<3. Key diagnostic strategies in H. pylori gastritis>
The unique properties of H. pylori enable infection to be dianosed in multiple ways using diverse modalities based on either direct visualisation in histology and culture or on metabolic pathways (13C-UBT) and immune (stool antigens, SAT) or immunoreactive parameters (serum antibodies) of the bacterium.
Gastroscopy, although per se not sufficient to diagnose H. pylori, is indispensable for the evaluation of the gastric mucosa and the proper selection of biopsy samples. Each of these diagnostic procedures has its allocation in clinical management strategies. Non-invasive tests such as the 13C-UBT and SAT determine the current H. pylori status and a positive test leads straight to eradication therapy. Conversely, the serological detection of anti-H. pylori antibodies cannot distinguish between current and past infection and thus requires confirmation (either by 13C-UBT or the slightly less accurate SAT).
A comprehensive assessment of gastritis requires histological examination with direct visualisation of H. pylori complemented by defining the degree of inflammation (low-grade vs high-grade) and severity of atrophy (staging). In the presence of alarm symptoms, H. pylori management strategies based on gastroscopy combined with histology are recommended in all patients aged 50 years or older. Since histology requires endoscopy for biopsy sampling, obtaining additional biopsies for conventional cultures or molecular antibiotic resistance testing, performed on fresh or formalin-fixed biopsy samples, could be considered.
" 위염의 진단과 단계를 결정하기 위해서는 적어도 antrum과 corpus에서 각각 2개의 조직을 얻어야 한다. 추가적으로 비정상적인 부위에서도 샘플링을 해야 한다. 생검 표본은 구역을 구분해야 하며 분리된 용기를 등록해야 한다. update Sydney System에서 권고하는 위각(incisura angularis)에서의 조직 생검은 선택적이다."
<Comment>
Original Sydney System과 updated Houston version에서는 gastroscopy하면서 최소한 antral mucosecreting mucosa와 oxyntic mucosa를 대표할 수 있는 2곳에서 생검 표본을 얻도록 권고 하고 있습니다. ‘Transitional zones’ (gastro-oesophageal junction & oxyntic–pyloric border)에 대한 명확한 경계는 embriological patterning 과 endoscopic landmark에 따라 영향을 받을 수 있습니다.
‘Basic’ biopsy set:
(a) Two antral biopsies from either predefined sites (one from the lesser curvature and one from the greater curvature) or, if changes are observed endoscopically, targeting those suggesting either atrophy or IM
(b) Two biopsies from the oxyntic compartment, one from the lesser curvature and one from the greater curvature
현재 유용하게 사용되는 atrophy (Kyoto, Kimura-Takemoto)와 IM (endoscopic grading of gastric intestinal metaplasia, EGGIM)에서의 분류법은 standard 한 방법은 아니지만, 조직학적 검사가 요구되는 report에는 포함되어야 할 내용입니다. 임상적으로 AI-based endoscopy reports (see section 2.9) 에서는 pathologist의 추가적인 information이 포함되어야 합니다.
"위축성 위염의 진단에는 위 내시경, 조직검사 및 혈청학적 data가 포함 되어야 한다."
<Comment>
* Gastric atrophy (precancerous condition)
: a loss of appropriate (synonym: native) gastric glands in a given gastric mucosa compartment
Atrophic changes의 different phenotypes (non-metaplastic atrophy, IM, pseudopyloric metaplasia)은 동시에 나타날 수 있고, 내시경 및 조직학적 결과에 포함되어 보고해야 하겠습니다.
* Gastroscopy: Standard parameters have been established to determine high-quality endoscopic assessment of the upper gastrointestinal tract. High-resolution endoscopes with virtual chromoendoscopy increase accuracy in assessing the phenotype and topography of atrophic changes, particularly IM (figures 3 and 5).
