<7. Gastritis and gastric microbiota>
The microbiota of the healthy stomach mainly consists of in-transit microorganisms originating from the oral cavity and transported to the small intestine with gastric fluids. There is currently no sufficient evidence for bacteria other than H. pylori causing gastritis (ie, H. pylori-negative gastritis). However, there are few observational studies that suggest this as a possibility of gastritis in a small subset of patients and thus for now remains a hypothesis to be addressed in future microbiome sequencing studies. This finding supports the hypothesis that, in normal conditions, the microorganisms are confined to the mucus layer with no permanent mucosal colonisation. It is currently unknown whether certain species of non-H. pylori gastric microbiota may be aetiologically involved in gastric mucosal inflammation (eg, H. pylori-negative gastritis).
In H. pylori infection, the microbial α-diversity decreases significantly, with elective dropping in the prevalence of some species. In H. pylori-eradicated subjects, the gastric microbiota remodulation differs according to the post-eradication gastritis phenotype (non-atrophic or atrophic gastritis) and correlates with gastric acidity. In atrophic gastritis, the microbial profile has a significant carcinogenetic potential. Microbiota and their functions for their potential role in management of H. pylori infection were addressed in our consensus and are discussed below.
"H. pylori 감염은 위 미생물총의 구성에 영향을 미친다."
<Comment>
Compared with non-infected gastric mucosa, H. pylori-positive gastric mucosal specimens feature reduced microbial diversity, an altered microbiota community and decreased interactions among gastric microbes.
The biodiversity of gastric bacteria with potential beneficial effects in the regulation of inflammation is high, and it is possible that some of them may become viable candidates for future probiotic management of H. pylori.
"위 미생물총은 위염에서 병원성으로써 역할을 할 수 있으며, 특히 위 위축과 무 위산증이 발생하면 더욱 그렇다."
<Comment>
Several studies have reported that, with advancing gastric atrophy and impaired acid secretion, the gastric microbiota become dominated by components of the oral and/or intestinal microbiome. In a hypochlorhydric gastric microenvironment, the expected discrepancy between the microbial profile adherent to the mucosa (as detected by testing mucosal biopsies) and that detected in juice aspirates disappears (see section 2.7.1). These findings support the hypothesis that the oral component of gastric bacteria, usually believed to pass through, may settle in an atrophic mucosa and act as co-players in the oncogenetic cascade.
"위 미생물군은 H. pylori 감염에 의해 시작된 위암 발생의 여러 단계에 영향을 미칠 수 있으며, 미생물군에 의한 발암 경로를 확인하기 위한 추가 연구가 필요하다."
<Comment>
The gastric microbiota population is ‘dynamic’, and it is modulated by acid production, mucosal inflammation, atrophic–metaplastic lesions and gastric cancer.
Dysbiotic microbial profiles that develop along with the progression of gastritis (ie, non-atrophic to atrophic) may carry a genotoxic potential (유전독성 가능성), acting as co-promoters of oncogenesis. Dysbiotic microbiota are also detected in H. pylori-positive mucosa associated with early and advanced gastric precancerous conditions and lesions (ie, high-stage atrophic gastritis and dysplasia) and can still be reversed by eradication (see section 2.1.4).
<8.Epidemiology of gastritis and related preneoplastic and neoplastic lesions >
The epidemiology of gastritis differs by geographical area and is intimately related to the regional prevalence of H. pylori infection. Gastritis subtypes feature similar trends: with several notable exceptions, high-stage atrophic gastritis, gastritis-associated precancerous lesions and gastric cancer have high incidence in areas with a high prevalence of H. pylori infection. H. pylori gastritis and its related lesions are a primary health issue involving more than half of the world’s population, and disproportionately affect at higher rates various populations and specific ethnic subgroups, particularly those with a high proportion of economically disadvantaged individuals.
The epidemiological impact of H. pylori-negative gastritis and NHPH (table 1; see section 2.6.1) is by far less significant. The variability of diagnostic criteria adopted for gastric autoimmunity results in controversial information (논란의 여지가 있음) on the prevalence of gastric autoimmunity in both the general and the endoscopic populations. Moreover, available data on the precancerous and neoplastic risks in patients with AIG are conflicting (명확하지 않음). Recent evidence supports the hypothesis that current or previous H. pylori comorbidity is a cardinal cofactor in increasing the risk of gastric cancer among patients with AIG. The epidemiological relevance of gastritis (both atrophic and non-atrophic) in viral infections, particularly those due to EBV, remains to be defined (see section 2.6.5).
