Part I: Classification of gastritis according to ICD-11
Clinical Question 1: Is the current classification of gastritis under ICD-10 appropriate.
Statement 1: The current ICD-10 classification of gastritis is outdated in view of the discovery of Hp.
Recommendation level: Strong
Evidence classification: high
Level of consensus: 100%
Comment.
The ICD-10 classification criteria for gastritis were developed in 1989 and are still deferred in most countries.The ICD-10 classification of gastritis and duodenitis is based mainly on visual and histological criteria, with the only etiological factor being alcohol (Box 1), and the histological classification of gastritis is mainly atrophic and autoimmune.
Hp was not included in ICD-10, probably because its role in the disease was still controversial at that time. It is now proven that Hp infection is the primary cause of chronic gastritis, so a classification of gastritis that does not include Hp as a cause is incomplete.
Clinical question 2: Is the ICD-11 classification criteria for gastritis appropriate.
Statement 2: The newly proposed ICD-11 classification criteria for gastritis is an improvement because it is based on etiologic factors.
Level of recommendation: strong
Level of evidence: Moderate
Level of consensus: 100%
Comment.
In the gastritis section of ICD11, gastritis caused by Hp should be considered as a specific classification based on its etiological features, considering that different etiologies have different pathophysiological manifestations. After the recognition of Hp as the main cause of chronic gastritis, the previous criteria relying on histopathological assessment of gastritis were changed, followed by the introduction of the Sydney system and its integration into clinical practice. To reflect the pathologic features of endoscopic biopsies, the Sydney classification of gastritis includes histologic inflammatory activity, degree of chronicity, atrophy, intestinal epithelial hyperplasia, distribution characteristics, and etiologic information.
In summary, the three most important types of gastritis should be: (i) Hp-induced gastritis; (ii) drug-induced gastritis; and (iii) autoimmune gastritis. the classification of gastritis established by the ICD11β version is mainly based on etiologic features (Box 2), and physicians adopt different management and treatment strategies according to the different etiologies. Hp is a causative agent of gastric cancer and its eradication is gaining attention. In addition to Hp, we need to know more about other causes of gastritis, which are called Hp-negative or idiopathic gastritis.
The consensus meeting went further to summarize the etiology-based classification of gastritis in the beta version of ICD11 (Box 3), but clinical practice is still needed to determine the validity of the new classification. In addition, duodenitis in the gastritis section of ICD10 is now classified as a separate category. although the combined linearization of prevalence and lethality in ICD11β is widely used, this linear classification does not use the principles of etiologic classification, so further revision is still needed.
Clinical Question 3: Is it necessary to classify gastritis according to the site of the stomach.
Statement 3: The risk of gastric cancer and peptic ulcer is influenced by the site of gastritis; therefore, Hp gastritis should be classified according to the site of the stomach.
Level of recommendation: strong
Level of evidence: high
Level of consensus: 97.4%
Comments.
The site and severity of Hp gastritis can assess an individual’s risk of developing peptic ulcers and gastric cancer. Different sites of gastritis involvement lead to different gastric dysfunctions, especially gastric acid secretion, resulting in gastric acid hypersecretion, decreased secretion or even gastric acid deficiency.
After Hp eradication, severe gastric body atrophic gastritis (with or without intestinal epithelial hyperplasia) and severe gastric body-dominant gastritis also carry a high risk of developing intestinal or diffuse gastric cancer, requiring routine endoscopic and tissue biopsy follow-up.
Clinical question 4: Is it necessary to classify gastritis according to histology (severity) and/or endoscopic presentation.
Statement 4: Classification of gastritis by histology is recommended because the risk of Hp gastritis developing into gastric cancer can vary depending on its degree of inflammation and atrophy.
Level of recommendation: strong
Level of evidence: high
Level of consensus: 100%
Comments.
The updated Sydney system, which is widely used in clinical practice, allows assessment of the degree of atrophy and intestinal epithelial metaplasia at different sites in Hp gastritis. Different histological features determine the degree of risk of progression to peptic ulcer and gastric cancer, so the classification of gastritis should include histological features. The severity of atrophic gastritis and intestinal epithelial hyperplasia correlates with the degree of risk of developing gastric cancer. Similarly, severe Hp gastritis is associated with gastric carcinogenesis. The new histologic stage grading system for gastritis will assess clinical gastric cancer risk based on the degree of atrophy or intestinal epithelial hyperplasia at different sites. These two systems will be discussed further in Part III.