Figure 5. Kimura and Takemoto classification of gastric mucosa atrophy. Kimura-Takemoto classification recognises two main atrophic topographical patterns: (1) closed (C type) and (2) open type (O type). Both patterns are further subdivided into three grades (C-1, C-2 and C-3; and O-1, O-2 and O-3). In C-1, atrophy is found only in the antrum, while in C-2 and C-3, the atrophic border (also known as pyloric–oxyntic border) starts from the greater curvature of the antrum, spreads to the anterior wall crossing the lesser curvature and enclosing the incisura almost symmetrically. In C-2, the location of the atrophic border is below the middle of the stomach on the lesser curvature, while in C-3, the atrophic border lies above it. In open types, the endoscopic atrophic area is more widespread, with the atrophic border lying between the lesser curvature and the anterior wall in type O-1, on the anterior wall in type O-2, and between the anterior wall and the greater curvature in type O-3. The severity of atrophy is often classified in three grades: mild (C-1; C-2), moderate (C-3; O-1) and severe (O-2; O-3). The figure is inspired by a drawing published by Nakajima et al.
"위염의 정확한 진단과 위염의 중증도, 범위, 유형 및 병인을 확인하기 위해서는 위 생검과 함께 높은 질을 갖는 내시경 검사가 필요하며 적극 권장된다."
"비화생성 위축과 IM 모두 내시경 적으로 확인할 수 있으며 영향을 받은 위 점막의 비율 추정치가 보고서에 포함되어야 한다. 현재 EGGIM, Kyoto, Kimura-Takemoto와 같은 시스템은 몇 가지 제한 사항(예: AIG)을 갖고 있지만 조직학적 평가 및 위암에 대한 위험과 밀접한 상관관계가 있다."
The report on atrophic lesions, irrespective of their aetiology, should include (figures 6 and 7) :
(1) topography (eg, compartmental distribution; ‘closed’ (ie, C pattern) vs ‘open’ (ie, O pattern))
(2) extent of the mucosal involvement
(3) the phenotype, as seen on magnified endoscopy (eg, non-metaplastic or metaplastic)
Figure 6. Gastroscopy showing prominent atrophic non-metaplastic mucosa. White-light gastroscopy: atrophic non-metaplastic mucosa in antrum (A) and corpus (B). Narrow-band imaging: focal loss of pit pattern in atrophic antral mucosa (C) and severe corpus atrophy (D).
Figure 7. Gastroscopy in atrophic gastritis due to Helicobacter pylori infection. White-light gastroscopy: H. pylori atrophic gastritis in antral (A) and corpus mucosa (B). Atrophic gastritis in antrum (C) and corpus mucosa (D) in narrow-band imaging gastroscopy; in the square, atrophic intestinalised mucosa and yellow star next to light-blue crest. IM, intestinal metaplasia.
"IM의 범위는 불완전한 IM의 비율과 상관관계가 있다는 증거가 있다. 따라서 IM 하위 유형 지정은 OLGA/OLGIM 병기 설정에 따라 평가된 암 위험 평가를 통합하는 데 사용될 수 있다."
"OLGA 및 OLGIM 병기 결정 시스템은 장형 및 미만형 위암의 위험 예측에 유용하다."
Gastric cancers, classified by Laurén as intestinal type (I-GC) and diffuse type (D-GC), have distinct clinical, histopathological and epidemiological characteristics. Both subtypes are strongly associated with H. pylori infection.
* Related to serologically diagnosed atrophy
large long term prospective cohort study of healthy asymptomatic males
: increased risk of both I-GC and D-GC among patients with extensive atrophic gastritis, as assessed by serum PgI/II levels (HR=3.1, 95% CI: 1.9 to 5.3; HR=2.7, 95% CI: 1.3 to 5.7, respectively).
"위암의 위험도를 평가하기 위해서, 전체적인 점막 관찰과 OLGA 및/또는 OLGIM에 따른 지형적 생검의 조직학적 분석을 포함한 내시경 검사가 권장된다."
Individuals at risk of gastric cancer can be evaluated by serology, histology and image-enhanced endoscopy.
