Predictors of heartburn resolution and erosive esophagitis in patients with GERD

ABSTRACT

Objectives: The primary objective was to assess gastroesophageal reflux disease (GERD) symptom resolution rates with esomeprazole by erosive esophagitis (EE) status, and the secondary objective was to evaluate potential predictors of the presence of EE and heartburn resolution.

Background: Patients with GERD who have EE have higher reported symptom resolution rates than those with nonerosive reflux disease (NERD) when treated with proton pump inhibitors (PPIs).

Study: This open-label multicenter study included adults with GERD symptoms. Patients were stratified by EE status after endoscopy and received once-daily esomeprazole 40 mg for 4 weeks. Questionnaires determined symptom response rates, and baseline predictors of EE or heartburn resolution were evaluated. Potential predictors, including years with GERD, history of EE, and time to relief with antacids, were examined.

Results: Heartburn resolution rates at 4 weeks were higher for patients with EE than NERD (69% [124/179] vs. 48% [85/177]; p < 0.0001). Multivariate models had moderate predictive ability for EE (c-index, 0.76) and poor predictive ability (c-index, 0.57) for heartburn resolution. However, faster heartburn relief with antacid use, particularly within 15 min, was predictive of EE and heartburn resolution.

Conclusions: Patients with EE have higher heartburn resolution rates than patients with NERD after treatment, although recall bias may be possible. Fast relief with antacid use is predictive of EE and heartburn resolution with a PPI and suggests that a history of antacid relief may provide corroborative evidence to empiric PPI therapy in determining whether patients with heartburn have acid reflux disease.

Trial registration: ClinicalTrials.gov identifier: NCT00242736.

Key words: :

• Erosive esophagitis
• Esomeprazole
• GERD
• Heartburn
• Predictive modeling
• PPI

Transparency

Declaration of funding

The study was funded by AstraZeneca LP, Wilmington, DE, USA.

Declaration of financial/other relationships

R.C.O. has disclosed that he has or has had in the recent past financial relationships (consulting, lecture bureau, research support, stock ownership) with Amicus Therapeutics, AstraZeneca LP, Boston Scientific, Merck, Novartis, Pfizer, Procter & Gamble, Santarus, and Sirna. J.T.M. and D.G.S. have disclosed that they are employees of AstraZeneca LP.

All peer reviewers receive honoraria from CMRO for their review work. The peer reviewers have disclosed that they have no relevant financial relationships.

Acknowledgment

The authors have disclosed that Christopher Langford, PAREXEL MMS Europe, UK, and Anny Wu, PharmD, Scientific Connexions, Newtown, PA, USA, provided medical writing support funded by AstraZeneca LP, and that John Tumas and Mary Wiggin, both from AstraZeneca LP, provided editorial assistance.

The authors thank Wilfred M. Weinstein, MD, for his role as the central reader for biopsy processing and evaluation; Shawn Jones (AstraZeneca LP) for study management; the patients, the study-site staff members, and the following primary investigators (all USA): A. Caos, Ocoee, FL; S.L. Duckor, Orange, CA; M.S. Eisner, Zephyrhills, FL; V.S. Jayanty, Houston, TX; F.T. Wootton, III, Norfolk, VA; R.A. Krause, Chattanooga, TN; T. Liebermann, Austin, TX; J.E. Lowe, Ogden, UT; T.F. Mendolia, Elkin, NC; P.B. Miner, Jr., Oklahoma City, OK; S.E. Moussa, Tucson, AZ; J.M. Provenza, Shreveport, LA; M. Raikhel, Torrance, CA; D.S. Riff, Anaheim, CA; M.A. Ringold, Christiansburg, VA; H.I. Schwartz, Miami, FL; D.J. Sales, Arlington Heights, IL; U.K. Shah, Hollywood, MD; R.D. Shepard, Tampa, FL; G.A. Spiegelman, Knoxville, TN; D.B. Stanton, Orange, CA; S.A. Wofford, North Little Rock, A.R., and R.D. Marks, Alabaster, AL.

Notes

*This manuscript was presented as a podium talk at American College of Gastroenterology Annual Meeting and Postgraduate Course, Philadelphia, PA, USA, October 12–17, 2007