scholarly journals Clinicopathological Characteristics and Endoscopic Features of Early Gastric Cancers Diagnosed After Helicobacter pylori Eradication: A Retrospective Study

2020 ◽  
Author(s):  
Hideki Ishibashi ◽  
Hidetoshi Takedatsu ◽  
Taro Tanabe ◽  
So Imakiire ◽  
Hiroki Matsuoka ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Risk Factor ◽  
Clinicopathological Characteristics ◽  
Depressed Type ◽  
Helicobacter Pylori Eradication ◽  
Positive Group ◽  
Careful Patient ◽  
H Pylori

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.

scholarly journals Clinicopathological Characteristics and Endoscopic Features of Early Gastric Cancers Diagnosed After Helicobacter pylori Eradication

2021 ◽  
Author(s):  
Hideki Ishibashi ◽  
Hidetoshi Takedatsu ◽  
Taro Tanabe ◽  
So Imakiire ◽  
Hiroki Matsuoka ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Risk Factor ◽  
Clinicopathological Characteristics ◽  
Depressed Type ◽  
Helicobacter Pylori Eradication ◽  
Positive Group ◽  
Careful Patient ◽  
H Pylori

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.

scholarly journals Clinicopathological Characteristics and Endoscopic Features of Early Gastric Cancers Diagnosed After Helicobacter pylori Eradication: A Retrospective Study

2020 ◽  
Author(s):  
Hideki Ishibashi ◽  
Hidetoshi Takedatsu ◽  
Taro Tanabe ◽  
So Imakiire ◽  
Hiroki Matsuoka ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Risk Factor ◽  
Retrospective Study ◽  
Clinicopathological Characteristics ◽  
Depressed Type ◽  
Helicobacter Pylori Eradication ◽  
Positive Group ◽  
H Pylori

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.

scholarly journals Helicobacter pylori Eradication in Patients Undergoing Gastrectomy: Diagnosis and Therapy

2020 ◽  
Vol 20 (3) ◽  
pp. 204-209
Author(s):  
Youn I Choi ◽  
Jun-Won Chung
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Diagnostic Tests ◽  
Remnant Stomach ◽  
Optimal Timing ◽  
Helicobacter Pylori Eradication ◽  
Metachronous Gastric Cancer ◽  
H Pylori

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.

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 ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Incidence Rate Ratio ◽  
Gastric Atrophy ◽  
Diffuse Type ◽  
Gastric Cancer Risk ◽  
Helicobacter Pylori Eradication ◽  
H Pylori ◽  
Diffuse Type Gastric Cancer

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.

scholarly journals Effect of Helicobacter pylori eradication after subtotal gastrectomy on the survival rate of patients with gastric cancer: follow-up for up to 15 years

2020 ◽  
Vol 23 (6) ◽  
pp. 1051-1063
Author(s):  
Yonghoon Choi ◽  
Nayoung Kim ◽  
Chang Yong Yun ◽  
Yoon Jin Choi ◽  
Hyuk Yoon ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Survival Rate ◽  
Subtotal Gastrectomy ◽  
Helicobacter Pylori Eradication

scholarly journals Effect of Helicobacter pylori Eradication on Epigenetic Changes in Gastric Cancer-related Genes

2021 ◽  
Vol 21 (4) ◽  
pp. 256-266
Author(s):  
Ji Min Choi ◽  
Sang Gyun Kim
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Gastric Carcinogenesis ◽  
Point Of View ◽  
Epigenetic Changes ◽  
Epigenetic Alterations ◽  
Helicobacter Pylori Eradication ◽  
Gastric Cancer Prevention ◽  
H Pylori

It is known that gastric carcinogenesis results from the progressive changes from chronic gastritis to gastric atrophy, intestinal metaplasia, dysplasia, and invasive carcinoma. Several genetic and epigenetic alterations are involved in this process, and Helicobacter pylori (H. pylori) infection is believed to induce the initiation and progression of these steps. From an epigenetic point of view, H. pylori induces hypermethylation of genes involved in the development of gastric cancer and regulates the expression of various microRNAs (miRNAs). These H. pylori-related epigenetic changes are accumulated not only at the site of neoplasm but also in the adjacent non-cancerous gastric mucosa. Thereby, a state vulnerable to gastric cancer known as an epigenetic field defect is formed. H. pylori eradication can have an effective chemopreventive effect in gastric carcinogenesis. However, the molecular biological changes that occur in the stomach environment during H. pylori eradication have not yet been established. Several studies have reported that H. pylori eradication can restore infection-related changes, especially epigenetic alterations in gastric cancer-related genes, but some studies have shown otherwise. Simply put, it appears that the recovery of methylated gastric cancer-related genes and miRNAs during H. pylori eradication may vary among genes and may also differ depending on the histological subtype of the gastric mucosa. In this review, we will discuss the potential mechanism of gastric cancer prevention by H. pylori eradication, mainly from an epigenetic perspective.