Clinical Question 5: How do we elaborate on gastric erosion in chronic gastritis.
Statement 5: Gastric erosion should be presented separately in the report, and its natural course and clinical features depend on etiology, but this area is less studied and needs further elucidation.
Level of recommendation: strong
Level of evidence: low
Level of consensus: 100%
Comment.
Gastric erosion is defined as a rupture of the mucosal layer <3 mm or 5 mm in diameter. Because of its small extent, erosions are generally not easily confused with ulcers involving the mucosal muscle layer. Gastric erosion can be caused by Hp infection or, more commonly, by the administration of drugs that damage the mucosa, mainly aspirin and NSAIDs.
It is important to note that after Hp eradication the gastric sinus can present with non-drug erosions, including (1) flat, (2) elevated, (3) bleeding, and (4) focal bleeding spots, which may be related to the hyperacidic state after Hp eradication therapy. It is the NSAIDs drugs that are most likely to cause gastric mucosal erosion clinically and can further develop into ulcers.
There are few studies on the clinical features and natural history of gastric and duodenal erosions, so it is important to conduct separate prospective studies of gastric and duodenal erosions in conjunction with the classification of gastritis to better understand the natural history of gastric erosions and the underlying mechanisms of their progression to ulcers and bleeding, and to apply a grading of the degree of erosion at the time of the study.
Clinical Question 6: Is Hp gastritis an infectious disease, regardless of symptoms and complications.
Statement 6: Hp gastritis should be defined as an infectious disease regardless of the presence or absence of symptoms, with or without peptic ulcer and gastric cancer.
Level of recommendation: strong
Level of evidence: high
Level of consensus: 100%
Comments.
Hp gastritis is an infectious disease that can lead to chronic active gastritis of varying degrees in almost all infected individuals. The manifestation of structural damage to the gastric mucosa varies greatly among individuals, as well as the clinical manifestations, some of which can be without significant clinical symptoms, but which can progress to peptic ulcers and gastric cancer.
Hp gastritis can be cured, and the probability of its development into peptic ulcer and gastric cancer can be reduced after curing. If Hp gastritis progresses to a more severe form of gastritis, such as atrophic gastritis with or without intestinal epithelial hyperplasia, or gastric body-dominant gastritis, the risk of gastric cancer can be increased, and close follow-up is needed after Hp eradication at this stage.
Part II Indigestion associated with Hp infection
Clinical question 7: Can Hp cause dyspepsia.
Statement 7: Hp gastritis is the cause of dyspepsia in some patients.
Level of recommendation: strong
Level of evidence: high
Level of consensus: 100%
Comment.
Numerous observations confirm that Hp infection may be the cause of dyspeptic symptoms in a subset of patients.1 Acute medical or self-administered infection with Hp can produce acute dyspeptic symptoms. However, persistent Hp colonization usually leads to chronic gastritis, and severe dyspeptic symptoms are transient in most individuals. ② Most epidemiological investigations show that Hp infection is associated with dyspeptic symptoms. Eradication therapy in unscreened and FD populations infected with Hp showed statistically significant differences in symptom control. There are no criteria to predict whether eradication therapy is effective in improving dyspeptic symptoms; therefore, the only method in clinical practice is to observe whether symptoms are relieved or require additional treatment after Hp eradication. Because recovery from gastritis takes time, clinical effects cannot be observed until at least 6 months after eradication therapy.
Clinical Question 8: Should we classify Hp-associated dyspepsia into a special category.
Statement 8A: In patients with Hp infection with dyspepsia, we consider these symptoms to be caused by Hp gastritis if successful eradication therapy can maintain symptom remission.
Level of recommendation: strong
Level of evidence: high
Level of consensus: 97.4%
Statement 8B: Hp-associated dyspepsia (as described in statement 8A) is a separate group of diseases.
Level of recommendation: strong
Level of evidence: Moderate
Level of consensus: 92.1%
Comment.
