Risk of Progression of Gastric Intestinal Metaplasia Is Significantly Greater When Detected in Both Antrum and Body
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ORIGINAL ARTICLE
Risk of Progression of Gastric Intestinal Metaplasia Is Significantly Greater When Detected in Both Antrum and Body Anthony O’Connor1 · Adam Bowden1 · Eoin Farrell1 · Joshua Weininger1 · Stephen Crowther2 · Deirdre McNamara1 · Paul Ridgway3 · Colm O’Morain1 Received: 18 February 2020 / Accepted: 6 October 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Background Gastric cancer (GC) is the fifth leading cause of cancer-related death worldwide. GC is usually preceded by a cascade of well-defined precursor lesions, set in place by an environmental trigger (H. pylori) including intestinal metaplasia (GIM) and dysplasia. Aims To investigate the rates of progression of GIM to dysplasia and GC in a region of low gastric cancer incidence. Methods We identified all patients diagnosed with GIM between January 1, 2008, and June 30, 2012. Any repeat upper endoscopy more than 1 year after index diagnosis and before December 31, 2018, was considered follow-up. Carcinomas the bulk of which were macroscopically located below the OGJ were considered primary gastric cancer. Results Progression to more advanced lesions was observed in six patients (0.6%). Four patients (three male) developed GC at median age 74 years (SD 6). Two patients progressed to dysplasia (one male) at median age 71 years (SD 4). Patients with GIM in both gastric antrum and body were significantly more likely to progress than those with GIM in only one location (3.1% vs. 0.4%) (p value 0.017). Fifty-eight patients who had H. pylori eradicated were followed up. No progression to dysplasia or GC was noted in this group, with 28 patients having persistent GIM at follow-up. Conclusion Patients with GIM in both antrum and body had a significantly increased risk of progression and warrant close attention. This is comparable to routinely followed premalignant conditions such as Barrett’s esophagus and Colonic Polyps, and appropriate surveillance protocols should be followed in this group. Keywords Gastric cancer · Gastric intestinal metaplasia · Dysplasia · H. pylori
Introduction Gastric cancer, despite a declining incidence, was the fifth most common cancer, and the third most common cause of cancer death worldwide in 2012 and is thought to be responsible for almost three-quarters of a million deaths annually [1]. The current accepted model for gastric carcinogenesis is an expansion of that first published by Correa et al. in 1975 * Anthony O’Connor [email protected] 1
Gastroenterology Department, Trinity College Dublin, Tallaght University Hospital, Belgard Avenue, Tallaght, Dublin D24 NR0A, Ireland
2
Histopathology Department, Trinity College Dublin, Tallaght University Hospital, Dublin, Ireland
3
Upper Gastrointestinal Surgery Department, Trinity College Dublin, Tallaght University Hospital, Dublin, Ireland
[2]. This model proposes that gastric cancer is the end result of a number of mutations that begin with an unknown environmental trigger in early life, now known to be infection with H
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