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Non-alcoholic fatty liver disease and hypertension: coprevalent or correlated?

Oikonomou, Dimitriosa,*; Georgiopoulos, Georgiosb,*; Katsi, Vassilikib; Kourek, Chrisb; Tsioufis, Constantinosb; Alexopoulou, Alexendrab; Koutli, Evaggeliac; Tousoulis, Dimitriosb

European Journal of Gastroenterology & Hepatology: September 2018 - Volume 30 - Issue 9 - p 979–985
doi: 10.1097/MEG.0000000000001191
Review Articles

Objective To provide a comprehensive review summarizing the existing evidence on the association between nonalcoholic fatty liver disease (NAFLD) and hypertension (HT) independent of other components of metabolic syndrome.

Methods We searched the literature through Medline and the Cochrane Library for studies evaluating the relationship between hypertension and fatty liver disease.

Results Studies testing this association are limited, but agree that HT and fatty liver disease are inter-related independent of other components of the metabolic syndrome such as obesity and diabetes mellitus. Clinical evidence shows that NAFLD is associated with new-onset HT, whereas increased blood pressure is related to the development of fatty liver disease and the possible subsequent progression to liver fibrosis. Insulin resistance and activation of the renin–angiotensin–aldosterone system (RAAS) might provide potential pathophysiologic links between these clinical entities. Until further evidence is available, patients with HT should be meticulously evaluated and treated for fatty liver disease and vice versa. RAAS inhibitors have been tested in NAFLD, presenting a favorable profile by decreasing insulin resistance and fibrosis progression.

Conclusion NAFLD and HT are associated independent of traditional cardiovascular risk factors. Insulin resistance appears to be the main linking mechanism. Although RAAS inhibitors are the most beneficial treatment option for HT in patients with NAFLD, randomized studies on the administration of these agents in HT patients with NAFDL are warranted to provide optimal treatment options in these high cardiovascular risk individuals.

aDepartment of Cardiology, ‘Evaggelismos’ General Hospital of Athens

bFirst Department of Cardiology

cDepartment of Internal Medicine, ‘Hippokration’ Hospital, University of Athens, Medical School, Athens, Greece

* Dimitrios Oikonomou and Georgios Georgiopoulos contributed equally to the writing of this article.

Correspondence to Dimitrios Oikonomou, MD, ‘Evaggelismos’ General Hospital of Athens, Ipsilantou 45-47, 10676 Athens, Greece Tel: +30 213 204 1457; fax: +30 213 204 1433; e-mail: jimoik4@hotmail.com

Received December 28, 2017

Accepted March 27, 2018

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