2022 Top Story in Gastroenterology: Preventing Decompensation in Patients With Compensated Cirrhosis
Written by
Scott J. Cotler MD
A study by Villanueva et al published in the Journal of Hepatology in October addresses the important goal of preventing decompensation in patients with compensated cirrhosis.1 Decompensated cirrhosis, defined by development of ascites, variceal bleeding, or hepatic encephalopathy is associated with a high mortality rate. Patients with clinically significant portal hypertension (CSPH; ie, hepatic vein portal gradient >10 mm Hg) are at risk for hepatic decompensation. Villanueva et al performed an individual participant data meta-analysis including four randomized controlled trials comprising patients with compensated cirrhosis and CSPH who received the non-selective beta blocker carvedilol (n = 181) versus endoscopic variceal ligation (EVL) or no active treatment (n = 171). Patients who received carvedilol had a lower risk of hepatic decompensation, primarily owing to a reduction in the development of ascites, and lower rates of mortality and liver-related mortality than those who underwent EVL or received no active treatment.
The first consideration in reducing the risk of hepatic decompensation in patients with compensated cirrhosis is to treat the underlying cause of liver disease. The study by Villanueva et al suggests a role for carvedilol in decreasing hepatic decompensation in patients with CSPH. Carvedilol has anti-adrenergic vasodilatory effects that decrease intrahepatic vascular resistance, and it offers an advantage over propranolol and nadolol in reducing portal pressures.
A practical consideration in implementing the findings of Villanueva et al in clinical practice is to identify patients with compensated cirrhosis and CSPH, as measurements of the hepatic vein portal gradient are not routinely taken at most centers. Surrogate markers of CSPH include the findings of gastroesophageal varices (including small varices) on endoscopy, portosystemic collaterals on imaging, or reversal of flow in the portal vein by Doppler, and, in patients with alcohol, viral, or non-obese NASH-related cirrhosis, liver stiffness >25 kPa by transient elastography.2,3 Prospective studies are needed to build on these important findings.