Editorial
Copyright ©2012 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Hepatol. Dec 27, 2012; 4(12): 327-331
Published online Dec 27, 2012. doi: 10.4254/wjh.v4.i12.327
Nonalcoholic fatty liver disease and the renin-angiotensin system: Implications for treatment
Paschalis Paschos, Konstantinos Tziomalos
Paschalis Paschos, Konstantinos Tziomalos, First Propedeutic Department of Internal Medicine, Medical School, Aristotle University of Thessaloniki, AHEPA Hospital, 54636 Thessaloniki, Greece
Author contributions: Paschos P drafted the paper; Tziomalos K revised the draft critically for important intellectual content.
Correspondence to: Paschalis Paschos, MD, First Propedeutic Department of Internal Medicine, Medical School, Aristotle University of Thessaloniki, AHEPA Hospital, 54636 Thessaloniki, Greece. pashospas@hotmail.com
Telephone: +30-2310-435316 Fax: +30-2310-992937
Received: October 18, 2011
Revised: October 18, 2012
Accepted: November 17, 2012
Published online: December 27, 2012
Abstract

Nonalcoholic fatty liver disease (NAFLD) is the commonest liver disease in Western countries. Treatment of NAFLD is currently based on lifestyle measures and no effective pharmacologic treatment is available so far. Emerging evidence, mainly from animal studies, suggests that the renin-angiotensin-aldosterone system may be of major importance in the pathogenesis of NAFLD and indicates that angiotensin-converting enzyme inhibitors (ACE-I) and angiotensin receptor blockers (ARBs) as a potentially useful therapeutic approach. However, data from human studies are limited and contradictory. In addition, there are few randomized controlled trials (RCTs) on the effects of ACE-I or ARB in patients with NAFLD and most data are from retrospective studies, pilot prospective studies and post hoc analyses of clinical trials. Accordingly, more and larger RCTs are needed to directly assess the effectiveness of ACE-I and ARBs in NAFLD.

Keywords: Nonalcoholic fatty liver disease, Non alcoholic steatohepatitis, Renin-angiotensin-aldosterone system, Angiotensin-converting enzyme inhibitors, Angiotensin receptor blockers, Fibrosis