Image-enhanced endoscopy with histological staging according to OLGA or OLGIM staging systems is considered the best approach. A meta-analysis showed that subjects with stages III–IV of OLGA or OLGIM were at increased risk of gastric cancer compared with those with stages 0–II. In countries of intermediate-high gastric cancer incidence, the OR was 2.64 (95% CI: 1.84 to 3.79) for OLGA stages III–IV and 3.99 (95% CI: 3.0 to 5.21) for OLGIM stages III–IV. (Yue H, Shan L, Bin L. The significance of OLGA and OLGIM staging systems in the risk assessment of gastric cancer: a systematic review and meta-analysis. Gastric Cancer 2018;21:579–87.)
A systematic review and meta-analysis revealed that subjects with severe and open-type endoscopic atrophy (according to the Kimura-Takemoto classification) had an increased risk of gastric cancer; the pooled risk ratios (RRs) were 3.89 (95% CI: 2.92 to 5.17) and 8.02 (95% CI: 2.39 to 26.88), respectively. (Xiao S, Fan Y, Yin Z, et al. Endoscopic grading of gastric atrophy on risk assessment of gastric neoplasia: a systematic review and meta-analysis. J Gastroenterol Hepatol 2021;36:55–63.)
In a multicentre validation study involving 250 consecutive patients, EGGIM by using NBI correlated with OLGIM stages III–IV, with area under the receiver operating characteristic curve of 0.96 (95% CI: 0.93 to 0.98).
<4. H. pylori gastritis clinicopathological outcome>
H. pylori gastritis is a specific infectious disease. Successful eradication of the bacterium leads to the resolution of the active (PMNs) component of gastritis; the mononuclear inflammatory component (lymphocytes, histiocytes and plasma cells) decreases slower. Complete recovery is unlikely when extensive atrophy has already developed (ie, high-stage gastritis).
The interaction of different genotypes of H. pylori with host genetic, environmental and lifestyle factors results in different phenotypes of gastritis. Depending on these variables, H. pylori gastritis may develop distinct outcomes and complications. Most clinical signs and symptoms associated with H. pylori gastritis are potentially reversible when the infection is cured. This section focuses on the essential aspects of H. pylori gastritis and its potential to progress to gastric cancer. Its purpose is to provide knowledge, to create awareness of the types of gastritis that confer increased cancer risk, and to promote proper management for adequate surveillance and the early detection of neoplasia.
"H. pylori 위염은 비위축성 위염에서 위축성 위염으로 진행될 수 있으며 위암으로 진행될 가능성이 있다. 만성 위축성 위염의 심각도와 정도는 위암 발생 위험과 상관관계가 있다."
"비위축성 위염은 위암 위험이 최소화된 잠재적으로 가역적인 염증 상태이다. 진단은 위축 예방을 위한 관리 및 전략을 결정할 수 있는 타당하거나 의심되는 병인이 포함되어야 한다."
"병인을 제거하면 위축성 병변이 회복 될 수 있다는 혈청학적, 내시경적 및 조직학적 근거가 있다. 회복의 존재와 범위를 평가하고 정량화하는 가장 신뢰할 수 있는 방법을 결정하기 위한 연구가 앞으로 필요하다."
"H. pylori의 박멸은 점막 손상의 진행을 멈추고 위의 구조와 기능에 대한 회복을 갖게한다."
<Comment>
H. pylori eradication is highly effective in arresting and reversing inflammation and histological damage, particularly in active H. pylori gastritis with or without atrophy (figure 8).
Figure 8. Metaplastic atrophy following Helicobacter pylori eradication (biopsy samples obtained from incisural mucosa 2months after successful H. pylori eradication). The native mucosa is partially replaced by intestinalised glands of complete and incomplete subtypes; metaplastic atrophy covers about 40–45% of the biopsy specimen. After bacterial eradication, a vaguely nodular, low-grade lymphocytic infiltrate remains (interalveolar area in the left corner). In a serial section of the same specimen, Alcian-PAS histochemistry shows native mucosa coexisting with atrophic–metaplastic glands ((A) H&E; (B) Alcian-PAS; original magnifications 10×). PAS, periodic acid–Schiff.
