In the daily practice of gastroenterology, early detection of gastric cancer is especially difficult because of the flat morphology, rapid submucosal invasion and relatively short duration (about 1.5 years) of an asymptomatic stage. This presents a small window for gastroenterologists to identify early gastric cancer.1
The cause of gastric cancer is now recognized as chronic infection with Helicobacter pylori (H. pylori), and eradication of this pathogen from the population can reduce more than 75 percent of the disease burden. Therefore, as gastroenterologists, we have gradually focused our attention on H. pylori-induced gastritis, which had long been considered a vague endoscopic description and its significance virtually ignored.
In 2014, a global consensus meeting held in Kyoto, Japan, substantially increased the awareness of H. pylori gastritis by delivering new statements on the diagnosis and management of gastritis with special reference to dyspepsia symptoms and gastric cancer prevention.2
First, the Kyoto consensus emphasizes the etiology-based investigation of gastritis and recommends that we classify gastritis into “H. pylori-induced” and “H. pylori-negative” or “-idiopathic.” This requires careful evaluation of an H. pylori infection using multiple, parallel tests, a detailed review of medication history and a thorough exclusion of other possible causes. Reliable eradication regimens can be selected according to the antibiotic resistance patterns in different geographic areas and all tests for a cure should be confirmed. H. pylori infection causes gastritis in all infected subjects, and when symptoms of dyspepsia are present, eradication may improve the symptoms. However, this may somewhat underestimate the benefits of treatment, since the regression of gastritis after H. pylori eradication may take at least six months.
Second, the use of histological grading systems (e.g., the updated Sydney System and OLGA/ OLGIM stage distribution) is recommended to evaluate the severity and extent of gastritis. For high-risk populations, we usually take biopsy samples at different gastric subsites (both antral and corpus mucosa).2 In addition to increasing the diagnostic yield of H. pylori infection, the topographic distribution of inflammation, atrophic mucosa and intestinal metaplasia are associated with the increased risk of peptic ulcers and gastric cancer, and help us determine the need for endoscopic surveillance. The use of image-enhanced endoscopy and targeted biopsy may increase the diagnostic accuracy after appropriate training. This may prevent adverse events by pathological evaluation, such as bleeding.
Third, the consensus indicates that H. pylori gastritis is an infectious disease regardless of symptoms and complications, and that all H. pylori-infected individuals should be offered eradication therapy, unless competing considerations (e.g., advanced age and clinical comorbidity) are present. In fact, when large numbers of individuals receive eradication, non-infected individuals will be protected and the spread of the disease will be slowed. In our community-based eradication program, when the infection rate declined from 60 to 10 percent, the re-infection rate diminished from 10 to three per 1,000 people.2 However, this statement should be interpreted cautiously as a recommendation for mass screening and eradication in any given population. Whether or not to institute a screening program is a complex decision that must consider issues such as disease burden, cost-benefit ratio, infrastructure for delivering screening tests and competition with other health-care priorities. The consensus also highlights that the maximum benefit of H. pylori eradication can be obtained when mucosal damage is still non-atrophic. In screening participants, H. pylori is present in some individuals for decades (mucosa may become atrophic) and curing H. pylori cannot completely eliminate gastric cancer risk in those patients. Although the extent and severity of baseline gastritis may provide a clue, atrophic mucosa may regenerate over time after eradication. Therefore, reliable methods are needed to determine which patients need long-term follow-ups. Serological tests based on pepsinogen I and II levels, which reflect loss of the gastric gland and the presence of hypoacidity, may be an option. In our experience, the positivity rate was only about 3 to 4 percent for such a population and among those who tested positive, atrophic gastritis was indeed prevalent and gastric cancer was found. Another promising approach is the measurement of epigenetic alterations in the mucosa; this approach has been found useful in predicting the risk of metachronous gastric cancer after endoscopic resection.3
In gastric cancer, the carcinogenic process starts with gastritis, progressing to precancerous lesions and then cancer, while the development of preventive methods follows the reverse sequence.
The Kyoto Consensus on H. pylori gastritis is of particular importance to everyday gastroenterology practices in the Asia/Pacific region. It is a cornerstone in practice for the prevention of gastric cancer and provides important recommendations and guidance on our diagnosis and treatment of gastritis, and of the risk factors for H. pylori-associated gastric cancer.
Dr. Lee has no conflicts to disclose
1. Lee YC, Chiang TH, Liou JM, et al. Mass eradication of Helicobacter pylori to prevent gastric cancer: Theoretical and practical considerations. Gut Liver 2016;10:12-26.
2. Sugano K, Tack J, Kuipers EJ, et al faculty members of Kyoto Global Consensus Conference. Kyoto global consensus report on Helicobacter pylori gastritis. Gut 2015;64:1353-1367
3. Lee YC, Chen TH, Chiu HM, et al. The benefit of mass eradication of Helicobacter pylori infection: a communitybased study of gastric cancer prevention. Gut 2013;62:676- 682.