Retrospective Study
Copyright ©The Author(s) 2025.
World J Gastrointest Endosc. Mar 16, 2025; 17(3): 99540
Published online Mar 16, 2025. doi: 10.4253/wjge.v17.i3.99540
Figure 1
Figure 1 Flow diagram of the enrolled study patients. ESD: Endoscopic submucosal dissection; MGC: Metachronous gastric cancer; H. pylori: Helicobacter pylori.
Figure 2
Figure 2 Cumulative incidences of metachronous gastric cancer after curative endoscopic submucosal dissection between different risk factors. A: The presence or absence of metabolic dysfunction-associated steatotic liver disease; B: Different Helicobacter pylori infection status; C: Degrees of mucosal atrophy; D: Differentiation of the lesions. MASLD: Metabolic dysfunction-associated steatotic liver disease; MGC: Metachronous gastric cancer; PD: Poorly differentiated; WD: Well differentiated; MD: Moderately differentiated.
Figure 3
Figure 3 A subgroup analyses forest plot of the risk factors for metabolic dysfunction-associated steatotic liver disease associated with metachronous gastric cancer. MASLD: Metabolic dysfunction-associated steatotic liver disease; PD: Poorly differentiated; WD: Well differentiated; MD: Moderately differentiated; HR: Hazard ratio; CI: Confidence interval; H. pylori: Helicobacter pylori.
Figure 4
Figure 4 Cumulative incidence of metachronous gastric cancer according to the risk stratification based on the risk factors. MGC: Metachronous gastric cancer.