"위염의 진행을 가속화시키는 관련된 요인으로는 감염을 일으키는 H. pylori 계통의 균주, 특정 숙주 유전적 감수성, 위암 병력이 있는 1차 직계, 건강하지 못한 생활 방식 및 사회적 습관 등이 있다."
<Comment>
* Japanese long-term prospective follow-up study after H. pylori eradication (5-year cumulative cancer risks)
: 0.7% (none/mild AG), 1.9% (moderate AG), 10% (severe AG)
(Shichijo S, Hirata Y, Niikura R, et al. Histologic intestinal metaplasia and endoscopic atrophy are predictors of gastric cancer development after helicobacter pylori eradication. Gastrointest Endosc 2016;84:618–24.)
* Nationwide cohort study from the Netherlands, the annual incidence rate of gastric cancer
: 0.1% (AG), 0.25% (IM), 0.6% (mild to moderate dysplasia), 6% (severe dysplasia)
(de Vries AC, van Grieken NCT, Looman CWN, et al. Gastric cancer risk in patients with premalignant gastric lesions: a nationwide cohort study in the Netherlands. Gastroenterology 2008;134:945–52.)
* Observational cohort study from Sweden, the incidence rates
: 0.1% (AG), 0.13% (IM), 0.26% (Dysplasia)
(Song H, Ekheden IG, Zheng Z, et al. Incidence of gastric cancer among patients with gastric precancerous lesions: observational cohort study in a low risk western population. BMJ 2015;351:h3867.)
* H. pylori infections were eradicated, approximately 89% of non-cardia gastric cancers, 29% of cardia gastric cancers and 74% of gastric non-Hodgkin’s lymphomas would be prevented.
(Plummer M, de Martel C, Vignat J, et al. Global burden of cancers attributable to infections in 2012: a synthetic analysis. Lancet Glob Health 2016;4:e609–16.)
(de Martel C, Georges D, Bray F, et al. Global burden of cancer attributable to infections in 2018: a worldwide incidence analysis. Lancet Glob Health 2020;8:e180–90.)
"고위험 내시경 소견이나 OLGA/OLGIM의 III~IV기 및/또는 광범위한 불완전 IM이 있는 사람은 3년 간격으로 또는 현지 권장 사항에 따라 내시경/조직학적 검사를 받는 것을 제안한다."
<Comment>
H. pylori eradication decreases the risk of gastric cancer. However, patients who have already developed atrophic gastritis likely retain a risk level similar to that present at the time of H. pylori eradication.
A systematic review and meta-analysis reported that the incidence rates of gastric cancer in atrophic gastritis and IM were 2.25 (95% CI: 1.67 to 2.90) and 7.58 (95% CI: 4.10 to 11.91) per 1000 person-years in Asia and 0.74 (95% CI: 0.13 to 1.71) and 1.72 (95% CI: 0.36 to 3.70) per 1000 person-years in Europe. (Akbari M, Tabrizi R, Kardeh S, et al. Gastric cancer in patients with gastric atrophy and intestinal metaplasia: a systematic review and meta-analysis. PLoS One 2019;14:e0219865.)
A cost-effectiveness analysis in Singapore suggested that the optimal interval was annual surveillance for subjects with OR 5.46–21.5 of gastric cancer, and 2-year intervals for surveillance for those with OR 2.4–5.46. Thus, a 2-year endoscopic surveillance interval for patients with OLGA/OGLIM stages III–IV may be optimal. However, in East Asia, gastric cancer may be more likely develop from early stages of atrophy or IM, such as OLGIM stage II.
Patients with low/high-grade dysplasia or early gastric cancer after endoscopic mucosal resection or endoscopic submucosal dissection remain at risk of the development of synchronous or metachronous gastric cancer, with reported incidence rates of between 7.7 and 33.9 per 1000 person-years. The interval of endoscopic surveillance after endoscopic mucosal resection at 1year, 5years or 10years proved cost-effective for Asian patients, and at 5years or 10years was also cost-effective for subjects of Hispanic ancestry in the USA.
