Advanced gastric cancer detected during regular follow-up after eradication of Helicobacter pylori

Tanaka, Masami; Kikuchi, Daisuke; Odagiri, Hiroyuki; Hosoi, Atsuko; Suzuki, Yugo; Okamura, Takayuki; Ochiai, Yasutoshi; Hayasaka, Junnosuke; Mitsunaga, Yutaka; Nomura, Kosuke; Yamashita, Satoshi; Matsui, Akira; Takazawa, Yutaka; Hoteya, Shu

doi:10.1007/s12328-021-01577-2

Cited by 2 publications

(3 citation statements)

References 14 publications

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“…Endoscopic or histological findings of early-stage gastric cancer after H. pylori eradication are becoming clearer with more previous reports. [2][3][4][5][6][7][8][9] After H. pylori eradication, few reports of invasive gastric cancer exist, 12,13 and its characteristics are unknown. To our knowledge, this is the first study to compare the clinicopathological features of invasive gastric cancer diagnosed ≥10 years after H. pylori eradication with those detected <10 years after eradication.…”

Section: Discussionmentioning

confidence: 99%

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Multicenter study of invasive gastric cancer detected after 10 years of Helicobacter pylori eradication in Japan: Clinical, endoscopic, and histopathologic characteristics

Kobayashi,

Fujisaki,

Namikawa

et al. 2024

DEN Open

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ObjectivesGastric cancer can be diagnosed even in patients long after Helicobacter pylori eradication. Most cases involve intramucosal lesions; however, some are invasive and require surgery. To clarify appropriate long‐term surveillance methods, this study compared invasive gastric cancer diagnosed ≥10 and <10 years after eradication.MethodsThis retrospective multicenter study included 14 institutions. We included 377 patients with gastric cancer with submucosal or deep invasion after surgical or endoscopic resection. Ordered logistic regression analysis was used to explore the factors contributing to the pathological stage and histological type.ResultsInvasive gastric cancer was detected in 84 patients (Group L) and 293 patients (Group S) ≥10 and <10 years after H. pylori eradication, respectively. Endoscopic mucosal atrophy at the time of cancer detection was similar in both groups; 50% of the patients had severe atrophy. Annual endoscopy correlated with early pathological stage (odds ratio [OR] 0.28, 95% confidence interval [CI] 0.14–0.54, p < 0.001). Group L exhibited an independent correlation with the advanced pathological stage (OR 2.27, 95% CI 1.06–4.88, p = 0.035) and the undifferentiated type (OR 2.12, 95% CI 1.16–3.90, p = 0.015). The pure differentiated type and early pathological stage significantly (p = 0.001) correlated with severe mucosal atrophy in Group S but not in Group L.ConclusionsInvasive cancers diagnosed ≥10 years after H. pylori eradication were likely to be more malignant in histological type and pathological stage. Gastric cancer surveillance should continue regardless of endoscopic atrophy, particularly ≥10 years after eradication.

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Section: Discussionmentioning

confidence: 99%

“…8,9 However, some lesions are invasive cancer and require surgery, making them a growing concern. [9][10][11] No comprehensive studies have examined invasive gastric cancer after H. pylori eradication 12,13 ; therefore, its characteristics are unknown. An appropriate surveillance method for long-term post-H. pylori eradication is required.…”

Section: Introductionmentioning

confidence: 99%

Multicenter study of invasive gastric cancer detected after 10 years of Helicobacter pylori eradication in Japan: Clinical, endoscopic, and histopathologic characteristics

Kobayashi,

Fujisaki,

Namikawa

et al. 2024

DEN Open

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“…Oxyntic atrophy and intestinal metaplasia are associated with risk of gastric cancer, although the latter is not necessarily a precursor (28-30). There have during the last few years been multiple reports of increased risk of gastric cancer after H. pylori eradication (31)(32)(33)(34). The fact that the risk of cancer development continues after H. pylori eradication if oxyntic atrophy is present suggests that H. pylori itself is not carcinogenic, but that the inflammation it causes leads to atrophy of the acid, producing mucosa which predisposes individuals to cancer.…”

Section: H Pylorimentioning

confidence: 99%

The central role of gastrin in gastric cancer

Waldum,

Mjønes

2023

Front. Oncol.

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The prevalence of gastric cancer has markedly declined, but due to the high mortality rates associated with gastric cancer, it is still a serious disease. The preferred classification of gastric cancer is according to Lauren into either the intestinal type, which has a glandular growth pattern, or the diffuse type, which does not have glandular structures. Both types have been classified as adenocarcinomas, with the latter type based on periodic acid–Schiff (PAS) positivity presumed to reflect mucin. However, the presence of mucin in the diffuse type, in contrast to neuroendocrine/enterochromaffin-like (ECL) cell markers, has not been confirmed by immunohistochemistry and in situ hybridization. The ECL cells are probably prone to becoming cancerous because they do not express E-cadherin. Gastric cancer is unique in that a bacterium, Helicobacter pylori, is thought to be its main cause. H. pylori predisposes infected individuals to cancer only after having caused oxyntic atrophy leading to gastric hypoacidity and hypergastrinemia. No single H. pylori factor has been convincingly proved to be carcinogenic. It is probable that gastrin is the pathogenetic factor for gastric cancer due to H. pylori, autoimmune gastritis, and long-term prolonged inhibition of gastric acid secretion. Hypergastrinemia induces ECL cell hyperplasia, which develops into neuroendocrine tumors (NETs) and then into neuroendocrine carcinomas in rodents, a sequence that has also been described in humans. During carcinogenesis, the tumor cells lose specific traits, requiring that sensitive methods be used to recognize their origin. Gastric cancer occurrence may hopefully be prevented by H. pylori eradication at a young age, and by the reduced use of inhibitors of acid secretion and use of a gastrin antagonist in those with previous long-term H. pylori infection and those with autoimmune gastritis.

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Advanced gastric cancer detected during regular follow-up after eradication of Helicobacter pylori

Cited by 2 publications

References 14 publications

Multicenter study of invasive gastric cancer detected after 10 years of Helicobacter pylori eradication in Japan: Clinical, endoscopic, and histopathologic characteristics

Multicenter study of invasive gastric cancer detected after 10 years of Helicobacter pylori eradication in Japan: Clinical, endoscopic, and histopathologic characteristics

The central role of gastrin in gastric cancer

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