takedatsu ◽  
Taro Tanabe ◽  
So Imakiire ◽  
Hiroki Matsuoka ◽  
...  

Abstract Background: Helicobacter pylori (H. pylori) infection is an important risk factor for developing gastric cancer. However, even after H. pylori eradication, early gastric cancer (EGC) can develop. We elucidated the characteristics of EGCs diagnosed after H. pylori eradication. Methods: Thirty-six EGCs in 32 patients diagnosed after H. pylori eradication were defined as the eradication group (H. pylori-EG). The clinicopathological and endoscopic features were compared with those of 156 EGCs in 140 patients in the H. pylori-positive group (H. pylori-PG). Twenty-nine EGC lesions in the H. pylori-EG were further divided into two subgroups: the first included six lesions of no to mild atrophic mucosa around the EGC, and the second included 23 lesions of moderate to severe atrophic mucosa around the EGC. We compared them between the two subgroups. Results: Endoscopic features of EGCs in the H. pylori-EG were characterized as small (P = 0.049) and of the depressed type (P = 0.022) compared with those in the H. pylori-PG. EGCs in the H. pylori-EG were detected in the upper region of the stomach more frequently than those in the H. pylori-PG (P = 0.002). Submucosal ECGs in the H. pylori-EG were more likely to be seen in the no to mild atrophic mucosa subgroup (4/6, 67%) compared with the moderate to severe atrophic gastric mucosa subgroup (1/23, 4%) (P = 0.003). Conclusions: Careful follow-up endoscopies are necessary after H. pylori eradication.


2017 ◽  
Vol 85 (5) ◽  
pp. AB303
Author(s):  
Tomomitsu Tahara ◽  
Sayumi Tahara ◽  
Tetsuya Tsukamoto ◽  
Noriyuki Horiguchi ◽  
Tomohiko Kawamura ◽  
...  

2018 ◽  
Vol 111 (5) ◽  
pp. 484-489 ◽  
Author(s):  
Ka Shing Cheung ◽  
Esther W Chan ◽  
Angel Y S Wong ◽  
Lijia Chen ◽  
Wai Kay Seto ◽  
...  

2020 ◽  
Vol 23 (6) ◽  
pp. 1051-1063
Author(s):  
Yonghoon Choi ◽  
Nayoung Kim ◽  
Chang Yong Yun ◽  
Yoon Jin Choi ◽  
Hyuk Yoon ◽  
...  

PLoS ONE ◽  
2020 ◽  
Vol 15 (9) ◽  
pp. e0237515
Author(s):  
Rolando Herrero ◽  
Katy Heise ◽  
Johanna Acevedo ◽  
Paz Cook ◽  
Claudia Gonzalez ◽  
...  

2018 ◽  
Vol 19 (8) ◽  
pp. 2424 ◽  
Author(s):  
Shamshul Ansari ◽  
Boldbaatar Gantuya ◽  
Vo Tuan ◽  
Yoshio Yamaoka

Gastric cancer is the third leading cause of cancer-related deaths and ranks as the fifth most common cancer worldwide. Incidence and mortality differ depending on the geographical region and gastric cancer ranks first in East Asian countries. Although genetic factors, gastric environment, and Helicobacter pylori infection have been associated with the pathogenicity and development of intestinal-type gastric cancer that follows the Correa’s cascade, the pathogenicity of diffuse-type gastric cancer remains mostly unknown and undefined. However, genetic abnormalities in the cell adherence factors, such as E-cadherin and cellular activities that cause impaired cell integrity and physiology, have been documented as contributing factors. In recent years, H. pylori infection has been also associated with the development of diffuse-type gastric cancer. Therefore, in this report, we discuss the host factors as well as the bacterial factors that have been reported as associated factors contributing to the development of diffuse-type gastric cancer.


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