"위암 발생률과 사망률은 전 세계적으로 상당한 지리적 차이가 있으며, 새로운 사례의 약 75%가 아시아에서 발생한다."
<Comment>
In 2020, there were 1.1million new cases of gastric cancer worldwide, which accounted for 770,000 cancer deaths, making it the fifth most common cancer and the fourth most common cause of cancer death. It ranks among the top three most common cancers in 19 countries and the three most common causes of cancer death in 42 countries. Based on the GLOBOCAN 2020 database, the majority of gastric cancer cases occurred in Asia (n=819,944, 75%); China accounted for 44% of all gastric cancer cases in the world, followed by Europe (12.5%), South America and the Caribbean (6.2%), Africa (3%), North America (2.7%) and Oceania (0.3%). Similarly, 75% of all gastric cancer deaths were observed in Asia (n=575,206), of which 49% occurred in China alone.
Countries with the highest incidence rates in men included Japan (age-standardised incidence rates (ASIR), 48.1), Mongolia (47.2) and the Republic of Korea (39.7), while the highest incidence in females was observed in Mongolia (20.7) and Tajikistan (18.8).
When the gastric cancer burden was estimated by anatomical subsite, non-cardia gastric cancer was globally dominant, accounting for >80% of all gastric cancer cases, with a high case burden in Asia, but also in South and Central America. The global distribution of cardia gastric cancers had a different pattern, with the highest incidence rates being observed in East Asia, parts of Oceania, Western Europe and Western Asia.
Given its often late detection, the 5-year survival proportions remain poor, in the range of 20–30% in most countries worldwide, except in Japan and Korea, where endoscopic screening is widely practised.
In Korea, for example, implementation of national screening programmes has led to an increasing number of cases diagnosed at an early, curable stage and high 5-year survival proportions of over 76% between 2013 and 2017.
"전 세계적으로 발병률이 감소하고 있음에도 불구하고 위암 부담은 증가할 것으로 예상되며 전 세계적으로 공중 보건에 대한 주요 과제로 남을 것이다. 특히 일부 젊은 인구 집단, 특히 서구 지역에서 위암 발병률이 증가하고 있다."
<Comment>
(이번 Review에서 유일하게 agreement 100%를 받은 문항입니다)
Gastric cancer incidence rates have been declining in many parts of the world. A recent study using the longitudinal high-quality cancer registry data from 92 cancer registries in 34 countries found that the overall incidence rates will continue to fall until 2035 in most countries, regardless of their background incidence rates.
Nonetheless, the absolute number of new cases is predicted to further increase in many countries due to growing populations and ageing. If current rates remain stable, 1.8million cases and 1.3million deaths are expected to occur in 2040, which is 66% and 71% higher than estimated in 2020. Even with an assumed 2% annual decrease in rates, there would be an increased burden with 1.18million new cases and 0.85million deaths predicted by 2040.
It is noteworthy that the observed stable or declining trends were more evident in older age groups, while this was not always the case in the younger age groups. Increases in incidence in individuals aged <50 years are predicted in 15 out of 34 countries of both low and high incidence, including Belarus, Chile, the Netherlands, Canada and the UK. A US population-based registry study reported increasing incidence of non-cardia gastric cancer in non-Hispanic white patients aged <50 years (estimated annual percentage change for 1995–2013, 1.3%). The increase was more pronounced in females (2.6%). Notably, the largest increases were observed for proximal malignancies. These observations, however, require a critical interpretation, given the large proportion (50% on average globally) of cancers with unspecified anatomical location.
Foreign birth, daily consumption of ethnic food, slower acculturation (느린 문화적응) and low socioeconomic status were important predictors of gastric cancer cases in US multiethnic populations. Gastric cancer may therefore need to be recognised as an important disease for prevention even in lower risk countries.
"종양 전 위 질환(상태) 및 병변의 유병률은 인구 집단에 따라 다르며 일반적으로 위암 발생률, H. pylori 감염 유병률, 위암 가족력, 환경(예: 흡연 및 식이) 및 숙주 관련 위험 요인과 상관관계가 있다."
