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Pathogenesis and potential reversibility of intestinal metaplasia − a milestone in gastric carcinogenesis

Jan Drnovsek
Jan Drnovsek
, 
Matjaz Homan
Matjaz Homan
, 
Nina Zidar
Nina Zidar
 and 
Lojze M Smid
Lojze M Smid
   | Apr 21, 2024
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Article Category: Review
Published Online: Apr 21, 2024
Page range: -
Received: Nov 03, 2023
Accepted: Mar 19, 2024
DOI: https://doi.org/10.2478/raon-2024-0028
Keywords
© 2024 Jan Drnovsek et al., published by Sciendo
This work is licensed under the Creative Commons Attribution 4.0 International License.

FIGURE 1.

Gastric intestinal metaplasia, endoscopic (A, B) and histological (C, D) appearance. Gastric intestinal metaplasia is endoscopically characterized by the presence of grey-white velvety or slightly nodular elevated patches, which are clearly demarcated against the surrounding pink gastric mucosa, as illustrated in image A of antral gastric mucosa under white light. Narrow band imaging (NBI, depicted in image B) further enhances the visualization of mucosal and vascular patterns by employing optical filters to narrow the bandwidth of light. This technique offers superior contrast compared to white light endoscopy, thereby improving the detection of metaplastic transformation. Histologically, gastric intestinal metaplasia can be classified into either complete (as seen in image C) or incomplete types (as shown in image D). Image C demonstrates preserved oxyntic mucosa (on the left) adjacent to intestinal metaplasia of the complete type, which features enterocytes with a well-defined brush border, alongside well-formed goblet cells and Paneth cells. In contrast, image D illustrates the intestinal metaplasia of the gastric mucosa of the incomplete type, characterized by goblet cells of variable size and intervening mucin-secreting columnar cells that lack a brush border (both images are hematoxylin and eosin-stained, original magnification 10x).
Gastric intestinal metaplasia, endoscopic (A, B) and histological (C, D) appearance. Gastric intestinal metaplasia is endoscopically characterized by the presence of grey-white velvety or slightly nodular elevated patches, which are clearly demarcated against the surrounding pink gastric mucosa, as illustrated in image A of antral gastric mucosa under white light. Narrow band imaging (NBI, depicted in image B) further enhances the visualization of mucosal and vascular patterns by employing optical filters to narrow the bandwidth of light. This technique offers superior contrast compared to white light endoscopy, thereby improving the detection of metaplastic transformation. Histologically, gastric intestinal metaplasia can be classified into either complete (as seen in image C) or incomplete types (as shown in image D). Image C demonstrates preserved oxyntic mucosa (on the left) adjacent to intestinal metaplasia of the complete type, which features enterocytes with a well-defined brush border, alongside well-formed goblet cells and Paneth cells. In contrast, image D illustrates the intestinal metaplasia of the gastric mucosa of the incomplete type, characterized by goblet cells of variable size and intervening mucin-secreting columnar cells that lack a brush border (both images are hematoxylin and eosin-stained, original magnification 10x).

FIGURE 2.

Pathogenesis of intestinal metaplasia and gastric adenocarcinoma – the Corea cascade. This stepwise process starts with chronic gastritis triggered by H. pylori infection. The likelihood of developing gastric cancer is higher in individuals infected with virulent strains of H. pylori, unhealthy diets (rich in salt and smoked foods), low iron levels, and harmful lifestyle choices, including smoking. Persistent inflammation results in the damage and eventual loss of acid-producing parietal cells, causing reduced stomach acidity (hypochlorhydria) and eventually no stomach acid production (achlorhydria). This reduction in acidity allows for the colonization of the stomach by detrimental, pro-inflammatory microbiota. These bacteria can produce genotoxic and pro-inflammatory metabolites and carcinogens, directly contributing to the transformation of stomach epithelial cells into malignant cells.
Pathogenesis of intestinal metaplasia and gastric adenocarcinoma – the Corea cascade. This stepwise process starts with chronic gastritis triggered by H. pylori infection. The likelihood of developing gastric cancer is higher in individuals infected with virulent strains of H. pylori, unhealthy diets (rich in salt and smoked foods), low iron levels, and harmful lifestyle choices, including smoking. Persistent inflammation results in the damage and eventual loss of acid-producing parietal cells, causing reduced stomach acidity (hypochlorhydria) and eventually no stomach acid production (achlorhydria). This reduction in acidity allows for the colonization of the stomach by detrimental, pro-inflammatory microbiota. These bacteria can produce genotoxic and pro-inflammatory metabolites and carcinogens, directly contributing to the transformation of stomach epithelial cells into malignant cells.

Patients’ related predictive risk factors for gastric intestinal metaplasia

Risk Factor Odds ratio (OD) Key findings References
Race
  White 1 Hispanic and Asian patients have an increased risk for GIM Tan MC et al. (2022)94
  Asian 2.83–3 Akpoigbe K et al. (2022)95
  Hispanic 2.10–5.6
Age (> 50 years) 1.5–2.03 Risk increases with age, possibly due to accumulated exposure to risk factors. Aumpan N et al. (2021)96
Tan MC et al. (2020)97
Male gender 1.55–2.09 Probably due to genetics and exposure to other risk factors Aumpan N et al. (2020)98
Leung WK et al. (2005)99
Chronic gastritis 3.68–5.76 Chronic inflammation is leads to IM. Yoo YE et al. (2013)100
Tatsuta M et al. (1993)101
H. pylori infection 2.47–3.65 Strong correlation with IM, especially with CagA positive strains. Aumpan N et al. (2021)96
Nguyen T et al. (2021)102
Family history of gastric cancer 1.5–3.8 Patients with a first-degree relative with gastric cancer have an increased risk of neoplastic progression Nieuwenburg SAV et al. (2021)103
Reddy KM et al. (2006)104
Alcohol consumption 1.27–1.54 Alcohol intake was independently associated with increased risk of developing AG and IM Holmes HM et al. (2021)105
Kim K et al. (2020)106
Tobacco smoking 1.54–2.75 Tobacco smoking is a risk factor for gastric IM. Morais S et al. (2014)107
Thrift AP et al. (2022)108
Blood group A 1.39–1.42 Blood group A is associated with higher risk of GIM Mao Y et al. (2019)109
Rizatto C et al. (2013)110
Bile reflux unknown Bile acids not only interefere with gastric mucosa but also regulate multiple carcinogenic pathways Wang M et al. (2023)111
Yu J et al. (2019)112
Salt consumption 0.37–1.53 Salt intake may increase progression to advanced gastric precancerous lesions Dias-Neto M et al. (2010)113
Song JH et al. (2017)114
Industrially processed food unknown Dietary exposure to N-nitroso–containing compounds has been shown to increase the promotion of gastric carcinogenesis Wiseman M (2008)115
Jencks DS et al. (2018)116
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