You could be reading the full-text of this article now if you...

If you have access to this article through your institution,
you can view this article in

Helicobacter pylori-negative Gastritis in Erosive Esophagitis, Nonerosive Reflux Disease or Functional Dyspepsia Patients

Peura, David A. MD*; Haber, Marian M. MD; Hunt, Barbara MS; Atkinson, Stuart MB ChB

Journal of Clinical Gastroenterology:
doi: 10.1097/MCG.0b013e3181ac9830
ALIMENTARY TRACT: Original Articles
Abstract

Background: Although Helicobacter pylori infection is believed to be the main cause of chronic gastritis, a US clinical trial investigating the long-term effects of lansoprazole as maintenance therapy for erosive esophagitis revealed a surprisingly high prevalence (over 90%) and severity of chronic gastritis in H. pylori-negative subjects.

Goals: This study aims to compare prevalence and severity of chronic gastritis of the body and antrum in H. pylori-negative subjects with erosive esophagitis, nonerosive reflux disease, or functional dyspepsia from several trials.

Study: Pretreatment gastric histology was compared in 1595 H. pylori-negative subjects with erosive esophagitis (≥ grade 2; n=196), nonerosive reflux disease (n=688), or functional dyspepsia (n=711) who participated in US Takeda-sponsored lansoprazole trials.

Results: Pretreatment histology data from US clinical studies showed that 67.5% and 75.0% of H. pylori-negative adult subjects with erosive esophagitis had moderate or severe body and antral chronic gastritis, respectively. Chronic gastritis was also observed in H. pylori-negative subjects with nonerosive reflux disease or functional dyspepsia, although prevalence was significantly less (P<0.001) than in erosive esophagitis.

Conclusions: Chronic gastritis in H. pylori-negative subjects is more common than previously appreciated. These results highlight the need for better characterization of gastric mucosal histology in these gastrointestinal disorders.

Author Information

*University of Virginia Health System, Charlottesville, VA

Department of Pathology, Drexel University College of Medicine, Philadelphia, PA

Takeda Global Research & Development Center, Inc., Deerfield, IL

Declaration of Funding Interests: (i) This study was funded in full by Takeda Global Research & Development Center, Inc. Takeda Studies M94-140, M96-619, M97-671, M96-519, and M96-521. (ii) The preparation of this paper was funded in full by Takeda Global Research & Development Center, Inc. (iii) Writing support was provided by Caroline Spencer of Rx Communications, UK, and funded by Takeda Global Research & Development Center, Inc.

Reprints: David A. Peura, MD, University of Virginia Health System, PO Box 800708, Charlottesville, VA 22908-0708 (e-mail: dap8v@virginia.edu).

Received for publication February 5, 2009

accepted May 1, 2009

Statement of Interests: Authors' declaration of personal interests: (i) David A. Peura has served as a speaker, a consultant, and an advisory board member for Takeda Global Research & Development Center, Inc. (TAP Pharmaceutical Products Inc. is now a part of Takeda Global Research & Development Center, Inc.) and has received research funding from Takeda Global Research & Development Center, Inc. Marian M. Haber has served as a consultant for Takeda Global Research & Development Center, Inc. (ii) David A. Peura is an employee of University of Virginia Health System, Charlottesville, VA. Marian M. Haber is an employee of Drexel University College of Medicine, Philadelphia, PA. Barbara Hunt and Stuart Atkinson are employees of Takeda Global Research & Development Center, Inc.

© 2010 Lippincott Williams & Wilkins, Inc.