Cancer precursor lesions in intact stomach Helicobacter pylori gastritis and in resected stomach gastritis

Andrea Giuliani, S. Spada, M. Corona, M. Demoro, M. Di Bari, T. Ricciardulli, G. Galati, A. Caporale, A. Tocchi, F. Angelico

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Hemigastrectomy for benign disease and Helicobacter pylori infection are risk conditions for the development of gastric cancer. Aim of the study was to compare gastric histology and precursor lesions of malignancy in these two conditions. The hemigastrectomy group included 351 consecutively endoscoped subjects operated for gastroduodenal benign disease. Six to ten biopsy specimens were routinely taken from the residual gastric mucosa. The intact stomach group included 2097 consecutively endoscoped symptomatic subjects, who did not receive eradication therapy against H. pylori. The histological findings were classified as normal mucosa (NM), chronic non atrophic gastritis (CNAG), chronic atrophic gastritis (CAG), intestinal metaplasia (IM) and dysplasia (DYS). One thousand and three intact stomachs were H. pylori negative, and 1094 showed H. pylori colonization. The age over fifty was a significant risk factor for the occurrence of IM (OR 2.52, P≤0.001) and DYS (OR 3.46, P≤0.001), while Hp-positivity was a risk factor for CNAG (OR 1.81, P≤0.001) and CAG (OR 3.88, P≤0.001). Gastroresection was associated to higher risk for CNAG (OR 1.53, P≤0.001) and DYS (OR 4.31, P≤0.001) and to a lower risk of CAG (OR 0.49, P≤0.001). Both in males and females the risk for CNAG was significantly higher in Hp-positive (males OR 1.92, P=0.000; females OR 1.70, P=0.000) and gastrectomized subjects (males OR 2.06, P=0.000; females OR 2.43, P=0.000). Gastrectomized males, furthermore, showed an increased risk for DYS (OR 5.82, P=0.000). The aged Hp-negative and Hp-positive subjects evidenced a significant risk for IM (respectively OR's 3.42, P=0.000 and 4.85, P=0.000); the risk for DYS was significant in aged Hp-negative subjects (OR 4.09 P≤0.020). The Hp-positive individuals evidenced a significant risk for metaplastic mucosal changes (OR 38.17, P=0.000). Subjects aged over forty at the time of surgery and those with a longer postoperative follow up endoscopy presented an increased risk for CNAG of the residual mucosa (respectively OR's 2.75, P=0.000 and 5.25, P=0.000). CNAG and IM were the most frequently observed mucosal lesions both in subjects operated for duodenal and gastric ulcer (respectively OR's 4.02, P=0.000 and 3.00, P=0.000). Our data support that hemigastrectomy for benign disease and H. pylori infection may induce an increased incidence for histological precursor lesions for gastric malignancy and suggest that carcinogenesis in a resected stomach may be different from that in the intact stomach.

Original languageEnglish
Pages (from-to)371-378
Number of pages8
JournalJournal of Experimental and Clinical Cancer Research
Volume22
Issue number3
Publication statusPublished - Sep 2003

Fingerprint

Atrophic Gastritis
Gastritis
Helicobacter pylori
Stomach
Metaplasia
Neoplasms
Helicobacter Infections
Mucous Membrane
Gastric Stump
Stomach Ulcer
Duodenal Ulcer
Gastric Mucosa
Endoscopy
Stomach Neoplasms
Histology
Carcinogenesis
Biopsy

Keywords

  • Atrophic gastritis
  • Gastric cancer
  • Gastric stump
  • Gastritis
  • Helicobacter pylori

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Giuliani, A., Spada, S., Corona, M., Demoro, M., Di Bari, M., Ricciardulli, T., ... Angelico, F. (2003). Cancer precursor lesions in intact stomach Helicobacter pylori gastritis and in resected stomach gastritis. Journal of Experimental and Clinical Cancer Research, 22(3), 371-378.

Cancer precursor lesions in intact stomach Helicobacter pylori gastritis and in resected stomach gastritis. / Giuliani, Andrea; Spada, S.; Corona, M.; Demoro, M.; Di Bari, M.; Ricciardulli, T.; Galati, G.; Caporale, A.; Tocchi, A.; Angelico, F.

In: Journal of Experimental and Clinical Cancer Research, Vol. 22, No. 3, 09.2003, p. 371-378.

Research output: Contribution to journalArticle

Giuliani, A, Spada, S, Corona, M, Demoro, M, Di Bari, M, Ricciardulli, T, Galati, G, Caporale, A, Tocchi, A & Angelico, F 2003, 'Cancer precursor lesions in intact stomach Helicobacter pylori gastritis and in resected stomach gastritis', Journal of Experimental and Clinical Cancer Research, vol. 22, no. 3, pp. 371-378.
Giuliani, Andrea ; Spada, S. ; Corona, M. ; Demoro, M. ; Di Bari, M. ; Ricciardulli, T. ; Galati, G. ; Caporale, A. ; Tocchi, A. ; Angelico, F. / Cancer precursor lesions in intact stomach Helicobacter pylori gastritis and in resected stomach gastritis. In: Journal of Experimental and Clinical Cancer Research. 2003 ; Vol. 22, No. 3. pp. 371-378.
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T1 - Cancer precursor lesions in intact stomach Helicobacter pylori gastritis and in resected stomach gastritis

AU - Giuliani, Andrea

AU - Spada, S.

AU - Corona, M.

AU - Demoro, M.