Based on the Rome III consensus, FD is defined as “symptoms of chronic dyspepsia (postprandial fullness, early satiety, epigastric pain or burning sensation) without evidence of organic disease (including upper gastrointestinal endoscopy) to explain these symptoms” (Figure 1). dyspeptic symptoms of the disease, which can be alleviated by removing the causative agent or treating the primary cause.
The Rome III consensus refers to Hp gastritis as organic dyspepsia if it is effective for eradication therapy. If Hp gastritis does not resolve after Hp eradication, it is considered FD. As mentioned above, studies of eradication therapy suggest that patients with Hp infection with dyspeptic symptoms need at least 6 months after the end of eradication therapy to see benefit.
Based on these considerations, sustained symptom remission after successful eradication suggests that Hp is the organic cause of symptoms in these patients and argues for Hp-associated dyspepsia as a separate clinical condition. Patients with Hp infection accompanied by chronic dyspepsia symptoms and negative endoscopic findings should be treated for eradication and attribution determined by post-treatment response.
Clinical Question 9: Is Hp eradication the first-line option for the treatment of dyspeptic symptoms.
Statement 9: Hp eradication is the first-line treatment option for patients with co-infection with Hp and dyspeptic symptoms.
Level of recommendation: strong
Level of evidence: high
Level of consensus: 94.7%
Comment.
The lack of reliable and durable treatment modalities for FD is evident from statement 8. If a class of FD patients can have symptom relief after Hp eradication, we consider Hp as the cause of symptoms. Although some patients have slower clinical remission, this is the only way patients can be cured. Finally, eradication therapy is a short-term treatment with an acceptable cost-benefit ratio in controlling dyspeptic symptoms while preventing peptic ulcers and gastric cancer. Based on these considerations, eradication therapy can be a first-line treatment option for Hp-infected dyspeptic patients, which is in line with the recent conclusions of the Rome meeting.
Clinical question 10: How effective is Hp eradication in relieving dyspeptic symptoms in the short and long term? How does it compare with other treatment options (e.g., PPI)?
Statement 10: In Hp-infected patients with dyspepsia, eradication is a better regimen than placebo for the relief of dyspeptic symptoms.
Level of recommendation: strong
Level of evidence: high
Level of consensus: 97.47%
Comments.
Eradication studies confirm that patients with Hp infection with FD have relief of dyspeptic symptoms after eradication therapy. There are only a limited number of studies directly comparing the efficacy of eradication therapy with other treatment options for FD, such as PPI and prokinetic therapy. Therefore, Hp eradication is the treatment of choice, although symptomatic gains require at least 6 months. In patients with Hp infection with chronic dyspeptic symptoms and negative endoscopy, future studies should further compare eradication therapy with other non-placebo treatment options.
Clinical Question 11: After Hp has been successfully eradicated, should the presence of FD be considered if the patient continues to have dyspeptic symptoms?
Statement 11: The presence of FD should be considered if a patient continues to have dyspeptic symptoms after Hp has been successfully eradicated.
Level of recommendation: weak
Level of evidence: Moderate
Level of consensus: 97.47%
Comment.
In statements 8A, 8B and Rome III criteria, patients with endoscopy-negative dyspepsia with Hp infection are considered to have Hp-associated dyspepsia if their symptoms are controlled after treatment. Conversely, if symptoms do not improve during long-term observation after successful eradication, it means that Hp gastritis does not cause symptoms in such patients, so that they can still be called FD.
Part III: Diagnosis of gastritis
Clinical question 12: Can atrophy and/or intestinal epithelial hyperplasia be diagnosed by endoscopy?
Statement 12: After appropriate training, mucosal atrophy and intestinal epithelial hyperplasia can be accurately determined by image-enhanced endoscopy.
Level of recommendation: strong
Level of evidence: high
Level of consensus: 84.2%
Comments.
Conventional endoscopy cannot accurately diagnose atrophy and chemosis in most cases, so tissue biopsy and histomorphological evaluation of the gastric mucosa based on Sydney criteria must be performed. However, image-enhanced endoscopy offers greater accuracy and reproducibility in the diagnosis of precancerous lesions of the gastric mucosa. Image-enhanced endoscopy includes pigmented endoscopy, high-resolution magnification endoscopy, and high-definition endoscopy combined with magnification technology (Figure 2). These techniques have been widely used in Japan and will be gradually expanded around the world. Endoscopists need certain specialized training to use these techniques for accurate assessment of the gastric mucosa and to take full advantage of their precision biopsies.
