Association between severe portal hypertension and risk of liver decompensation in patients with hepatitis C, regardless of response to antiviral therapy
Lens S.
Clinical Gastroenterology and Hepatology 2015;13:1846–1853.

Hepatic venous pressure gradient (HVPG) is associated with a risk of liver events in patients with chronic hepatitis C. Antiviral therapies that lead to a sustained virologic response (SVR) reduce portal pressure and prevent liver disease progression. However, it is not clear to what extent the progression of hepatitis C is modified once patients develop cirrhosis with severe portal hypertension (CSPH) (HVPG ≥ 10 mm Hg). This study assessed the effects of HVPG and SVR on the risk of liver decompensation, hepatocellular carcinoma, and/or death in patients with hepatitis C–related cirrhosis.

Data from 100 patients with hepatitis C and compensated cirrhosis who underwent HVPG measurement 3 months or less before (baseline) and 24 weeks after therapy with pegylated interferon alfa-2a and ribavirin at 4 hospitals in Spain, from 2001 through 2009. SVR was defined as undetectable serum HCV RNA level 24 weeks after treatment ended. Clinical data were collected until death, liver transplantation, or December 2012 (median, 5 y; interquartile range, 1.4–7 y).

Among the 74 patients with CSPH at baseline, 35% achieved an SVR. During the follow-up period, 19 patients developed liver decompensation (ascites, variceal bleeding, or encephalopathy). The actuarial probability values for liver decompensation at 1, 5, and 7 years were 3%, 19% and 22%, respectively. The baseline level of HVPG, but not SVR, was associated independently with the risk of liver decompensation.

In conclusion, patients with CSPH, regardless of an SVR to therapy for hepatitis C, remain at risk for liver decompensation within the first 5 years after treatment, and should be monitored closely.

Expert's Perspective

«  In the era of Interferon free oral combination therapy with direct antiviral agents (DAAs), patients with compensated and decompensated liver cirrhosis have been the first to receive therapy due to the severity of the liver disease and the high rates of Sustained Virologic response (SVR) with DAAs. However, the effect of viral suppression on long-term clinical outcomes in these patients particularly with clinical significant portal hypertension (CSPH) remains to be established. This study gives some light in the long term follow up of these patients particularly for those with CSPH that means HVPG > 10 mm Hg. The authors show that CSPH before antiviral treatment is a strong predictor of liver decompensation during follow-up, and evaluation of hepatic venous pressure gradient is superior to the presence of esophageal varices or platelet count. All patients developing liver decompensation during follow-up evaluation had CSPH at baseline. However, neither hepatic venous pressure gradient nor SVR predicted the development of HCC during follow-up. The degree of portal hypertension could be a relevant parameter for defining “ a non return” point f or developing clinical complications of portal hypertension despite achieving SVR. Indeed, prospective studies including new tools available in many centres such as transient elastography, are needed. In the meantime, patients with cirrhosis and CSPH have to be considered at high risk for developing liver decompensation even achieving an SVR, and need to be regularly monitored  »

Pr Maria Butti, Hospital General Universitari Valle Hebron, Barcelona