<3. Key diagnostic strategies in H. pylori gastritis>
The unique properties of H. pylori enable infection to be dianosed in multiple ways using diverse modalities based on either direct visualisation in histology and culture or on metabolic pathways (13C-UBT) and immune (stool antigens, SAT) or immunoreactive parameters (serum antibodies) of the bacterium.
Gastroscopy, although per se not sufficient to diagnose H. pylori, is indispensable for the evaluation of the gastric mucosa and the proper selection of biopsy samples. Each of these diagnostic procedures has its allocation in clinical management strategies. Non-invasive tests such as the 13C-UBT and SAT determine the current H. pylori status and a positive test leads straight to eradication therapy. Conversely, the serological detection of anti-H. pylori antibodies cannot distinguish between current and past infection and thus requires confirmation (either by 13C-UBT or the slightly less accurate SAT).
A comprehensive assessment of gastritis requires histological examination with direct visualisation of H. pylori complemented by defining the degree of inflammation (low-grade vs high-grade) and severity of atrophy (staging). In the presence of alarm symptoms, H. pylori management strategies based on gastroscopy combined with histology are recommended in all patients aged 50 years or older. Since histology requires endoscopy for biopsy sampling, obtaining additional biopsies for conventional cultures or molecular antibiotic resistance testing, performed on fresh or formalin-fixed biopsy samples, could be considered.
" 위염의 진단과 단계를 결정하기 위해서는 적어도 antrum과 corpus에서 각각 2개의 조직을 얻어야 한다. 추가적으로 비정상적인 부위에서도 샘플링을 해야 한다. 생검 표본은 구역을 구분해야 하며 분리된 용기를 등록해야 한다. update Sydney System에서 권고하는 위각(incisura angularis)에서의 조직 생검은 선택적이다."
<Comment>
Original Sydney System과 updated Houston version에서는 gastroscopy하면서 최소한 antral mucosecreting mucosa와 oxyntic mucosa를 대표할 수 있는 2곳에서 생검 표본을 얻도록 권고 하고 있습니다. ‘Transitional zones’ (gastro-oesophageal junction & oxyntic–pyloric border)에 대한 명확한 경계는 embriological patterning 과 endoscopic landmark에 따라 영향을 받을 수 있습니다.
‘Basic’ biopsy set:
(a) Two antral biopsies from either predefined sites (one from the lesser curvature and one from the greater curvature) or, if changes are observed endoscopically, targeting those suggesting either atrophy or IM
(b) Two biopsies from the oxyntic compartment, one from the lesser curvature and one from the greater curvature
현재 유용하게 사용되는 atrophy (Kyoto, Kimura-Takemoto)와 IM (endoscopic grading of gastric intestinal metaplasia, EGGIM)에서의 분류법은 standard 한 방법은 아니지만, 조직학적 검사가 요구되는 report에는 포함되어야 할 내용입니다. 임상적으로 AI-based endoscopy reports (see section 2.9) 에서는 pathologist의 추가적인 information이 포함되어야 합니다.
<Comment>
* Gastric atrophy (precancerous condition)
: a loss of appropriate (synonym: native) gastric glands in a given gastric mucosa compartment
Atrophic changes의 different phenotypes (non-metaplastic atrophy, IM, pseudopyloric metaplasia)은 동시에 나타날 수 있고, 내시경 및 조직학적 결과에 포함되어 보고해야 하겠습니다.
* Gastroscopy: Standard parameters have been established to determine high-quality endoscopic assessment of the upper gastrointestinal tract. High-resolution endoscopes with virtual chromoendoscopy increase accuracy in assessing the phenotype and topography of atrophic changes, particularly IM (figures 3 and 5).