A. Narrow band imaging (NBI) of the gastric mucosa, a circular, uniformly sized glandular depression surrounded by a regular network of microvessels (left), a morphological feature of the gastric mucosa (regular network of microvessels) called “RAC”, which is highly suggestive of Hp negativity. In the Hp-infected mucosa with inflammation, the glandular dimples are prolonged, vary in size and shape, and the distance between dimples is widened. The microvascular network also becomes blurred due to inflammation (middle). As intestinalization continues to progress, the hollows are further extended and a pale blue light (pale blue crown) is seen at the edge of the hollows (right). These images are courtesy of Dr. Kazuyoshi Yagi. b. Blue laser imaging (BLI) of the gastric mucosa. BLI is a new modality for high-definition imaging. the BLI bright mode allows for better acquisition of lower magnification images, similar to NBI images, in A (left). Using BLI magnification mode, more mucosal alterations such as periglandular capillary network (red circles around the gastric minor concavity) can be detected (middle). BLI endoscopy can be used to identify areas of intestinalization, which appear as areas dominated by a pale green extended minor concavity (right). These images are courtesy of Dr. Hiroyuki Osawa, from Jichi Medical University.
Clinical Question 13: Are the New Sydney criteria applicable to the histological diagnosis of gastritis?
Statement 13: Accurate histologic evaluation of gastritis requires biopsy sampling of both the gastric sinus and the body of the stomach.
Level of evidence: High
Level of recommendation: strong
Level of consensus: 92.1%
Opinion.
Gastric precancerous lesions are often unevenly distributed; therefore, accurate histologic evaluation of gastritis requires simultaneous biopsy sampling of the gastric sinus and gastric body, which may facilitate the classification and grading of gastric precancerous lesions. Several studies have shown that multipoint biopsy improves the detection rate of precancerous lesions and provides a more accurate picture of the severity and distribution of these precancerous lesions. The practical clinical limitations of multi-point biopsy have led to the creation of the New Sydney Criteria, which clarify specific methods for biopsy and histopathologic grading of individual lesions – specifically, inflammation, glandular reduction, and intestinal epithelial metaplasia. The new Sydney criteria recommend that five gastric biopsy specimens be routinely obtained: the greater and lesser curvatures of the gastric sinus, the gastric horn notch, and the greater and lesser curvatures of the gastric body, and that the resulting specimens be sent separately and labeled with the different sites or lesions. The most common modification of the Sydney criteria in widespread use is that separate sampling of the gastric horn notch is often ignored. It is particularly important to sample the lesion site for biopsy at endoscopy. Operation of high-definition endoscopy by a specially trained endoscopist can further improve the positive rate of accurate biopsies.
Clinical Question 14: Are grading systems such as OLGA and OLGIM effective for risk stratification?
Statement 14A: The risk of gastric cancer is related to the severity and extent of atrophic gastritis.
Level of recommendation: strong
Level of evidence: high
Level of consensus: 94.7%
Statement 14B: Histologic staging criteria such as OLGA and OLGIM are valid for risk stratification.
Level of recommendation: strong
Level of evidence: low
Level of consensus: 97.3%
Comment.
Most gastric cancers develop primarily from chronic gastritis due to Hp infection, often undergoing multiple and evolutionary precancerous lesions such as atrophic gastritis, intestinal epithelial hyperplasia and heterogeneous hyperplasia/intraepithelial neoplasia. Several studies have shown that patients with precancerous lesions are at increased risk of developing gastric cancer. For example, a national study from the Netherlands that included 98,000 patients with precancerous lesions showed that the risk of developing gastric cancer could reach an average of 2 to 3 percent after 10 years. This risk varied with the type of precancerous lesion, such as 0.8%, 1.8%, 3.9% and 32.7% for gastric cancer in atrophic gastritis, intestinal epithelial metaplasia, mild to moderate heterogeneous hyperplasia and severe heterogeneous hyperplasia, respectively.
