Shunsuke Takata

Low Prevalence of Helicobacter pylori-negative Gastric Cancer among Japanese

Background and Aims:  The true prevalence of Helicobacter pylori‐negative gastric cancer (HpNGC) is unknown. We attempt to clarify the prevalence and clinicopathologic features of HpNGC in Japanese.

Clinical prevention of gastric cancer by Helicobacter pylori eradication therapy: a systematic review

Helicobacter pylori (H. pylori) infection plays an important role in gastric carcinogenesis. We conducted a systematic review concerning gastric cancer development after H. pylori eradication therapy. In total 15 papers matched our criteria, the results were reviewed. The H. pylori eradication therapy statistically diminished the prevalence of clinical gastric cancer by approximately one-third. The studies from Japan supported this conclusion; however, studies from overseas reported conflicting results. The differences in these conclusions lie in the diagnostic ability of endoscopic examination, since the clinical stage was quite different between these studies. Gastric cancer that developed after eradication revealed a mainly intestinal type histology and depressed-type appearance. The following are possible reasons for reduced gastric cancer: (1) eradication therapy inhibits the new occurrence of gastric cancer, (2) eradication regresses or inhibits the growth of gastric cancer, and (3) eradication interferes with the discovery of gastric cancer. Considering the biological nature of cancer cell proliferation, a sufficiently long-term follow-up may clarify the effect of eradication therapy on inhibition of the development (not discovery) of gastric cancer and reduction of gastric cancer-related mortality.

Morphological changes in human gastric tumours after eradication therapy of Helicobacter pylori in a short-term follow-up

Background : It is controversial as to whether the development of gastric cancer is influenced by Helicobacter pylori eradication. If eradication itself influences the tumour morphology, this may affect the tumour discovery rate.

Gastric Cancer Development after Helicobacter pylori Eradication Therapy: A New Form of Gastric Neoplasia

Background and Aim: Along with the widespread use of eradication for Helicobacter pylori (H. pylori), the incidence of gastric cancer after eradication has also been increasing. There is a need for clarification of the clinical and biological characteristics of these neoplasms. Patients and Methods: We studied 27 cases of gastric cancer that developed after eradication (group AE). Out of the 27, we selected 26 with early-stage gastric cancer and compared them with 78 age-matched gastric cancer patients with H. pylori infection (group Pos) and 20 patients without H. pylori (group Neg). The patient with autoimmune gastritis was not included. Clinicopathological features, mucus patterns and Wnt5a expressions were compared among these groups. Results: Among group AE patients, there were more males than females, and the tumor histology was mainly intestinal type, a significant difference from group Neg. In contrast, macroscopically, the tumors were predominantly of the flat-depressed type, a feature similar to that of group Neg but significantly different from that of group Pos. MUC2 and Wnt5a expression was significantly lower in group AE than in group Pos. Conclusion: Gastric cancer development after eradication may have a carcinogenic pathway similar to that in cancer with H. pylori infection, though macroscopic/biological features may be modified by eradication therapy.

A combination of the Helicobacter pylori stool antigen test and urea breath test is useful for clinical evaluation of eradication therapy: A multicenter study

Background:  Helicobacter pylori stool antigen (HpSA) test is a new tool for evaluating the H. pylori infection. The present study was carried out to investigate the clinical usefulness of the HpSA test in the evaluation of eradication therapy by comparing it with the 13C‐urea breath test (UBT).

Host factors contributing to the discovery of gastric cancer after successful eradication therapy of Helicobacter pylori: Preliminary report

Background and Aim:  Clinical features of patients who develop gastric cancer after successful eradication of Helicobacter pylori are still unclear. We attempted to identify host factors associated with the discovery of gastric cancer, including changes in the background gastric mucosa in patients with atrophic gastritis.

The effect of Helicobacter pylori eradication therapy on gastric ulcer healing after endoscopic mucosal resection.