<Comment>
Among asymptomatic patients, a meta-analysis including endoscopic and serological studies showed a prevalence of atrophic gastritis and IM of 33% and 25%, respectively. The prevalence of IM was significantly higher in East Asia (21%) and South America (23.9%) than in Northern Europe (3.4%), Western Europe (3.2%) and North America (4.8%). A more recent meta-analysis of 14 studies (years 2010–2020) reported that 25% of study population had atrophic gastritis. The risk of atrophic gastritis was about 2.4-fold higher in H. pylori-positive versus negative subjects.
Overall, the local prevalence of atrophic gastritis and IM correlated well with the prevalence of H. pylori infection and the incidence of gastric cancer. Moreover, the prevalence of atrophic gastritis and IM is usually higher in males, in individuals aged 40 years or above and with a family history of gastric cancer. Individuals who consume a diet high in salt, and with smoking or drinking habits are also at higher risk.
"H. pylori의 유병률은 세계 여러 지역, 특히 젊은층에서 감소하고 있다. H. pylori가 없거나 박멸된 후 만성 위염의 역학에 대한 기여하는 다른 요인들은 아직 결정된 것이 없다."
<Comment>
Systematic reviews and meta-analyses estimated that up to 4billion people worldwide were infected with H. pylori, but the prevalence of H. pylori infection is declining in many developed countries, particularly in the younger populations. With the gradual decline in the prevalence of H. pylori infection due to both successful eradication and reduced new infection, there might be a shift in the relative proportion and importance of other agents contributing to gastritis, whose characterisation will require more epidemiological studies to characterise. Currently, the role of other microorganisms within the gastric microbiota in the pathogenesis of gastritis and preneoplastic lesions remains uncertain (see section 2.7.3).
"전암성 위 병변의 진행 위험은 활동성 H. pylori 감염의 존재 여부, 병변의 지형학적 범위 및 심각도, IM 유형, 다양한 숙주 및 환경 요인에 따라 다르다."
<Comment>
Dysplasia (synonym: IEN; non-invasive neoplasia) is the most advanced neoplastic non-invasive lesion. In a meta analysis, the annual progression rate to gastric cancer was 40.4 (95% CI: 27.1 to 55.7) per 1000 person-years, while for high grade dysplasia and low-grade dysplasia was 186.4 (95% CI: 106.6 to 285.6) and 11.3 (95% CI: 3.9 to 21.2), respectively. For atrophic gastritis, the pooled incidence rate of progression to gastric cancer was 1.24 (95% CI: 0.80 to 1.76) per 1000 person-years, and to IM and dysplasia, it was estimated as 41.4 (95% CI: 3.1 to 64.5) and 6.2 (95% CI: 2.34 to 11.5) per 1000 person-years. For IM, a cardinal lesion belonging to the spectrum of gastric atrophy, the incidence of gastric cancer was 3.38 (95% CI: 2.13 to 4.85) per 1000 person-years, while the progression rate to dysplasia was 12.51 (95% CI: 5.45 to 22.03) per 1000 person-years.
IM can be subtyped into complete and incomplete. Incomplete IM has been found to be associated with a 3.3-fold (RR 3.33, 95% CI: 1.96 to 5.64) higher risk of gastric cancer compared with complete IM during follow-up ranging from 3 to 12.8 years. Incomplete IM has been significantly associated with extensive gastric intestinalisation, which assimilates widespread incomplete IM to high-risk OLGA/ OLGIM gastritis stages (see section 2.3.5).
Family history of gastric cancer, dietary habits and smoking also contribute to the risk of progression. In a meta-analysis of nine randomised controlled trials, H. pylori eradication alone has been shown to improve both atrophic gastritis (OR 2.61, 95% CI: 1.41 to 4.81) and IM (OR 2.61, 95% CI: 1.66 to 4.11) when compared with placebo (see section 2.4.3).
Although gastric cancer of the intestinal type is considered to be associated with premalignant gastric lesions, a recent meta analysis suggested a similar association with diffuse-type gastric cancer. Furthermore, high-risk patients with OLGA/OLGIM stages III and IV are at higher risk of metachronous gastric cancer following curative endoscopic submucosal dissection for early gastric cancer.
