scholarly journals Detection of Early Gastric Cancer after Helicobacter pylori Eradication

Digestion ◽  
2021 ◽  
pp. 1-8
Author(s):  
Satoki Shichijo ◽  
Noriya Uedo ◽  
Tomoki Michida

<b><i>Background:</i></b> Based on evidence that <i>Helicobacter pylori</i> eradication reduces the development of gastric cancer and other diseases such as peptic ulcer, eradication therapy has prevailed. However, gastric cancer can develop even after successful eradication. <b><i>Summary:</i></b> In this review article, we searched for studies that identified the characteristics of primary and metachronous gastric cancers after <i>H. pylori</i> eradication, the risk factors for the development of these cancers after successful <i>H. pylori</i> eradication, and whether image-enhanced endoscopy is useful for diagnosing gastric cancer after eradication. A gastritis-like appearance is seen as a characteristic endoscopic finding, which corresponds to an epithelium with low-grade atypia – also known as nonneoplastic epithelium – covering the surface of the cancerous glands. This finding may make endoscopic detection of early gastric cancer difficult after <i>H. pylori</i> eradication. Similar risk factors, such as the male sex, endoscopic atrophy, histologic intestinal metaplasia, and late eradication, have been reported as predictors for the development of both primary and metachronous gastric cancers. Image-enhanced endoscopy, such as linked color imaging, may be useful for the detection and risk stratification of gastric cancer after eradication. <b><i>Key Messages:</i></b> Based on these findings, we believe that effective surveillance of high-risk patients leads to early detection of gastric cancer in the era of <i>H. pylori</i> eradication.

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Liang Wang ◽  
Jinfeng Wang ◽  
Sha Li ◽  
Fei Bai ◽  
Hailong Xie ◽  
...  

Abstract Objective To investigate the effect of Helicobacter pylori (H. pylori) eradication on the prognosis of postoperative early gastric cancer (EGC). Methods This is a retrospective study based on data from 6 hospitals. We identified 429 patients with EGC who underwent curative gastrectomy from January 2010 to December 2016. All of the patients were tested for H. pylori. Patients were divided into two groups, the successful H. pylori eradication group (group A, 268 patients) and the non-H. pylori eradication group (group B, 161 patients), for calculating the disease-free survival (DFS) and overall survival (OS) of each group. Result Positive node metastasis (hazard ratio (HR), 3.13; 95% confidence interval (CI), 1.84–5.32; P < 0.001), undifferentiated type (HR, 2.54; 95% CI, 1.51–4.28; P < 0.001), and non-H. pylori eradication (HR, 1.73; 95% CI, 1.08–2.77; P = 0.023) were statistically significantly independent risk factors of recurrence. Patient’s age ≥60 years old (HR, 3.32; 95% CI, 2.00–5.53; P < 0.001), positive node metastasis (HR, 3.71; 95% CI, 2.25–6.12; P < 0.001), undifferentiated type (HR, 3.06; 95% CI, 1.79–5.23; P < 0.001), and non-H. pylori eradication (HR, 1.83; 95% CI, 1.11–3.02; P = 0.018) were statistically significantly independent risk factors of overall survival. Conclusion H. pylori eradication treatment could prevent the recurrence of postoperative EGC to prolong the overall survival of patients with EGC.


Cancers ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1779
Author(s):  
Masaki Katsurahara ◽  
Ichiro Imoto ◽  
Yuhei Umeda ◽  
Hiroshi Miura ◽  
Junya Tsuboi ◽  
...  

Background: The role of Helicobacter pylori in the pathogenesis of reflux esophagitis is controversial. This study investigated the frequency of reflux esophagitis before and after H. pylori eradication in patients having endoscopic submucosal dissection for early gastric cancer. Methods: This study included 160 patients that fulfilled the study’s criteria. Endoscopy was performed before and after H. pylori eradication, and reflux esophagitis was evaluated during the follow-up period. Results: Seropositivity for H. pylori in patients with early gastric cancer was 68.8%, 101 of them received eradication therapy. During the follow-up period, the incidence of reflux esophagitis increased from 3.1% to 18.8% in the successful eradication group but no case of reflux esophagitis was observed in the failed eradication group. The univariate and multivariate analyses showed a significant correlation between successful H. pylori eradication rate and the development of reflux esophagitis. Conclusions: This study demonstrated that a successful H. pylori eradication therapy is a risk factor for newly developed reflux esophagitis in patients with endoscopic submucosal dissection for early gastric cancer.


2017 ◽  
Vol 55 (07) ◽  
pp. 653-656 ◽  
Author(s):  
Caspar Franck ◽  
Armin Hoffmann ◽  
Alexander Link ◽  
Christian Schulz ◽  
Kerstin Wuttig ◽  
...  