Background and Aim It remains unclear whether Helicobacter pylori eradication therapy accelerates the healing of acute gastric ulcer after endoscopic mucosal resection (EMR) of gastric tumor. We examined the effect of H. pylori eradication therapy on ulcer healing after EMR. Methods Twenty-six patients who underwent successful H. pylori eradication therapy before EMR were followed prospectively. Patients underwent endoscopic examination 1 or 2 months after EMR, during which the ulcer status and reduction rate were assessed. The effect of H. pylori eradication on the quality of ulcer healing was also evaluated. Six patients in whom eradication therapy failed and 26 patients who underwent EMR without eradication therapy served as control subjects. Results Endoscopically, 18 (75%) of 24 ulcers in the eradication group were at the healing stage 1 month after EMR. The ulcer reduction rates were 85.0±2.6% and 96.9±1.1% at 1 and 2 months after EMR, respectively. Ulcer stage and reduction rate did not differ significantly between the eradication group and control group. However, we frequently observed a better quality of ulcer healing in the eradication group than in the control groups (P<0.01). Conclusion H. pylori eradication therapy does not accelerate ulcer healing after EMR but may improve the quality of ulcer healing of gastric ulcer after EMR.

Relationship between Helicobacter pylori Tyrosine-Phosphorylated CagA-Related Markers and the Development of Diffuse-Type Gastric Cancers: A Case-Control Study

Background/Aims: Tyrosine phosphorylation of the EPIYA motif in Helicobacter pylori CagA (CagA-P) plays an important role in toxic reaction. Diffuse-type gastric cancer (DGC) has a poor prognosis. We tried to clarify the expression level of CagA-P in DGC patients. Methods: We enrolled 42 early-stage DGC patients (DGC group; 20 males, 22 females, mean age 58.2 years) and 42 age- and gender-matched atrophic gastritis (AG) patients (AG group) as controls. We evaluated histological and serological gastritis and examined two markers; the serum titer of anti-CagA-P antibody and CagA-P expression in gastric mucosa. Results: In the DGC group, we found significantly higher corpus histological gastritis scores for activity, atrophy, and intestinal metaplasia. The titer of anti-CagA-P antibody and CagA-P expression in the corpus were significantly higher in the DGC group, especially in females (p < 0.05). Sixteen patients (38.1%) in the DGC group showed both positive markers, and the odds ratio for DGC occurrence was 4.00 (95% CI = 1.07–14.91), while that for females was 9.00 (95% CI = 1.29–62.97). Conclusions: CagA-P plays a role in active corpus gastritis, which may link to DGC carcinogenesis. Clinical quantification of CagA-P-related markers may be useful for the evaluation of DGC risk, especially in females.

Serum screening for detection of high‐risk group for early‐stage diffuse type gastric cancer in Japanese

Background and Aim:  Serum screening systems are beneficial for gastric cancer mass surveys; however, the marker for diffuse type gastric cancer (DGC) is not defined. We attempted to define the high‐risk group for DGC by using serum markers of anti‐Helicobacter pylori antibody and pepsinogens (PG).

Helicobacter pylori cagA polymorphism and gastric inflammation: An international comparison between Japanese and Brazilian patients

Abstract Objective. Gastritis induced by Helicobacter pylori can cause the onset of gastric cancer, and H. pylori cytotoxin associated gene A (cagA) is considered to be an important factor for its development. We investigated the relationship between the grades of gastritis and cagA phenotype in Japanese and Brazilian patients. Material and methods. We studied 47 Brazilian and 47 age-, gender-matched Japanese patients. Status of H. pylori infection, the degree of histologic gastritis, and the levels of serum pepsinogen levels were evaluated. DNA was extracted from paraffin-embedded sections and a portion of the cagA gene was amplified using the polymerase chain reaction, followed by direct sequencing of the fragment. We investigated the cagA subtype using a newly developed restriction fragment length polymorphism (RFLP) system. Results. In H. pylori-positive patients, the grades of histological and serological gastritis were more prominent in the Japanese subjects than their Brazilian counterparts, although no difference was detected in the H. pylori-negative subjects. According to cagA phenotype analysis, our RFLP system was helpful for evaluating cagA phenotype, and we found that the prevalence of the East Asia subtype was significantly higher in the Japanese subjects than in the Brazilian. Conclusion. Infection with H. pylori possessing the East Asian cagA gene contributes to the progression of gastritis.