<9. AI in gastritis clinical management>
Supercomputers combined with last-generation sophisticated software make reality the dream of ‘a machine capable of perceiving, recognising and identifying its surroundings without any human training or control’. AI promises revolutionary changes in almost all fields of human activities, including medicine and, more specifically, clinical gastroenterological practice. Deep structured learning may accomplish the task of exploiting in real time enormous amounts of information, including high-resolution epidemiological data, host-related and environmental risk factors, clinical signs and symptoms, and predictive or prognostic values coming from both traditional and omics-provided biomarkers. The expected results are a superhuman improvement in disease recognition, a cost–benefit balanced therapeutic decisions and trustworthy prediction of disease outcome.
Worldwide, however, the inequality of the available technology, the lack of standardised taxonomy and clinical procedures, the discrepancies of laws and policies for data protection, and the variability of human rights obligations are still far from being consistent. Systematically addressing all these issues is the precondition for ensuring that AI will eventually fulfil its potential promises.
In clinical gastroenterology, AI performance has been explored in inflammatory, precancerous and neoplastic diseases. By addressing the AI-assisted diagnosis of atrophic gastritis, Zhang et al constructed an AI model of a convolutional neural network whose accuracy (94.2%), sensitivity (94,5%) and specificity (94.0%) outperformed those of expert endoscopists. Similar findings were obtained by a study that applied a deep-learning system based on a training dataset of 200 real-time white-light images. In the same gastritis setting, a Thai real-time semantic segmentation network for IM showed sensitivity, specificity, positive and negative predictive values, and accuracy consistently higher than 90%. A meta-analysis on the AI’s performance in the diagnosis of both H. pylori infection and gastric precancerous lesions has shown a pooled accuracy of 79.6% (95% CI: 66.7% to 90.0%) and 90.3% (95% CI: 84.3% to 94.9%), respectively. Based on these results, the authors concluded that their AI system could be a valuable adjunctive diagnostic resource. By applying scSE-CatBoost (ie, Spatial and Channel Squeeze and Excitation) models for H. pylori status assessment in a cohort of 302 endoscopy subjects, a recent Taiwanese experience has achieved an accuracy of 0.90, sensitivity of 1.00, specificity of 0.81, positive predictive and negative values of 0.82 and 1.00, respectively.
Traditionally, diagnosis and therapeutic choices combine scientific evidence with a patient-centred approach. The latter implies a person-to-person relationship capable of empathically pondering those patients’ needs; this part would necessarily be neglected by the simulating setting of a clinical vignette. Effectively integrating AI in the clinical workflow can potentially improve quality of care. However, in its current form and in the largest part of the eastern and western world, the actual potential advantages of AI are only partially exploited in real-world clinical practice. In conclusion, while fascinated by AI’s potential scientific horizons, we also think that in patient-centred care, AI should, at best parallel, not replace, human involvement, despite its inherent risk of error prone intelligence.
(결론적으로, 우리는 AI의 잠재적인 과학적 지평에 매료되어 오류가 발생하기 쉬운 지능이라는 고유한 위험에도 불구하고 환자 중심 치료에서 AI가 인간의 개입을 대체해서는 안 된다고 생각합니다.)
Conclusions
For decades, classifications of gastritis suffered criticism or indifference. The realisation that H. pylori was the most common cause of chronic gastritis, the evidence that H. pylori was strongly related to gastric cancer, and new insights into the aetiology and pathogenesis of several other types of gastritis set the Sydney System (1990), its updated Houston version (1994) and the Kyoto Global Consensus (2014) apart from all past classifications. These three systems, flanked by the six editions of the Maastricht-Florence conference devoted to H. pylori, are founded on the crucial characteristic that makes classifications relevant: its ability to influence the management of a disease. A forum of gastritis scholars from five continents participated in the multidisciplinary RE.GA.IN. consensus to build on the biological, clinicopathological, epidemiological and technical advances matured in the past three decades. It also addressed the importance of agreeing on a uniform nomenclature of gastric inflammatory diseases. After lively debates on the most controversial aspects of the gastritis spectrum, the group amalgamated (한데 모았습니다) their comprehensive (포괄적이고) and diverse (다양한) knowledge to distil (추출하기 위해) patient centred, evidence-based statements to assist health professionals in their real-world clinical practice. Its success will be measured by how widely it is used.