Abstract Background In the federal state of Saxony-Anhalt, gastric cancer (GC) incidence ranks among the highest in Germany. Helicobacter pylori prevalence is a surrogate marker for GC risk in a given population. In 2010 we reported an H. pylori seroprevalence of 44.4 % in patients at the emergency ward of the University Hospital of Magdeburg, the capital of Saxony-Anhalt. Our aim is to update these findings in a cohort of healthy blood donors from the same region. Materials and methods The sera of 516 consecutive blood donors (40.1 ± 14.1 years; 286 males and 230 females) were tested for antibodies against H. pylori and CagA. Data on demographics and previous H. pylori eradication therapy were obtained by means of a structured questionnaire. Blood donors with positive serology for H. pylori or CagA and/or history of eradication therapy were classified as H. pylori-positive. Results Overall, 28.9 % of the study cohort were H. pylori-positive. The prevalence was higher in older generations (9 % in 18 – 20 years up to 47 % in 61 – 70 years). In 44.4 % of H. pylori IgG-positive donors, CagA serology was also positive. This proportion was not age-dependent. Study participants with siblings were by trend more often H. pylori-positive (p = 0.066). Conclusion Compared to our previous study in patients at the emergency ward, we found by trend lower age-related H. pylori prevalence rates. In our cohort of healthy blood donors, we confirmed a lower H. pylori prevalence in younger generations.


2019 ◽  
Vol 41 (1) ◽  
pp. 97-108 ◽  
Author(s):  
Fujiao Duan ◽  
Chunhua Song ◽  
Jintao Zhang ◽  
Peng Wang ◽  
Hua Ye ◽  
...  

Abstract Eradication of Helicobacter pylori colonization has been reported to affect the progression of gastric cancer. A comprehensive literature search was performed from 1997 to 2017 using electronic databases. All randomized controlled trials (RCTs) and nonrandomized controlled trials (non-RCT) evaluated the effect of H. pylori eradication on development of gastric cancer. Four RCTs and 9 non-RCTs were included (n = 40,740 participants; 321,269 person-years). Overall, H. pylori eradication therapy was associated with a significantly reduced risk of gastric cancer (incidence rate ratio (IRR) = 0.52, 95% confidence interval (CI): 0.41, 0.65). Results of mixed-effect Poisson regression meta-analysis were similar to those of traditional meta-analyses. In stratified analyses, the IRRs were 0.59 (95% CI: 0.41, 0.86) in RCTs and 0.48 (95% CI: 0.36, 0.64) in non-RCTs. The IRRs were 0.45 (95% CI: 0.34, 0.61) in patients and 0.63 (95% CI: 0.44, 0.90) in the general population. Moreover, the relative risk reduction was approximately 77% on the development of noncardiac gastric cancer with H. pylori eradication therapy in China. Attributable risk percentage and population attributable risk percentage for Chinese patients were 77.08% and 75.33%, respectively, and for Japanese patients were 57.80% and 45.99%, respectively. H. pylori eradication therapy reduces the risk of noncardiac gastric cancer development. The findings indicate the importance of early intervention with H. pylori eradication therapy from the perspective of epidemiology.


2021 ◽  
Vol 12 ◽  
Author(s):  
Mariagrazia Piscione ◽  
Mariangela Mazzone ◽  
Maria Carmela Di Marcantonio ◽  
Raffaella Muraro ◽  
Gabriella Mincione

Worldwide, gastric cancer (GC) represents the fifth cancer for incidence, and the third as cause of death in developed countries. Indeed, it resulted in more than 780,000 deaths in 2018. Helicobacter pylori appears to be responsible for the majority of these cancers. On the basis of recent studies, and either alone or combined with additional etiological factors, H. pylori is considered a “type I carcinogen.” Over recent decades, new insights have been obtained into the strategies that have been adopted by H. pylori to survive the acidic conditions of the gastric environment, and to result in persistent infection, and dysregulation of host functions. The multistep processes involved in the development of GC are initiated by transition of the mucosa into chronic non-atrophic gastritis, which is primarily triggered by infection with H. pylori. This gastritis then progresses into atrophic gastritis and intestinal metaplasia, and then to dysplasia, and following Correa’s cascade, to adenocarcinoma. The use of antibiotics for eradication of H. pylori can reduce the incidence of precancerous lesions only in the early stages of gastric carcinogenesis. Here, we first survey the etiology and risk factors of GC, and then we analyze the mechanisms underlying tumorigenesis induced by H. pylori, focusing attention on virulence factor CagA, inflammation, oxidative stress, and ErbB2 receptor tyrosine kinase. Moreover, we investigate the relationships between H. pylori eradication therapy and other diseases, considering not only cardia (upper stomach) cancers and Barrett’s esophagus, but also asthma and allergies, through discussion of the “hygiene hypothesis. ” This hypothesis suggests that improved hygiene and antibiotic use in early life reduces microbial exposure, such that the immune response does not become primed, and individuals are not protected against atopic disorders, asthma, and autoimmune diseases. Finally, we overview recent advances to uncover the complex interplay between H. pylori and the gut microbiota during gastric carcinogenesis, as characterized by reduced bacterial diversity and increased microbial dysbiosis. Indeed, it is of particular importance to identify the bacterial taxa of the stomach that might predict the outcome of gastric disease through the stages of Correa’s cascade, to improve prevention and therapy of gastric carcinoma.


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