Long‐term follow up of serum pepsinogens in patients with gastric cancer or dysplasia after Helicobacter pylori eradication

2020 ◽  
Vol 35 (9) ◽  
pp. 1540-1548 ◽  
Author(s):  
Gitark Noh ◽  
Nayoung Kim ◽  
Yonghoon Choi ◽  
Hye Seung Lee ◽  
Young Jae Hwang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Helicobacter Pylori Eradication ◽  
Serum Pepsinogens ◽  
Long Term Follow Up

THE ASSOCIATION OF THE COMBINATION OF TP53 GENE CODON 72 POLYMORPHISM AND HELICOBACTER PYLORI INFECTION WITH GASTRIC CANCER

2017 ◽  
pp. 47-52
Author(s):  
Thi Minh Thi Ha ◽  
Van Huy Tran ◽  
Viet Nhan Nguyen
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Risk Factor ◽  
Tp53 Gene ◽  
Codon 72 ◽  
Codon 72 Polymorphism ◽  
Pcr Rflp ◽  
Two Factors ◽  
Risk Patients ◽  
H Pylori

Background: The interaction of environment factor and host factor plays the important role in the pathogenesis of gastric cancer (GC). This study aimed to evaluate the association of the combination of TP53 gene codon 72 polymorphism and the H. pylori infection with GC risk. Patients and methods: 112 patients with GC and 136 patients without GC were extracted DNA from specimens of gastric mucosa, then were determined TP53 gene codon 72 polymorphism by PCR-RFLP and diagnosed H. pylori infection by PCR with ureC gene-specific primers. Results: There was no significant association between TP53 gene codon 72 polymorphism and GC risk, as well as between H. pylori infection and GC risk. The combination of two factors (TP53 gene codon 72 polymorphism and H. pylori infection) was found to be associated with GC risk: The combination of Pro/Pro genotype and H. pylori (+) was the GC risk factor, OR = 2.62 (95%CI: 1.20–5.71) as compared to other combinations. In the group of H. pylori-positive patients, Pro/Pro genotype was the GC risk factor, OR = 2.42 (95%CI: 1.05 – 5.59) as compared to (Arg/Arg + Arg/Pro) group, and OR = 3.48 (95%CI: 1.23 – 9.78) as compared to Arg/Arg genotype. Conclusion: The factors of TP53 gene codon 72 polymorphism and H. pylori infection were not associated with GC risk as assessed separately, but they had the interaction associated with GC risk. Key words: TP53 gene codon 72 polymorphism, Helicobacter pylori, gastric cancer

DETERMINATION OF HELICOBACTER PYLORI CAGA GENE AND VACA GENOTYPES IN PATIENTS WITH GASTRIC CANCER

2013 ◽  
pp. 118-125
Author(s):  
Quy Hung Le ◽  
Thi Minh Thi Ha
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Signet Ring Cell ◽  
Tubular Adenocarcinoma ◽  
Negative Group ◽  
Caga Gene ◽  
Positive Group ◽  
Histopathological Classification ◽  
Vaca Gene ◽  
H Pylori

Background: H. pylori is the first cause of gastric cancer (GC). However, the role of cagA gene and vacA gene in GC is still controversial. This study is aimed at determining the rates of H. pylori infection, cagA gene, vacA genotypes in patients with GC; and evaluating the relationship between cagA gene, vacA genotypes and endoscopic and histopathological features of gastric cancer. Patients and methods: Fifty eight GC patients and one hundred and sixteen non-GC patients (controls) were enrolled. Infection of H. pylori was determined by PCR. cagA gene and vacA genotypes were determined by Multiplex PCR. Results: The rate of H. pylori was found in 55.2% in GC group. The rate of cagA gene and vacA gene in GC patients H. pylori positive were found in 78.1% and 100%, respectively. vac A genotypes s1/m1, s1/m2 and s1/m1m2 were found in 34.4%; 50% and 15.6%, respectively. The risk of GC of cagA positive group was higher than cagA negative group, with OR = 4,5; 95%CI = 1.6-12.2. The risk of GC of vacA s1/m1, cagA positive group was higher than vacA s1/m1, cagA negative group, OR = 7.1; 95%CI = 1.4-36. A statistically significative difference of rate of cagA positive was found between Borrmann III/IV group (100%) and Borrmann I/II group (46.2%). A statistically significative difference of rate of cagA positive was found between the tubular adenocarcinoma group (100%) and signet-ring cell carcinoma (44.4%, p = 0,002), and mucinous adenocarcinoma (50%, p =0,024). Conclusion: Gene cagA and vacA s1/m1 genotype were both risk factors in GC. A significative differences of rate of cagA positive were found between Borrmann groups, and between groups of WHO histopathological classification. Key words: cagA gene and vacA genotype, Helicobacter pylori, gastric cancer

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