The above data confirm the correlation between gastric precancerous lesions and gastric cancer development, but also indicate that patients with precancerous lesions have a small risk of progression to gastric cancer (2-6 cases of gastric cancer out of 1000 precancerous lesions per year). Therefore, risk stratification methods need to be used. Gastric biopsy specimens can provide the most important information for risk assessment (OLGA staging system). the OLGA histological staging system stages patients with gastritis according to their corresponding gastric cancer risk gastritis. Studies have shown that this staging system provides accurate clinical information. Although the incidence of atrophic gastritis is high in high-risk groups, the repeatability of histological diagnosis of atrophic gastritis is limited, and different observers may make different judgments about atrophic gastritis, so scholars have further proposed the OLGIM system according to the degree and distribution of intestinal epithelial hyperplasia.
Compared with atrophic gastritis, there is relatively little variability in the judgment of intestinal epithelial hyperplasia by different observers, and intestinal epithelial hyperplasia is closely related to the severity of atrophic gastritis. Some studies have confirmed that patients with stage III or IV gastritis evaluated by the OLGA or OLGIM systems have a higher risk of gastric carcinogenesis. Therefore, upper gastrointestinal endoscopy should be performed in this group of patients.
Clinical Question 15: Can serological tests (pepsinogen I, II, I/II, Hp antibodies) be used for risk stratification of gastric cancer?
Statement 15: Serological tests (pepsinogen I, II, I/II, Hp antibody) can be used to identify people at high risk of developing gastric cancer.
Recommendation level: strong
Level of evidence: high
Level of consensus: 91.9%
Comments.
Serologic tests have been used for more than 25 years to diagnose chronic gastritis and gastric mucosal atrophy. These include: Hp serologic tests (crude antigen assay with or without anti-CagA antibodies) for the diagnosis of gastritis, serum pepsinogen I and II, and gastrin for the detection of hypogastric acidity status due to glandular reduction. These methods are often combined with other assays and are effective non-invasive diagnostic methods, and are also often used for population screening and follow-up. In a Japanese cohort study, a population was screened with Hp serological tests and measurement of serum pepsinogen I and II levels. The annual incidence of gastric cancer was low in populations with normal serum pepsinogen levels, regardless of whether they were positive or negative for Hp infection, whereas the incidence of gastric cancer increased yearly in populations with low serum pepsinogen levels (3.5 to 6 per 1000 people per year), which is consistent with the detection rate in atrophic gastritis. In this population, the incidence of gastric cancer was higher in the Hp serologically negative population than in the Hp serologically positive population, suggesting that atrophy and intussusception can affect Hp colonization when it is extended. This finding was also confirmed by the results of other studies.
Clinical Question 16: What is the appropriate time to search for and screen for Hp gastritis?
Statement 16: Based on local epidemiological surveys, the appropriate time to search for and screen for Hp gastritis should be before the onset of atrophic gastritis and intestinal epithelial metaplasia.
Level of recommendation: strong
Level of evidence: Moderate
Level of consensus: 97.3%
Comments.
Hp infection is most often acquired in childhood (up to 12 years of age), and the main route of transmission in developed countries is between family members. Hp infection and Hp gastritis will persist throughout life unless eradication therapy is performed or atrophic gastritis/intestinal epithelial metaplasia progresses to an end-stage with widespread distribution in the stomach. The risk of gastric cancer depends on the degree of gastric atrophy and intestinal epithelial metaplasia. Eradication of Hp reduces the risk of cancer, but is mainly limited to patients without atrophy and intestinal metaplasia. In patients with atrophy and intestinal metaplasia, Hp eradication reduces gastritis but does not prevent its progression to gastric cancer, so gastric cancer can occur 10 years after Hp eradication therapy.
Given this, the appropriate time to detect and screen for Hp gastritis should be between the age of relatively low infection rate (>12 years) and the onset of atrophic gastritis and intestinalization. The exact timing depends largely on geographic location and local epidemiologic findings, taking into account local Hp infection rates, as well as tumor incidence at different ages.
Part IV Treatment of gastritis
Clinical Question 17: Should all Hp-positive individuals receive eradication therapy?
Statement 17: Hp-infected individuals should be given eradication therapy unless there are antibiotic considerations.
Level of recommendation: strong
Level of evidence: high
Level of consensus: 100%
Comment.