Figure 5. Kimura and Takemoto classification of gastric mucosa atrophy. Kimura-Takemoto classification recognises two main atrophic topographical patterns: (1) closed (C type) and (2) open type (O type). Both patterns are further subdivided into three grades (C-1, C-2 and C-3; and O-1, O-2 and O-3). In C-1, atrophy is found only in the antrum, while in C-2 and C-3, the atrophic border (also known as pyloric–oxyntic border) starts from the greater curvature of the antrum, spreads to the anterior wall crossing the lesser curvature and enclosing the incisura almost symmetrically. In C-2, the location of the atrophic border is below the middle of the stomach on the lesser curvature, while in C-3, the atrophic border lies above it. In open types, the endoscopic atrophic area is more widespread, with the atrophic border lying between the lesser curvature and the anterior wall in type O-1, on the anterior wall in type O-2, and between the anterior wall and the greater curvature in type O-3. The severity of atrophy is often classified in three grades: mild (C-1; C-2), moderate (C-3; O-1) and severe (O-2; O-3). The figure is inspired by a drawing published by Nakajima et al.
"위염의 정확한 진단과 위염의 중증도, 범위, 유형 및 병인을 확인하기 위해서는 위 생검과 함께 높은 질을 갖는 내시경 검사가 필요하며 적극 권장된다."
"비화생성 위축과 IM 모두 내시경 적으로 확인할 수 있으며 영향을 받은 위 점막의 비율 추정치가 보고서에 포함되어야 한다. 현재 EGGIM, Kyoto, Kimura-Takemoto와 같은 시스템은 몇 가지 제한 사항(예: AIG)을 갖고 있지만 조직학적 평가 및 위암에 대한 위험과 밀접한 상관관계가 있다."
The report on atrophic lesions, irrespective of their aetiology, should include (figures 6 and 7) :
(1) topography (eg, compartmental distribution; ‘closed’ (ie, C pattern) vs ‘open’ (ie, O pattern))
(2) extent of the mucosal involvement
(3) the phenotype, as seen on magnified endoscopy (eg, non-metaplastic or metaplastic)
Figure 6. Gastroscopy showing prominent atrophic non-metaplastic mucosa. White-light gastroscopy: atrophic non-metaplastic mucosa in antrum (A) and corpus (B). Narrow-band imaging: focal loss of pit pattern in atrophic antral mucosa (C) and severe corpus atrophy (D).
Figure 7. Gastroscopy in atrophic gastritis due to Helicobacter pylori infection. White-light gastroscopy: H. pylori atrophic gastritis in antral (A) and corpus mucosa (B). Atrophic gastritis in antrum (C) and corpus mucosa (D) in narrow-band imaging gastroscopy; in the square, atrophic intestinalised mucosa and yellow star next to light-blue crest. IM, intestinal metaplasia.
"IM의 범위는 불완전한 IM의 비율과 상관관계가 있다는 증거가 있다. 따라서 IM 하위 유형 지정은 OLGA/OLGIM 병기 설정에 따라 평가된 암 위험 평가를 통합하는 데 사용될 수 있다."
"OLGA 및 OLGIM 병기 결정 시스템은 장형 및 미만형 위암의 위험 예측에 유용하다."
Gastric cancers, classified by Laurén as intestinal type (I-GC) and diffuse type (D-GC), have distinct clinical, histopathological and epidemiological characteristics. Both subtypes are strongly associated with H. pylori infection.
* Related to serologically diagnosed atrophy
large long term prospective cohort study of healthy asymptomatic males
: increased risk of both I-GC and D-GC among patients with extensive atrophic gastritis, as assessed by serum PgI/II levels (HR=3.1, 95% CI: 1.9 to 5.3; HR=2.7, 95% CI: 1.3 to 5.7, respectively).
"위암의 위험도를 평가하기 위해서, 전체적인 점막 관찰과 OLGA 및/또는 OLGIM에 따른 지형적 생검의 조직학적 분석을 포함한 내시경 검사가 권장된다."
Individuals at risk of gastric cancer can be evaluated by serology, histology and image-enhanced endoscopy.
