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Stage of fibrosis and portal pressure correlation in nonalcoholic steatohepatitis

Sourianarayanane, Achuthan; Talluri, Jyothsna; Humar, Abinav; McCullough, Arthur J.

European Journal of Gastroenterology & Hepatology: May 2017 - Volume 29 - Issue 5 - p 516–523
doi: 10.1097/MEG.0000000000000825
Original Articles: Metabolic Liver Disease

Background: Hepatic venous pressure gradient (HVPG) measurement correlates with staging of liver fibrosis. Patients with nonalcoholic steatohepatitis (NASH) have a different pattern of fibrosis compared with hepatitis C virus (HCV) with possible alterations in pressures.

Aim: The aim of this study was to compare portal pressures with the stage of fibrosis in NASH in comparison with other liver diseases.

Patients and methods: Records of all patients who had undergone transjugular liver biopsy with pressure measurements between January 2001 and June 2013 were reviewed. Wedge hepatic venous pressure (WHVP) and HVPG were compared with stages of fibrosis in liver diseases of different etiologies.

Results: Among 142 patients included in this study, the liver disease etiology was as follows: HCV (26.6%) and NASH (24.6%), with the remaining (38.7%) grouped under other categories. The mean age of the patients was 51.2±11.5 years, with more men with HCV (73.1%) compared with NASH (51.4%) in terms of etiology (P=0.046). There were strong correlations between the stage of fibrosis with both the HVPG (r=0.64; P<0.0001) and the WHVP (r=0.63; P<0.0001) in NASH patients. Compared with HCV patients, NASH patients had a lower HVPG (3.4±2.4 vs. 7.5±11 mmHg/stage; P=0.01) with a coefficient estimate of −0.24 (P=0.017) and WHVP (9.6±5.5 vs. 14.6±15.2 mmHg/stage; P=0.03) for the stage of fibrosis.

Conclusion: HVPG and WHVP measurements were strongly correlated with stages of fibrosis in NASH. Patients with NASH had lower HVPG and WHVP for each stage of fibrosis compared with HCV patients. This raises the concern of underestimation of pressures by HVPG in NASH etiology for the stage of disease or increased fibrosis despite lower pressures in them.

aDivision of Gastroenterology, Hepatology and Nutrition

bDepartment of Transplant Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania

cDivision of Gastroenterology and Hepatology, Medical College of Wisconsin, Milwaukee, Wisconsin

dDepartment of Gastroenterology and Hepatology, Digestive Disease Institute, Cleveland Clinic Foundation

eCleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, Ohio, USA

The study was presented as a poster presentation at DDW; 3–6 May 2014; Chicago, Illinois, USA.

Correspondence to Achuthan Sourianarayanane, MD, MRCP, Department of Gastroenterology and Hepatology, Medical College of Wisconsin, 9200 West Wisconsin Ave, Milwaukee, WI 53226, USA Tel: +1 414 955 6850; fax: +1 414 955 6215; e-mail: asourianar@mcw.edu

Received September 26, 2016

Accepted November 23, 2016

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