Hp is the major pathogen causing chronic, progressive gastric mucosal damage in humans and is involved in the development of peptic ulcers, gastric cancer and gastric atrophy, and is also closely associated with gastric MALT lymphoma, dyspepsia, gastric hyperplastic polyps and idiopathic thrombocytopenic purpura. hp-positive individuals are a major source of infection transmission.
The decision to proceed with Hp eradication treatment in a community should be based on quantitative data information on the consequences in the untreated infected population. chronic infections caused by Hp, similar to asymptomatic syphilis or tuberculosis, have outcomes that cannot be predicted in advance. Unlike other chronic infectious diseases, Hp infection is always contagious and therefore puts others at risk. Gastric mucosal damage is progressive and often lacks obvious clinical signs at the time of diagnosis, so there is no value in predicting risk for the patient, the patient’s family, or the community. the benefits of Hp eradication for the patient themselves depend in part on the extent and scope of pre-existing damage and the reversibility of that damage prior to eradication. The potential benefits of Hp eradication include halting the progression of mucosal damage, stabilizing or reducing the risk of gastric cancer development, improving mucosal inflammation, stabilizing or promoting gastric mucosal function, restoring normal acid secretion mechanisms, repairing Hp-associated peptic ulcers, reducing the risk of gastrointestinal complications from NSAID therapy, and preventing the development of Hp-associated ulcers.
For society, the benefits of Hp eradication include reducing the source of infection and reducing the cost of diagnosing and treating Hp-associated diseases and their complications. Therefore, patients with Hp infection should be treated for eradication unless other concerns such as co-morbidity, community re-susceptibility, other priority diseases to be treated, and economic costs are present. In addition, some of the side effects of eradication therapy on human health should be considered, such as increased incidence of allergy, obesity, and disruption of the intestinal flora.
Clinical Question 18: What is the best time to eradicate Hp in asymptomatic individuals?
Statement 18: Hp eradication before atrophy of the gastric mucosa damage has occurred provides the greatest benefit.
Level of recommendation: strong
Level of evidence: high
Level of consensus: 100%
Comment.
Hp eradication prevents further progression of gastric mucosal injury, reduces the source of infection, and reduces or prevents the development of Hp-associated disease. Hp eradication before atrophy of the gastric mucosal damage has occurred provides the greatest benefit, especially in populations in countries with a high incidence of gastric cancer and in younger age groups. The benefits of Hp eradication in adolescents or young adults also include the ability to reduce or prevent their transmission of Hp to the next generation.
As mentioned previously (Part III), the risk of gastric cancer is related to the extent and degree of atrophic gastritis, and it is not practical to define gastric cancer risk by age for individual patients; cancer risk in any population is related to the rate of progression of gastric mucosal damage, and this rate of progression is high in populations with high risk of cancer and low in populations with low risk of gastric cancer. Thus, although it is possible to predict the mean age of transition from a nonatrophic to an atrophic phenotype in a given population, there may be varying degrees (from normal mucosa to progressive gastric mucosal atrophy) of gastric mucosal damage at any age; this suggests that risk stratification assessment should be based on some objective parameter such as a histologic staging system, rather than age, to determine whether patients need to receive eradication therapy or still require surveillance follow-up.
The incidence of gastric cancer increases with age, and age is a surrogate indicator of the timing of progression to atrophic gastritis. When atrophic gastritis lesions are extensive and severe, the risk of cancer increases exponentially. Cancer is the result of long-term accumulation of genetic instability, with mutations in coding regions, somatic gene reorganization, and epigenetic alterations such as methylation within cancer cells. Current studies support the idea that Hp eradication blocks mucosal damage and reduces or eliminates Hp-associated damage that increases genetic instability in the gastric mucosa. These Hp-associated damages include: DNA double-strand breaks, damaged DNA mismatches; abnormal activation and expression of cytidine deaminase, which in turn causes DNA mutations through altered nucleotides; abnormal methylation of some gene promoters in the gastric mucosa, such as cell growth-associated genes, DNA repair genes, oncogenes, cell adhesion genes E-cadherin and CpG islands of microRNAs, and and abnormal microRNA expression.