AU - Di Bari, M.

AU - Ricciardulli, T.

AU - Galati, G.

AU - Caporale, A.

AU - Tocchi, A.

AU - Angelico, F.

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N2 - Hemigastrectomy for benign disease and Helicobacter pylori infection are risk conditions for the development of gastric cancer. Aim of the study was to compare gastric histology and precursor lesions of malignancy in these two conditions. The hemigastrectomy group included 351 consecutively endoscoped subjects operated for gastroduodenal benign disease. Six to ten biopsy specimens were routinely taken from the residual gastric mucosa. The intact stomach group included 2097 consecutively endoscoped symptomatic subjects, who did not receive eradication therapy against H. pylori. The histological findings were classified as normal mucosa (NM), chronic non atrophic gastritis (CNAG), chronic atrophic gastritis (CAG), intestinal metaplasia (IM) and dysplasia (DYS). One thousand and three intact stomachs were H. pylori negative, and 1094 showed H. pylori colonization. The age over fifty was a significant risk factor for the occurrence of IM (OR 2.52, P≤0.001) and DYS (OR 3.46, P≤0.001), while Hp-positivity was a risk factor for CNAG (OR 1.81, P≤0.001) and CAG (OR 3.88, P≤0.001). Gastroresection was associated to higher risk for CNAG (OR 1.53, P≤0.001) and DYS (OR 4.31, P≤0.001) and to a lower risk of CAG (OR 0.49, P≤0.001). Both in males and females the risk for CNAG was significantly higher in Hp-positive (males OR 1.92, P=0.000; females OR 1.70, P=0.000) and gastrectomized subjects (males OR 2.06, P=0.000; females OR 2.43, P=0.000). Gastrectomized males, furthermore, showed an increased risk for DYS (OR 5.82, P=0.000). The aged Hp-negative and Hp-positive subjects evidenced a significant risk for IM (respectively OR's 3.42, P=0.000 and 4.85, P=0.000); the risk for DYS was significant in aged Hp-negative subjects (OR 4.09 P≤0.020). The Hp-positive individuals evidenced a significant risk for metaplastic mucosal changes (OR 38.17, P=0.000). Subjects aged over forty at the time of surgery and those with a longer postoperative follow up endoscopy presented an increased risk for CNAG of the residual mucosa (respectively OR's 2.75, P=0.000 and 5.25, P=0.000). CNAG and IM were the most frequently observed mucosal lesions both in subjects operated for duodenal and gastric ulcer (respectively OR's 4.02, P=0.000 and 3.00, P=0.000). Our data support that hemigastrectomy for benign disease and H. pylori infection may induce an increased incidence for histological precursor lesions for gastric malignancy and suggest that carcinogenesis in a resected stomach may be different from that in the intact stomach.

AB - Hemigastrectomy for benign disease and Helicobacter pylori infection are risk conditions for the development of gastric cancer. Aim of the study was to compare gastric histology and precursor lesions of malignancy in these two conditions. The hemigastrectomy group included 351 consecutively endoscoped subjects operated for gastroduodenal benign disease. Six to ten biopsy specimens were routinely taken from the residual gastric mucosa. The intact stomach group included 2097 consecutively endoscoped symptomatic subjects, who did not receive eradication therapy against H. pylori. The histological findings were classified as normal mucosa (NM), chronic non atrophic gastritis (CNAG), chronic atrophic gastritis (CAG), intestinal metaplasia (IM) and dysplasia (DYS). One thousand and three intact stomachs were H. pylori negative, and 1094 showed H. pylori colonization. The age over fifty was a significant risk factor for the occurrence of IM (OR 2.52, P≤0.001) and DYS (OR 3.46, P≤0.001), while Hp-positivity was a risk factor for CNAG (OR 1.81, P≤0.001) and CAG (OR 3.88, P≤0.001). Gastroresection was associated to higher risk for CNAG (OR 1.53, P≤0.001) and DYS (OR 4.31, P≤0.001) and to a lower risk of CAG (OR 0.49, P≤0.001). Both in males and females the risk for CNAG was significantly higher in Hp-positive (males OR 1.92, P=0.000; females OR 1.70, P=0.000) and gastrectomized subjects (males OR 2.06, P=0.000; females OR 2.43, P=0.000). Gastrectomized males, furthermore, showed an increased risk for DYS (OR 5.82, P=0.000). The aged Hp-negative and Hp-positive subjects evidenced a significant risk for IM (respectively OR's 3.42, P=0.000 and 4.85, P=0.000); the risk for DYS was significant in aged Hp-negative subjects (OR 4.09 P≤0.020). The Hp-positive individuals evidenced a significant risk for metaplastic mucosal changes (OR 38.17, P=0.000). Subjects aged over forty at the time of surgery and those with a longer postoperative follow up endoscopy presented an increased risk for CNAG of the residual mucosa (respectively OR's 2.75, P=0.000 and 5.25, P=0.000). CNAG and IM were the most frequently observed mucosal lesions both in subjects operated for duodenal and gastric ulcer (respectively OR's 4.02, P=0.000 and 3.00, P=0.000). Our data support that hemigastrectomy for benign disease and H. pylori infection may induce an increased incidence for histological precursor lesions for gastric malignancy and suggest that carcinogenesis in a resected stomach may be different from that in the intact stomach.

KW - Atrophic gastritis

KW - Gastric cancer

KW - Gastric stump

KW - Gastritis

KW - Helicobacter pylori

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