<7. Gastritis and gastric microbiota>
The microbiota of the healthy stomach mainly consists of in-transit microorganisms originating from the oral cavity and transported to the small intestine with gastric fluids. There is currently no sufficient evidence for bacteria other than H. pylori causing gastritis (ie, H. pylori-negative gastritis). However, there are few observational studies that suggest this as a possibility of gastritis in a small subset of patients and thus for now remains a hypothesis to be addressed in future microbiome sequencing studies. This finding supports the hypothesis that, in normal conditions, the microorganisms are confined to the mucus layer with no permanent mucosal colonisation. It is currently unknown whether certain species of non-H. pylori gastric microbiota may be aetiologically involved in gastric mucosal inflammation (eg, H. pylori-negative gastritis).
In H. pylori infection, the microbial α-diversity decreases significantly, with elective dropping in the prevalence of some species. In H. pylori-eradicated subjects, the gastric microbiota remodulation differs according to the post-eradication gastritis phenotype (non-atrophic or atrophic gastritis) and correlates with gastric acidity. In atrophic gastritis, the microbial profile has a significant carcinogenetic potential. Microbiota and their functions for their potential role in management of H. pylori infection were addressed in our consensus and are discussed below.
<Comment>
Compared with non-infected gastric mucosa, H. pylori-positive gastric mucosal specimens feature reduced microbial diversity, an altered microbiota community and decreased interactions among gastric microbes.
The biodiversity of gastric bacteria with potential beneficial effects in the regulation of inflammation is high, and it is possible that some of them may become viable candidates for future probiotic management of H. pylori.
"위 미생물총은 위염에서 병원성으로써 역할을 할 수 있으며, 특히 위 위축과 무 위산증이 발생하면 더욱 그렇다."
<Comment>
Several studies have reported that, with advancing gastric atrophy and impaired acid secretion, the gastric microbiota become dominated by components of the oral and/or intestinal microbiome. In a hypochlorhydric gastric microenvironment, the expected discrepancy between the microbial profile adherent to the mucosa (as detected by testing mucosal biopsies) and that detected in juice aspirates disappears (see section 2.7.1). These findings support the hypothesis that the oral component of gastric bacteria, usually believed to pass through, may settle in an atrophic mucosa and act as co-players in the oncogenetic cascade.
"위 미생물군은 H. pylori 감염에 의해 시작된 위암 발생의 여러 단계에 영향을 미칠 수 있으며, 미생물군에 의한 발암 경로를 확인하기 위한 추가 연구가 필요하다."
<Comment>
The gastric microbiota population is ‘dynamic’, and it is modulated by acid production, mucosal inflammation, atrophic–metaplastic lesions and gastric cancer.
Dysbiotic microbial profiles that develop along with the progression of gastritis (ie, non-atrophic to atrophic) may carry a genotoxic potential (유전독성 가능성), acting as co-promoters of oncogenesis. Dysbiotic microbiota are also detected in H. pylori-positive mucosa associated with early and advanced gastric precancerous conditions and lesions (ie, high-stage atrophic gastritis and dysplasia) and can still be reversed by eradication (see section 2.1.4).
<8.Epidemiology of gastritis and related preneoplastic and neoplastic lesions >
The epidemiology of gastritis differs by geographical area and is intimately related to the regional prevalence of H. pylori infection. Gastritis subtypes feature similar trends: with several notable exceptions, high-stage atrophic gastritis, gastritis-associated precancerous lesions and gastric cancer have high incidence in areas with a high prevalence of H. pylori infection. H. pylori gastritis and its related lesions are a primary health issue involving more than half of the world’s population, and disproportionately affect at higher rates various populations and specific ethnic subgroups, particularly those with a high proportion of economically disadvantaged individuals.
The epidemiological impact of H. pylori-negative gastritis and NHPH (table 1; see section 2.6.1) is by far less significant. The variability of diagnostic criteria adopted for gastric autoimmunity results in controversial information (논란의 여지가 있음) on the prevalence of gastric autoimmunity in both the general and the endoscopic populations. Moreover, available data on the precancerous and neoplastic risks in patients with AIG are conflicting (명확하지 않음). Recent evidence supports the hypothesis that current or previous H. pylori comorbidity is a cardinal cofactor in increasing the risk of gastric cancer among patients with AIG. The epidemiological relevance of gastritis (both atrophic and non-atrophic) in viral infections, particularly those due to EBV, remains to be defined (see section 2.6.5).