Hp infection can also cause an inflammatory response in the gastric mucosa, leading to acute and chronic inflammatory cell infiltration within the gastric mucosa. Cancer risk is associated with strain virulence (e.g., strains containing Cag pathogenic islands); however, all strains causing inflammation and gastric cancer lack virulence factors recognized to be associated with infection. Therefore, all Hp infections should be considered pathogenic and eradicated.
Due to the presence of damage and precancerous lesions, Hp eradication does not “turn the clock back to zero” (no risk), but it can stop the progression of risk and stabilize or reduce the risk of follow-up.
Clinical Question 19: Should we choose the appropriate eradication regimen based on geography?
Statement 19: Eradication regimens should be based on the most effective local regimen, ideally based on the patient’s drug sensitivity test results, or community antibiotic sensitivity test data, or antibiotic use and efficacy data. The availability of drugs varies from region to region and in a sense determines the choice of regimen.
Level of recommendation: strong
Level of evidence: high
Level of consensus: 100%
Comments.
The efficacy of Hp eradication regimens depends on the drug resistance of the population and the genotype of the host drug-metabolizing enzyme. there is a wide geographical variation in the resistance of Hp to commonly used antibiotics, which is also related to local antibiotic use, so the preferred eradication regimen often varies between regions. In general, treatment regimens should be developed with reference to the results of antibiotic sensitivity testing. Regardless of location, only regimens with an eradication rate of ≥90% in the population should be used empirically.
Clinical Question 20: Can Hp eradication prevent gastric cancer?
Statement 20: Hp eradication can reduce the risk of gastric cancer. The degree of risk reduction depends on the degree and extent of atrophy at the time of eradication therapy.
Level of recommendation: strong
Level of evidence: high
Level of consensus: 100%
Comment.
Hp infection is the most important cause of gastric cancer. According to statistics, 89% of gastric cancers occurring in non-cardia sites, accounting for 78% of all gastric cancers, are attributed to chronic Hp infection. The effectiveness of Hp eradication therapy for gastric cancer prevention depends on the degree and extent of atrophic damage at the time of eradication, with the best prevention results obtained in patients with non-atrophic gastritis and stabilization or reduction of gastric cancer risk in patients with existing atrophic changes. Part III points out that different methods of risk stratification are available, such as the accepted histological stratification systems (e.g., OLGA or OLGIM), and that Hp eradication can stabilize risk and inhibit progression of risk. Primary prevention includes prevention of Hp infection and eradication of Hp infection before the onset of atrophy. Secondary prevention consists of identifying high-risk individuals and following them up with testing to detect intraepithelial lesions and early gastric cancer in a timely manner and giving timely treatment before they develop into aggressive lesions. Immunotherapy given for precancerous lesions may be able to stop the progression of the disease.
Clinical Question 21: Should the efficacy of eradication therapy be evaluated (e.g., to check for eradication or not)?
Statement 21: The efficacy of eradication therapy should always be evaluated, with non-invasive methods preferred.
Level of recommendation: strong
Level of evidence: high
Level of consensus: 100%
Comment.
Failure of Hp eradication therapy is common, allowing mucosal damage to continue to develop, so the efficacy of eradication should always be confirmed, with non-invasive tests preferred, such as urea breath tests and fecal antigen testing using recognized monoclonal antibodies. For patients requiring endoscopic follow-up (e.g., after endoscopic resection of gastric adenoma), tissue specimens may be used for testing. Evaluation of eradication efficacy also provides early and timely warning of increasing antibiotic resistance in a population year by year, as evidenced by increased rates of eradication failure.
Clinical Question 22: Which patients require long-term follow-up after eradication therapy?
Statement 22: Hp eradication may not completely eliminate the risk of gastric cancer. Endoscopy and histology should be given to patients who are still at risk (based on the degree and extent of atrophy).
Level of recommendation: strong
Level of evidence: high
Level of consensus: 97.3%
Comments.
The decision to perform long-term follow-up such as regular endoscopy should be based on the results of the risk stratification assessment for gastric cancer after Hp eradication; the risk of gastric cancer is related to the degree and extent of atrophic gastritis, and risk stratification should be performed using accepted histologic risk scoring systems such as OLGA and OLGIM. However, in areas with extensive experience with endoscopic scoring systems, the Kumura and Takemoto systems may be used for assessment first, but confirmation by histologic systems is still recommended. Histology should be considered in patients diagnosed with Hp infection by non-invasive methods such as urea breath test or antigen detection. In addition, patients in common age groups prone to atrophic changes, with a history of gastric ulcer, pepsinogen I ≤ 70 ng/mL and pepsinogen I:II ≤ 3, patients with intraepithelial neoplasia (heterogeneous hyperplasia), or patients with early gastric cancer need to undergo regular endoscopic testing.