Image-enhanced endoscopy with histological staging according to OLGA or OLGIM staging systems is considered the best approach. A meta-analysis showed that subjects with stages III–IV of OLGA or OLGIM were at increased risk of gastric cancer compared with those with stages 0–II. In countries of intermediate-high gastric cancer incidence, the OR was 2.64 (95% CI: 1.84 to 3.79) for OLGA stages III–IV and 3.99 (95% CI: 3.0 to 5.21) for OLGIM stages III–IV. (Yue H, Shan L, Bin L. The significance of OLGA and OLGIM staging systems in the risk assessment of gastric cancer: a systematic review and meta-analysis. Gastric Cancer 2018;21:579–87.)
A systematic review and meta-analysis revealed that subjects with severe and open-type endoscopic atrophy (according to the Kimura-Takemoto classification) had an increased risk of gastric cancer; the pooled risk ratios (RRs) were 3.89 (95% CI: 2.92 to 5.17) and 8.02 (95% CI: 2.39 to 26.88), respectively. (Xiao S, Fan Y, Yin Z, et al. Endoscopic grading of gastric atrophy on risk assessment of gastric neoplasia: a systematic review and meta-analysis. J Gastroenterol Hepatol 2021;36:55–63.)
In a multicentre validation study involving 250 consecutive patients, EGGIM by using NBI correlated with OLGIM stages III–IV, with area under the receiver operating characteristic curve of 0.96 (95% CI: 0.93 to 0.98).
<4. H. pylori gastritis clinicopathological outcome>
H. pylori gastritis is a specific infectious disease. Successful eradication of the bacterium leads to the resolution of the active (PMNs) component of gastritis; the mononuclear inflammatory component (lymphocytes, histiocytes and plasma cells) decreases slower. Complete recovery is unlikely when extensive atrophy has already developed (ie, high-stage gastritis).
The interaction of different genotypes of H. pylori with host genetic, environmental and lifestyle factors results in different phenotypes of gastritis. Depending on these variables, H. pylori gastritis may develop distinct outcomes and complications. Most clinical signs and symptoms associated with H. pylori gastritis are potentially reversible when the infection is cured. This section focuses on the essential aspects of H. pylori gastritis and its potential to progress to gastric cancer. Its purpose is to provide knowledge, to create awareness of the types of gastritis that confer increased cancer risk, and to promote proper management for adequate surveillance and the early detection of neoplasia.
"비위축성 위염은 위암 위험이 최소화된 잠재적으로 가역적인 염증 상태이다. 진단은 위축 예방을 위한 관리 및 전략을 결정할 수 있는 타당하거나 의심되는 병인이 포함되어야 한다."
"병인을 제거하면 위축성 병변이 회복 될 수 있다는 혈청학적, 내시경적 및 조직학적 근거가 있다. 회복의 존재와 범위를 평가하고 정량화하는 가장 신뢰할 수 있는 방법을 결정하기 위한 연구가 앞으로 필요하다."
"H. pylori의 박멸은 점막 손상의 진행을 멈추고 위의 구조와 기능에 대한 회복을 갖게한다."
<Comment>
H. pylori eradication is highly effective in arresting and reversing inflammation and histological damage, particularly in active H. pylori gastritis with or without atrophy (figure 8).
Figure 8. Metaplastic atrophy following Helicobacter pylori eradication (biopsy samples obtained from incisural mucosa 2months after successful H. pylori eradication). The native mucosa is partially replaced by intestinalised glands of complete and incomplete subtypes; metaplastic atrophy covers about 40–45% of the biopsy specimen. After bacterial eradication, a vaguely nodular, low-grade lymphocytic infiltrate remains (interalveolar area in the left corner). In a serial section of the same specimen, Alcian-PAS histochemistry shows native mucosa coexisting with atrophic–metaplastic glands ((A) H&E; (B) Alcian-PAS; original magnifications 10×). PAS, periodic acid–Schiff.