"위암 발생률과 사망률은 전 세계적으로 상당한 지리적 차이가 있으며, 새로운 사례의 약 75%가 아시아에서 발생한다."
<Comment>
In 2020, there were 1.1million new cases of gastric cancer worldwide, which accounted for 770,000 cancer deaths, making it the fifth most common cancer and the fourth most common cause of cancer death. It ranks among the top three most common cancers in 19 countries and the three most common causes of cancer death in 42 countries. Based on the GLOBOCAN 2020 database, the majority of gastric cancer cases occurred in Asia (n=819,944, 75%); China accounted for 44% of all gastric cancer cases in the world, followed by Europe (12.5%), South America and the Caribbean (6.2%), Africa (3%), North America (2.7%) and Oceania (0.3%). Similarly, 75% of all gastric cancer deaths were observed in Asia (n=575,206), of which 49% occurred in China alone.
Countries with the highest incidence rates in men included Japan (age-standardised incidence rates (ASIR), 48.1), Mongolia (47.2) and the Republic of Korea (39.7), while the highest incidence in females was observed in Mongolia (20.7) and Tajikistan (18.8).
When the gastric cancer burden was estimated by anatomical subsite, non-cardia gastric cancer was globally dominant, accounting for >80% of all gastric cancer cases, with a high case burden in Asia, but also in South and Central America. The global distribution of cardia gastric cancers had a different pattern, with the highest incidence rates being observed in East Asia, parts of Oceania, Western Europe and Western Asia.
Given its often late detection, the 5-year survival proportions remain poor, in the range of 20–30% in most countries worldwide, except in Japan and Korea, where endoscopic screening is widely practised.
In Korea, for example, implementation of national screening programmes has led to an increasing number of cases diagnosed at an early, curable stage and high 5-year survival proportions of over 76% between 2013 and 2017.
"전 세계적으로 발병률이 감소하고 있음에도 불구하고 위암 부담은 증가할 것으로 예상되며 전 세계적으로 공중 보건에 대한 주요 과제로 남을 것이다. 특히 일부 젊은 인구 집단, 특히 서구 지역에서 위암 발병률이 증가하고 있다."
<Comment>
(이번 Review에서 유일하게 agreement 100%를 받은 문항입니다)
Gastric cancer incidence rates have been declining in many parts of the world. A recent study using the longitudinal high-quality cancer registry data from 92 cancer registries in 34 countries found that the overall incidence rates will continue to fall until 2035 in most countries, regardless of their background incidence rates.
Nonetheless, the absolute number of new cases is predicted to further increase in many countries due to growing populations and ageing. If current rates remain stable, 1.8million cases and 1.3million deaths are expected to occur in 2040, which is 66% and 71% higher than estimated in 2020. Even with an assumed 2% annual decrease in rates, there would be an increased burden with 1.18million new cases and 0.85million deaths predicted by 2040.
It is noteworthy that the observed stable or declining trends were more evident in older age groups, while this was not always the case in the younger age groups. Increases in incidence in individuals aged <50 years are predicted in 15 out of 34 countries of both low and high incidence, including Belarus, Chile, the Netherlands, Canada and the UK. A US population-based registry study reported increasing incidence of non-cardia gastric cancer in non-Hispanic white patients aged <50 years (estimated annual percentage change for 1995–2013, 1.3%). The increase was more pronounced in females (2.6%). Notably, the largest increases were observed for proximal malignancies. These observations, however, require a critical interpretation, given the large proportion (50% on average globally) of cancers with unspecified anatomical location.
Foreign birth, daily consumption of ethnic food, slower acculturation (느린 문화적응) and low socioeconomic status were important predictors of gastric cancer cases in US multiethnic populations. Gastric cancer may therefore need to be recognised as an important disease for prevention even in lower risk countries.
"종양 전 위 질환(상태) 및 병변의 유병률은 인구 집단에 따라 다르며 일반적으로 위암 발생률, H. pylori 감염 유병률, 위암 가족력, 환경(예: 흡연 및 식이) 및 숙주 관련 위험 요인과 상관관계가 있다."
