Successful antiviral therapy may reduce hepatitis C-related portal hypertension

Last Updated: 2017-08-04

By Will Boggs MD

NEW YORK (Reuters Health) - Antiviral therapy that results in sustained viral response in patients with hepatitis C virus infection is associated with reduced, but not resolved, clinically significant portal hypertension (CSPH), researchers from Spain report.

CSPH is associated with a higher risk of clinical decompensation, development of hepatocellular carcinoma (HCC), and death. The impact of achieving sustained viral response (SVR) on various features of CSPH remains unclear.

Dr. Juan Carlos Garcia-Pagan, of the University of Barcelona, and colleagues investigated the impact of achieving SVR on hepatic, pulmonary, and systemic hemodynamics and sought to identify the predictors of hepatic venous pressure gradient (HVPG) changes and persistence of CSPH.

Among the 226 patients included in the final analysis, SVR after all-oral antiviral therapy was associated with significant reductions in HVPG from a median 15 mm Hg at baseline to 13.4 mm Hg 24 weeks after the end of treatment.

Despite reductions in HVPG after SVR, CSPH persisted in 78% of patients: 63% still had an HVPG of at least 12 mm Hg, and 25% still had an HVPG of at least 16 mm Hg; 17% showed increases in HVPG despite achieving SVR, the researchers report in Gastroenterology, online July 19.

The presence of lower baseline albumin levels was the only predictor of smaller HVPG responses after therapy.

Significant predictors of CSPH persistence included higher baseline HVPG, the presence of esophageal varices, and a lower decline in liver stiffness (which was otherwise not reliable for ruling out CSPH after SVR).

SVR was also associated with small increases in mean arterial pressure, mean pulmonary artery pressure, pulmonary vascular resistance and systemic vascular resistance, as well as decreases in cardiac output.

The researchers conclude that "the real impact of these regimens in patients with portal hypertension and elevated pulmonary arterial pressure should be further studied."

Dr. Markus Peck-Radosavljevic from the Medical University of Vienna, Austria, who has investigated the impact of antiviral and other treatments on CSPH, told Reuters Health by email, "The liver will improve after SVR, in particular, the inflammatory activity and the part of portal hypertension that is caused by inflammation; but the fibrosis is not acutely affected and might not improve at all or only slowly. Once more-advanced-stage liver disease is established, resolution of portal hypertension becomes much less likely and should not be hoped for any longer."

He said the study "helps to argue in favor of continuing care for these patients even after SVR, be it screening for varices or surveillance for HCC."

Dr. Garcia-Pagan and a co-corresponding author did not respond to a request for comment.

SOURCE: http://bit.ly/2vzo44W

Gastroenterology 2017.