Gastric Intestinal Metaplasia

Educational Objectives

The goal of this program is to improve surveillance of gastric intestinal metaplasia caused by Helicobacter pylori infection. After hearing and assimilating this program, the clinician will be better able to:

1. Identify host phenotypes that increase risk for gastric cancer caused by H pylori infection.

Summary

Gastric intestinal metaplasia: describes normal intestinal tissue in abnormal location; complete — gastric tissue identical to tissue in small intestine; incomplete — gastric tissue does not contain enterocytes and not absorptive; higher risk for cancer than with complete metaplasia

Helicobacter pylori: prevalence — ≈50% worldwide (world’s most common infection); more frequent in developing countries (≤90%) and acquired earlier in life; because of immigration, H pylori will remain present in United States; natural history of infection — after development of chronic infection, low production of gastric acid leads to corpus-predominant infection with atrophy, leading to intestinal metaplasia, dysplasia, and gastric cancer

Host phenotypes: meta-analysis — odds for gastric cancer 2.36-fold higher with H pylori infection, and odds ratio >2 times higher for cytotoxin-associated gene A (CagA)-positive vs CagA-negative infection; host response to infection — study showed proinflammatory polymorphisms associated with higher incidence of cancer; and among family members of patients with cancer, those who had gastric atrophy much more likely to have proinflammatory phenotypes; study of patients infected with H pylori — patients with nonulcerative dyspepsia, gastric ulceration, and hyperplastic polyps had high incidence of cancer at 8 yr follow-up; patients with antral-predominant infection did not develop gastric cancer

Cost-effectiveness of screening and treatment of H pylori infection: screening — expensive and not always effective; may show serologic scar of previous exposure; treatment — side effects and resistance common; intervening after development of metaplasia and atrophy has minimal effect; risk factors for progression — pan gastritis and atrophy in elderly patients; severe intestinal metaplasia, incomplete metaplasia, first-degree family members with gastric cancer, and smoking habit

Treatment of H pylori and risk for cancer: nonrandomized study — patients with early-stage cancer who underwent endoscopic mucosal resection (EMR) and cured of H pylori infection did not develop cancer, whereas patients who underwent EMR and were not cured of infection progressed to cancer; study in China — patients (many with premalignant lesions), randomized to receive antibiotics or placebo; incidence of cancer similar when analyzing all patients, but lower in those with premalignant lesions treated before atrophy and intestinal metaplasia developed

Surveillance for gastric adenocarcinoma: endoscopy performed annually over 3-yr period standard in Europe, but not cost-effective in United States; low risk — may screen every 3 yr (but may not be necessary); controversial; high risk — includes patients with partial gastrectomy, gastric intestinal metaplasia with dysplasia, gastric ulcers, family history of gastric cancer, or inherited syndromes; perform endoscopy with multiple biopsies from antrum, body, and incisura; narrow-band imaging improves detection of intestinal metaplasia (recommended)

American Society for Gastrointestinal Endoscopy guidelines for surveillance of intestinal metaplasia: early detection improves outcomes; recommends surveillance for patients with family history or proinflammatory phenotype, high-grade dysplasia (very high risk for cancer), or low-grade dysplasia (intermediate risk)

Readings

Evans JA et al: The role of endoscopy in the management of premalignant and malignant conditions of the stomach. Gastrointest Endosc. 2015 Jul;82(1):1-8; Khatoon J et al: Role of Helicobacter pylori in gastric cancer: Updates. World J Gastrointest Oncol. 2016 Feb 15;8(2):147-58; Suerbaum S and Michetti P: Helicobacter pylori infection. N Engl J Med. 2002 Oct 10;347(15):1175-86; Wroblewski LE et al: Helicobacter pylori and Gastric Cancer: Factors That Modulate Disease Risk. Clin Microbiol Rev. 2010 Oct;23(4):713–739.

Disclosures

For this program, the following has been disclosed: Dr. Metz is a consultant for Takeda Pharmaceuticals and receives grant/research support from AAA Pharmaceutical, Ipsen Limited, and Lexicon Pharmaceuticals. The planning committee reported nothing to disclose. In his lecture, Dr. Metz presents information that is related to the off-label or investigational use of a therapy, product, or device.

Acknowledgements

Dr. Metz was recorded at the 39th Annual New York Course, held December 17-18, 2015, in New York, NY, and presented by the Albert Einstein College of Medicine and the New York Society for Gastrointestinal Endoscopy. For information on future CME activities from the Albert Einstein College of Medicine, please visit einstein.yu.edu. For information about upcoming CME activities from the New York Society for Gastrointestinal Endoscopy, please visit nysge.org. The Audio Digest Foundation thanks the speakers and the sponsors for their cooperation in the production of this program.

CME/CE INFO

Accreditation:

The Audio- Digest Foundation is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

The Audio- Digest Foundation designates this enduring material for a maximum of 0 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Audio Digest Foundation is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's (ANCC's) Commission on Accreditation. Audio Digest Foundation designates this activity for 0 CE contact hours.

Lecture ID:

ON080903

Expiration:

This CME course qualifies for AMA PRA Category 1 Credits™ for 3 years from the date of publication.

Instructions:

To earn CME/CE credit for this course, you must complete all the following components in the order recommended: (1) Review introductory course content, including Educational Objectives and Faculty/Planner Disclosures; (2) Listen to the audio program and review accompanying learning materials; (3) Complete posttest (only after completing Step 2) and earn a passing score of at least 80%. Taking the course Pretest and completing the Evaluation Survey are strongly recommended (but not mandatory) components of completing this CME/CE course.

Estimated time to complete this CME/CE course:

Approximately 2x the length of the recorded lecture to account for time spent studying accompanying learning materials and completing tests.