"위염의 진행을 가속화시키는 관련된 요인으로는 감염을 일으키는 H. pylori 계통의 균주, 특정 숙주 유전적 감수성, 위암 병력이 있는 1차 직계, 건강하지 못한 생활 방식 및 사회적 습관 등이 있다."
<Comment>
* Japanese long-term prospective follow-up study after H. pylori eradication (5-year cumulative cancer risks)
: 0.7% (none/mild AG), 1.9% (moderate AG), 10% (severe AG)
(Shichijo S, Hirata Y, Niikura R, et al. Histologic intestinal metaplasia and endoscopic atrophy are predictors of gastric cancer development after helicobacter pylori eradication. Gastrointest Endosc 2016;84:618–24.)
* Nationwide cohort study from the Netherlands, the annual incidence rate of gastric cancer
: 0.1% (AG), 0.25% (IM), 0.6% (mild to moderate dysplasia), 6% (severe dysplasia)
(de Vries AC, van Grieken NCT, Looman CWN, et al. Gastric cancer risk in patients with premalignant gastric lesions: a nationwide cohort study in the Netherlands. Gastroenterology 2008;134:945–52.)
* Observational cohort study from Sweden, the incidence rates
: 0.1% (AG), 0.13% (IM), 0.26% (Dysplasia)
(Song H, Ekheden IG, Zheng Z, et al. Incidence of gastric cancer among patients with gastric precancerous lesions: observational cohort study in a low risk western population. BMJ 2015;351:h3867.)
* H. pylori infections were eradicated, approximately 89% of non-cardia gastric cancers, 29% of cardia gastric cancers and 74% of gastric non-Hodgkin’s lymphomas would be prevented.
(Plummer M, de Martel C, Vignat J, et al. Global burden of cancers attributable to infections in 2012: a synthetic analysis. Lancet Glob Health 2016;4:e609–16.)
(de Martel C, Georges D, Bray F, et al. Global burden of cancer attributable to infections in 2018: a worldwide incidence analysis. Lancet Glob Health 2020;8:e180–90.)
"고위험 내시경 소견이나 OLGA/OLGIM의 III~IV기 및/또는 광범위한 불완전 IM이 있는 사람은 3년 간격으로 또는 현지 권장 사항에 따라 내시경/조직학적 검사를 받는 것을 제안한다."
<Comment>
H. pylori eradication decreases the risk of gastric cancer. However, patients who have already developed atrophic gastritis likely retain a risk level similar to that present at the time of H. pylori eradication.
A systematic review and meta-analysis reported that the incidence rates of gastric cancer in atrophic gastritis and IM were 2.25 (95% CI: 1.67 to 2.90) and 7.58 (95% CI: 4.10 to 11.91) per 1000 person-years in Asia and 0.74 (95% CI: 0.13 to 1.71) and 1.72 (95% CI: 0.36 to 3.70) per 1000 person-years in Europe. (Akbari M, Tabrizi R, Kardeh S, et al. Gastric cancer in patients with gastric atrophy and intestinal metaplasia: a systematic review and meta-analysis. PLoS One 2019;14:e0219865.)
A cost-effectiveness analysis in Singapore suggested that the optimal interval was annual surveillance for subjects with OR 5.46–21.5 of gastric cancer, and 2-year intervals for surveillance for those with OR 2.4–5.46. Thus, a 2-year endoscopic surveillance interval for patients with OLGA/OGLIM stages III–IV may be optimal. However, in East Asia, gastric cancer may be more likely develop from early stages of atrophy or IM, such as OLGIM stage II.
Patients with low/high-grade dysplasia or early gastric cancer after endoscopic mucosal resection or endoscopic submucosal dissection remain at risk of the development of synchronous or metachronous gastric cancer, with reported incidence rates of between 7.7 and 33.9 per 1000 person-years. The interval of endoscopic surveillance after endoscopic mucosal resection at 1year, 5years or 10years proved cost-effective for Asian patients, and at 5years or 10years was also cost-effective for subjects of Hispanic ancestry in the USA.