Background: Since “Helicobacter pylori (H. pylori) infection” was set as the indication in the Japanese Society for Helicobacter Research (JSHR) Guidelines 2009, eradication treatment for H. pylori gastritis is covered under insurance since 2013 in Japan, and the number of H. pylori eradication has rapidly increased. Under such circumstances, JSHR has made the third revision to the “Guidelines for diagnosis and treatment of H. pylori infection” for the first time in 7 years.Methods: The Guideline Committee held 10 meetings. Articles published between the establishment of the 2009 Guidelines and March 2016 were reviewed and classified according to the evidence level; the statements were revised on the basis of this review. After inviting public comments, the revised statements were finalized using the Delphi method.Results: There was no change in the basic policy that H. pylori infectious disease is an indication for eradication. Other diseases presumed to be associated with H. pylori infection were added as indications. Serum pepsinogen level, endoscopic examination, and X‐ray examination were added to the diagnostic methods. The effects of 1‐week triple therapy consisting of potassium‐competitive acid blocker (P‐CAB), amoxicillin, and clarithromycin have improved, and high eradication rates can also be expected with proton pump inhibitors (PPI) or P‐CAB combined with amoxicillin and metronidazole. If the susceptibility test is not performed, the triple PPI or P‐CAB/amoxicillin/metronidazole therapy should be chosen, because the PPI/amoxicillin/metronidazole combination demonstrated a significantly higher eradication rate than PPI/amoxicillin/clarithromycin. In the proposal for gastric cancer prevention, we divided gastric cancer prevention measures by age from adolescent to elderly, who are at an increased gastric cancer risk, and presented measures for gastric cancer prevention primarily based on H. pylori eradication.Conclusion: We expect the revised guidelines to facilitate appropriate interventions for patients with H. pylori infection and accomplish its eradication and prevention of gastric cancer.
Background: It is clear that genetic variations in the fat mass and obesity-associated (FTO) gene affect body mass index and the risk of obesity. Given the mounting evidence showing a positive association between obesity and pancreatic cancer, this study aimed to investigate the relation between variants in the FTO gene, obesity and pancreatic cancer risk. Methods: We conducted a hospital-based case–control study in Japan to investigate whether genetic variations in the FTO gene were associated with pancreatic cancer risk. We genotyped rs9939609 in the FTO gene of 360 cases and 400 control subjects. An unconditional logistic model was used to estimate the odds ratio (OR) and 95% confidence interval (CI) for the association between rs9939609 and pancreatic cancer risk. Results: The minor allele frequency of rs9939609 was 0.18 among control subjects. BMI was not associated with pancreatic cancer risk. Compared with individuals with the common homozygous TT genotype, those with the heterozygous TA genotype and the minor homozygous AA genotype had a 48% (OR=1.48; 95%CI: 1.07–2.04), and 66% increased risk (OR=1.66; 95%CI: 0.70–3.90), respectively, of pancreatic cancer after adjustment for sex, age, body mass index, cigarette smoking and history of diabetes. The per-allele OR was 1.41 (95%CI: 1.07–1.85). There were no significant interactions between TA/AA genotypes and body mass index. Conclusions: Our findings indicate that rs9939609 in the FTO gene is associated with pancreatic cancer risk in Japanese subjects, possibly through a mechanism that is independent of obesity. Further investigation and replication of our results is required in other independent samples.
TCTokyo Research Group on Prevention of Gastric Cancer
Tokyo Research Group on Prevention of Gastric Cancer
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Midkine (MK) is one of a family of heparin‐binding growth factors, and increased MK expression is reported in various types of human carcinomas. To clarify the association between serum MK (S‐MK) concentrations and gastric cancer, we examined S‐MK concentrations of gastric cancer patients (n = 275) and healthy controls (n = 275). S‐MK concentrations of all subjects were measured by enzyme‐linked immunosorbent assay (elisa). The medians (25th and 75th percentiles) of S‐MK were 192 (123 and 314) pg/mL in the cases and 170 (81 and 273) pg/mL in the controls (P < 0.01). We also compared S‐MK concentrations in each group divided by the progression stage or histological type of cancer. A difference was observed in the median S‐MK concentrations between early and advanced cancers [182 (105 and 301) pg/mLvs203 (139 and 331) pg/mL,P = 0.07], but not between intestinal and diffuse type cancers [185 (121 and 306) pg/mLvs198 (127 and 323) pg/mL,P = 0.51]. We found that those progression stages affect S‐MK concentration more strongly than the histological types in gastric cancer patients. Because S‐MK seems to reflect the progression stage of gastric cancer, it may serve as a useful marker in the clinical follow‐up of gastric cancer patients. (Cancer Sci2005; 96: 54 –57)