In the Journals

SVR reduces hepatic venous pressure gradient, portal hypertension persists

Sustained virologic response correlated with reduced hepatic venous pressure gradient in patients with HCV-associated cirrhosis, according to a recently published study. However, clinically significant portal hypertension continued to persist in most patients.

“Development of [clinically significant portal hypertension] is a hallmark in the natural history of cirrhosis because it is associated with a higher risk of hepatic decompensation, and increased risk of hepatocellular carcinoma and death,” Sabela Lens, MD, from the Universidad de Barcelona, and colleagues wrote. “Our study was performed in [a] large cohort of patients with cirrhosis and CSPH, most of them with esophageal varices and/or previous clinical decompensation. The results clearly show that [hepatic venous pressure gradient] is significantly reduced when evaluated 24 weeks after obtaining SVR with the use of interferon-free regimens.”

Inclusion criteria for the multicenter prospective study of patients with HCV-related cirrhosis included presence of clinically significant portal hypertension within 6 months before treatment and SVR by 24 weeks after treatment.

All 226 patients included had a hepatic venous pressure gradient of 10 mmHg or higher (range, 12-18 mmHg). Hepatic venous pressure gradient values increased with the presence of varices and their size (P < .001) and were higher among patients with decompensated cirrhosis (P < .01).

Following SVR, 140 patients had a hepatic venous pressure gradient reduction of 10% or more from baseline and 90 patients had a reduction of 20% or more, while 176 patients had persistent clinically significant portal hypertension including 142 with hepatic venous pressure gradient of 12 mmHg or higher and 57 with a gradient of 16 mmHg or higher. Thirty-nine patients had an increase in hepatic venous pressure gradient.

On multivariate analysis, lower baseline levels were an independent negative predictor of a 10% or more reduction (OR = 0.52; 95% CI, 0.27-0.59). Baseline hepatic venous pressure gradient and liver stiffness measure were significantly lower among those with a 20% or more reduction (OR = 0.92; 95% CI, 0.85-0.98).

Patients with persistent clinically significant portal hypertension despite SVR had higher baseline hepatic venous pressure gradient (OR = 1.9; 95% CI, 1.5-2.5) and the presence of esophageal varices (OR = 3.2; 95% CI, 1.2-8.3). Those whose hepatic venous pressure gradient values increased had significantly higher previous instances of acute variceal bleeding (OR = 2.7; 95% CI, 1.1-6.7) and lower platelet count (OR = 0.99; 95% CI, 0.98-0.99).

“In spite of a significant [hepatic venous pressure gradient] reduction at 6 months after the end of therapy, [clinically significant portal hypertension] persisted in a high proportion of patients (78%), implying that these patients remain at high risk of developing complications of portal hypertension and hepatocellular carcinoma,” the researchers concluded. “It is relevant to closely monitor patients with [clinically significant portal hypertension] despite a relevant [liver stiffness measurement] reduction after SVR.” – by Talitha Bennett

Disclosure: Lens reports she received speaker and consultant fees from Gilead, AbbVie and Janssen. Please see the full study for the other researchers’ relevant financial disclosures.

Sustained virologic response correlated with reduced hepatic venous pressure gradient in patients with HCV-associated cirrhosis, according to a recently published study. However, clinically significant portal hypertension continued to persist in most patients.

“Development of [clinically significant portal hypertension] is a hallmark in the natural history of cirrhosis because it is associated with a higher risk of hepatic decompensation, and increased risk of hepatocellular carcinoma and death,” Sabela Lens, MD, from the Universidad de Barcelona, and colleagues wrote. “Our study was performed in [a] large cohort of patients with cirrhosis and CSPH, most of them with esophageal varices and/or previous clinical decompensation. The results clearly show that [hepatic venous pressure gradient] is significantly reduced when evaluated 24 weeks after obtaining SVR with the use of interferon-free regimens.”

Inclusion criteria for the multicenter prospective study of patients with HCV-related cirrhosis included presence of clinically significant portal hypertension within 6 months before treatment and SVR by 24 weeks after treatment.

All 226 patients included had a hepatic venous pressure gradient of 10 mmHg or higher (range, 12-18 mmHg). Hepatic venous pressure gradient values increased with the presence of varices and their size (P < .001) and were higher among patients with decompensated cirrhosis (P < .01).

Following SVR, 140 patients had a hepatic venous pressure gradient reduction of 10% or more from baseline and 90 patients had a reduction of 20% or more, while 176 patients had persistent clinically significant portal hypertension including 142 with hepatic venous pressure gradient of 12 mmHg or higher and 57 with a gradient of 16 mmHg or higher. Thirty-nine patients had an increase in hepatic venous pressure gradient.

On multivariate analysis, lower baseline levels were an independent negative predictor of a 10% or more reduction (OR = 0.52; 95% CI, 0.27-0.59). Baseline hepatic venous pressure gradient and liver stiffness measure were significantly lower among those with a 20% or more reduction (OR = 0.92; 95% CI, 0.85-0.98).

Patients with persistent clinically significant portal hypertension despite SVR had higher baseline hepatic venous pressure gradient (OR = 1.9; 95% CI, 1.5-2.5) and the presence of esophageal varices (OR = 3.2; 95% CI, 1.2-8.3). Those whose hepatic venous pressure gradient values increased had significantly higher previous instances of acute variceal bleeding (OR = 2.7; 95% CI, 1.1-6.7) and lower platelet count (OR = 0.99; 95% CI, 0.98-0.99).

“In spite of a significant [hepatic venous pressure gradient] reduction at 6 months after the end of therapy, [clinically significant portal hypertension] persisted in a high proportion of patients (78%), implying that these patients remain at high risk of developing complications of portal hypertension and hepatocellular carcinoma,” the researchers concluded. “It is relevant to closely monitor patients with [clinically significant portal hypertension] despite a relevant [liver stiffness measurement] reduction after SVR.” – by Talitha Bennett

Disclosure: Lens reports she received speaker and consultant fees from Gilead, AbbVie and Janssen. Please see the full study for the other researchers’ relevant financial disclosures.