<Comment>
Among asymptomatic patients, a meta-analysis including endoscopic and serological studies showed a prevalence of atrophic gastritis and IM of 33% and 25%, respectively. The prevalence of IM was significantly higher in East Asia (21%) and South America (23.9%) than in Northern Europe (3.4%), Western Europe (3.2%) and North America (4.8%). A more recent meta-analysis of 14 studies (years 2010–2020) reported that 25% of study population had atrophic gastritis. The risk of atrophic gastritis was about 2.4-fold higher in H. pylori-positive versus negative subjects.
Overall, the local prevalence of atrophic gastritis and IM correlated well with the prevalence of H. pylori infection and the incidence of gastric cancer. Moreover, the prevalence of atrophic gastritis and IM is usually higher in males, in individuals aged 40 years or above and with a family history of gastric cancer. Individuals who consume a diet high in salt, and with smoking or drinking habits are also at higher risk.
"H. pylori의 유병률은 세계 여러 지역, 특히 젊은층에서 감소하고 있다. H. pylori가 없거나 박멸된 후 만성 위염의 역학에 대한 기여하는 다른 요인들은 아직 결정된 것이 없다."
<Comment>
Systematic reviews and meta-analyses estimated that up to 4billion people worldwide were infected with H. pylori, but the prevalence of H. pylori infection is declining in many developed countries, particularly in the younger populations. With the gradual decline in the prevalence of H. pylori infection due to both successful eradication and reduced new infection, there might be a shift in the relative proportion and importance of other agents contributing to gastritis, whose characterisation will require more epidemiological studies to characterise. Currently, the role of other microorganisms within the gastric microbiota in the pathogenesis of gastritis and preneoplastic lesions remains uncertain (see section 2.7.3).
"전암성 위 병변의 진행 위험은 활동성 H. pylori 감염의 존재 여부, 병변의 지형학적 범위 및 심각도, IM 유형, 다양한 숙주 및 환경 요인에 따라 다르다."
<Comment>
Dysplasia (synonym: IEN; non-invasive neoplasia) is the most advanced neoplastic non-invasive lesion. In a meta analysis, the annual progression rate to gastric cancer was 40.4 (95% CI: 27.1 to 55.7) per 1000 person-years, while for high grade dysplasia and low-grade dysplasia was 186.4 (95% CI: 106.6 to 285.6) and 11.3 (95% CI: 3.9 to 21.2), respectively. For atrophic gastritis, the pooled incidence rate of progression to gastric cancer was 1.24 (95% CI: 0.80 to 1.76) per 1000 person-years, and to IM and dysplasia, it was estimated as 41.4 (95% CI: 3.1 to 64.5) and 6.2 (95% CI: 2.34 to 11.5) per 1000 person-years. For IM, a cardinal lesion belonging to the spectrum of gastric atrophy, the incidence of gastric cancer was 3.38 (95% CI: 2.13 to 4.85) per 1000 person-years, while the progression rate to dysplasia was 12.51 (95% CI: 5.45 to 22.03) per 1000 person-years.
IM can be subtyped into complete and incomplete. Incomplete IM has been found to be associated with a 3.3-fold (RR 3.33, 95% CI: 1.96 to 5.64) higher risk of gastric cancer compared with complete IM during follow-up ranging from 3 to 12.8 years. Incomplete IM has been significantly associated with extensive gastric intestinalisation, which assimilates widespread incomplete IM to high-risk OLGA/ OLGIM gastritis stages (see section 2.3.5).
Family history of gastric cancer, dietary habits and smoking also contribute to the risk of progression. In a meta-analysis of nine randomised controlled trials, H. pylori eradication alone has been shown to improve both atrophic gastritis (OR 2.61, 95% CI: 1.41 to 4.81) and IM (OR 2.61, 95% CI: 1.66 to 4.11) when compared with placebo (see section 2.4.3).
Although gastric cancer of the intestinal type is considered to be associated with premalignant gastric lesions, a recent meta analysis suggested a similar association with diffuse-type gastric cancer. Furthermore, high-risk patients with OLGA/OLGIM stages III and IV are at higher risk of metachronous gastric cancer following curative endoscopic submucosal dissection for early gastric cancer.
