Apfel T, Lopez R, Sanaka MR, Thota PN. Risk of progression of Barrett's esophagus in patients with cirrhosis. World J Gastroenterol 2017; 23(18): 3287-3294 [PMID: 28566888 DOI: 10.3748/wjg.v23.i18.3287]
Corresponding Author of This Article
Prashanthi N Thota, MD, FACG, Director, Esophageal Center, Department of Gastroenterology and Hepatology, Digestive Disease and Surgery Institute, Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195, United States. thotap@ccf.org
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Case Control Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. May 14, 2017; 23(18): 3287-3294 Published online May 14, 2017. doi: 10.3748/wjg.v23.i18.3287
Risk of progression of Barrett's esophagus in patients with cirrhosis
Tehilla Apfel, Rocio Lopez, Madhusudhan R Sanaka, Prashanthi N Thota
Tehilla Apfel, Department of General Internal Medicine, Cleveland Clinic Foundation, Cleveland, OH 44195, United States
Rocio Lopez, Department of Biostatistics, Cleveland Clinic Foundation, Cleveland, OH 44195, United States
Madhusudhan R Sanaka, Prashanthi N Thota, Department of Gastroenterology and Hepatology, Digestive Disease and Surgery Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, United States
Author contributions: Apfel T collected data, drafting this manuscript; Lopez R statistical analysis; Sanaka MR designed study, revised this manuscript; Thota PN designed and supervised this study, drafting and revised of manuscript.
Institutional review board statement: The study was reviewed and approved for publication by our Institutional Reviewer.
Informed consent statement: Informed consent waived by institutional review board as it is a retrospective case control study.
Conflict-of-interest statement: All the Authors have no conflict of interest related to the manuscript.
Data sharing statement: The original anonymous dataset is available on request from the corresponding author at thotap@ccf.org.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Prashanthi N Thota, MD, FACG, Director, Esophageal Center, Department of Gastroenterology and Hepatology, Digestive Disease and Surgery Institute, Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195, United States. thotap@ccf.org
Telephone: +1-216-4440780 Fax: +1-216-445-4222
Received: January 23, 2017 Peer-review started: January 27, 2017 First decision: February 23, 2017 Revised: March 11, 2017 Accepted: April 21, 2017 Article in press: April 21, 2017 Published online: May 14, 2017 Processing time: 112 Days and 0.3 Hours
Core Tip
Core tip: Fifty seven cirrhotic patients with Barrett’s esophagus (BE) were compared to 228 non-cirrhotic BE controls. Nonalcoholic steatohepatitis or cardiac cirrhosis was the most common causes of cirrhosis in this group. There were no differences in incidence rates of high-grade dysplasia (HGD)/esophageal adenocarcinoma (EAC) in nondysplastic BE between cirrhotic cases and noncirrhotic controls (1.4 vs 1.1 per 100 person -years, P = 0.8). In low grade dysplasia, cirrhotic patients were found to have higher rates of progression to HGD/EAC compared to control group though this did not reach statistical significance (13.7 vs 8.1 per 100 person- years, P = 0.51). There was approximately 8 times increased risk of progression for every one point increase in Child- Pugh class.