Discussion
The Global Consensus Conference on Hp Gastritis created a new milestone in gastritis, but inconsistencies between histologic presentation and upper abdominal symptoms remain with the clinical picture.
Despite the fact that gastritis has long been considered a clinically important disease, generations of gastroenterologists have ignored the importance of treating the taxonomy of this disease. Rudolph? The discovery of Hp revolutionized the original concept of gastritis, and it has become a specific cause of peptic ulcers and gastric cancer. Most of these serious diseases present with chronic gastritis caused by Hp as their sole causative factor. For peptic ulcers, guidelines consistently recommend eradication therapy first for those patients who are Hp positive. However, since most patients with chronic gastritis are usually asymptomatic and do not develop clinical symptoms until the development of severe complications, there is no consensus on how and when to treat individuals with Hp gastritis, which will be directly related to the effectiveness of gastric cancer prevention. In addition, gastritis and duodenitis are considered to be important causes of upper gastrointestinal bleeding, prompting an increasing focus on the complications associated with current antithrombotic therapy.
As an important clinical condition, we need to further define the concept of gastritis, a term that has historically been used incorrectly as an alternative clinical diagnosis for FD. However, studies from history have failed to demonstrate a relationship between histological findings of gastritis and dyspeptic symptoms. Thus, the potential pathogenic role of Hp in causing dyspeptic symptoms was initially questioned and its eradication in FD was controversial. The results of a meta-analysis of large controlled studies with long-term follow-up confirmed that Hp eradication therapy can benefit FD patients to some extent, with statistically significant differences. Therefore, dyspepsia attributed to Hp gastritis involves a histological etiology and should be excluded from the FD classification. Furthermore, patients with dyspepsia should not be casually labeled as “gastritis” without any histologic confirmation.
The recently introduced high-resolution endoscopy with image enhancement mode and magnification endoscopy have made the diagnostic evaluation of gastritis increasingly advanced and are now routinely used in major hospitals in Japan. This endoscopic technique allows us to more accurately identify mucosal changes (targeted biopsies) and thus more accurately assess the risk of cancer, such as precancerous lesions. The current widespread use of this new endoscopic system in countries other than Japan may still be limited by conditions.
The Kyoto Consensus Conference focused on four main topics including clinical presentation and management of gastritis: classification of gastritis in relation to the ICD codes being revised; FD and Hp infection, diagnosis and management of gastritis. The meeting used all modern methods to reach consensus, including an Internet-based Delphi method that provides access to the full cloth of published data in a completely neutral perspective.
In summary, the Kyoto meeting presented an etiologic basis for the classification of gastritis and concluded that Hp gastritis is an infectious disease. Therefore, Hp gastritis needs to be treated whether it is symptom-related or not, as it represents its potential to develop into serious complications including peptic ulcers and gastric tumors.
The consensus is reached that patients with dyspeptic symptoms due to Hp gastritis are an independent group of patients. In these patients, eradication therapy is recommended as the first line of treatment. Because of the diagnostic problems associated with gastritis, these patients should be labeled as having Hp-associated dyspepsia with sustained relief of symptoms after eradication therapy.
Scholars consider risk stratification systems such as OLGA and OLGIM as useful as other serological markers for the diagnosis of gastritis. Given recent technological advances, the use of image-enhanced endoscopy should be encouraged to identify mucosal lesions that are at high risk for progression to gastric neoplasia. Finally, it is recommended that eradication therapy should be performed as early as possible, ideally before the appearance of tumor changes. However, the implementation of this strategy should be site-specific. Since eradication therapy does not guarantee the elimination of gastric cancer risk, follow-up observation needs to be considered for those who have developed precancerous lesions.
Although many areas still need to be discussed, we believe that the results of the Kyoto Consensus Conference will improve patient care and will provide a basis for further refinement and research in the field of gastritis.