<9. AI in gastritis clinical management>
Supercomputers combined with last-generation sophisticated software make reality the dream of ‘a machine capable of perceiving, recognising and identifying its surroundings without any human training or control’. AI promises revolutionary changes in almost all fields of human activities, including medicine and, more specifically, clinical gastroenterological practice. Deep structured learning may accomplish the task of exploiting in real time enormous amounts of information, including high-resolution epidemiological data, host-related and environmental risk factors, clinical signs and symptoms, and predictive or prognostic values coming from both traditional and omics-provided biomarkers. The expected results are a superhuman improvement in disease recognition, a cost–benefit balanced therapeutic decisions and trustworthy prediction of disease outcome.
Worldwide, however, the inequality of the available technology, the lack of standardised taxonomy and clinical procedures, the discrepancies of laws and policies for data protection, and the variability of human rights obligations are still far from being consistent. Systematically addressing all these issues is the precondition for ensuring that AI will eventually fulfil its potential promises.
In clinical gastroenterology, AI performance has been explored in inflammatory, precancerous and neoplastic diseases. By addressing the AI-assisted diagnosis of atrophic gastritis, Zhang et al constructed an AI model of a convolutional neural network whose accuracy (94.2%), sensitivity (94,5%) and specificity (94.0%) outperformed those of expert endoscopists. Similar findings were obtained by a study that applied a deep-learning system based on a training dataset of 200 real-time white-light images. In the same gastritis setting, a Thai real-time semantic segmentation network for IM showed sensitivity, specificity, positive and negative predictive values, and accuracy consistently higher than 90%. A meta-analysis on the AI’s performance in the diagnosis of both H. pylori infection and gastric precancerous lesions has shown a pooled accuracy of 79.6% (95% CI: 66.7% to 90.0%) and 90.3% (95% CI: 84.3% to 94.9%), respectively. Based on these results, the authors concluded that their AI system could be a valuable adjunctive diagnostic resource. By applying scSE-CatBoost (ie, Spatial and Channel Squeeze and Excitation) models for H. pylori status assessment in a cohort of 302 endoscopy subjects, a recent Taiwanese experience has achieved an accuracy of 0.90, sensitivity of 1.00, specificity of 0.81, positive predictive and negative values of 0.82 and 1.00, respectively.
Traditionally, diagnosis and therapeutic choices combine scientific evidence with a patient-centred approach. The latter implies a person-to-person relationship capable of empathically pondering those patients’ needs; this part would necessarily be neglected by the simulating setting of a clinical vignette. Effectively integrating AI in the clinical workflow can potentially improve quality of care. However, in its current form and in the largest part of the eastern and western world, the actual potential advantages of AI are only partially exploited in real-world clinical practice. In conclusion, while fascinated by AI’s potential scientific horizons, we also think that in patient-centred care, AI should, at best parallel, not replace, human involvement, despite its inherent risk of error prone intelligence.
(결론적으로, 우리는 AI의 잠재적인 과학적 지평에 매료되어 오류가 발생하기 쉬운 지능이라는 고유한 위험에도 불구하고 환자 중심 치료에서 AI가 인간의 개입을 대체해서는 안 된다고 생각합니다.)
Conclusions
For decades, classifications of gastritis suffered criticism or indifference. The realisation that H. pylori was the most common cause of chronic gastritis, the evidence that H. pylori was strongly related to gastric cancer, and new insights into the aetiology and pathogenesis of several other types of gastritis set the Sydney System (1990), its updated Houston version (1994) and the Kyoto Global Consensus (2014) apart from all past classifications. These three systems, flanked by the six editions of the Maastricht-Florence conference devoted to H. pylori, are founded on the crucial characteristic that makes classifications relevant: its ability to influence the management of a disease. A forum of gastritis scholars from five continents participated in the multidisciplinary RE.GA.IN. consensus to build on the biological, clinicopathological, epidemiological and technical advances matured in the past three decades. It also addressed the importance of agreeing on a uniform nomenclature of gastric inflammatory diseases. After lively debates on the most controversial aspects of the gastritis spectrum, the group amalgamated (한데 모았습니다) their comprehensive (포괄적이고) and diverse (다양한) knowledge to distil (추출하기 위해) patient centred, evidence-based statements to assist health professionals in their real-world clinical practice. Its success will be measured by how widely it is used.