FibroScan: Where Does It Stand in US Practice
FibroScan: Where Does It Stand in US Practice
It is intuitive that increasing liver stiffness reflects increasing portal hypertension. VCTE can predict significant portal hypertension (hepatic venous pressure gradient ≥10 mm Hg), the presence of varices, and risk for variceal hemorrhage but is not recommended as a replacement for endoscopy. A recent meta-analysis found a pooled PPV and NPV of 88% for the ability of VCTE to predict the presence of significant portal hypertension. In the largest study to examine this question, Bureau et al prospectively studied 150 consecutive French patients undergoing transjugular liver biopsy and portal pressure measurement, 59% of whom were cirrhotic. Controlling for ALT, aspartate aminotransferase, albumin, international normalized ratio, and platelet count, LSM ≥21 kPa had OR of 120.4 for hepatic venous pressure gradient ≥10 mm Hg. A cutoff of 11.7 kPa had PPV and NPV of 77.4% and 93.1%, respectively, whereas 21.0 kPa had PPV and NPV of 92.5% and 90.7%, respectively. In a retrospective study of 124 Americans with cirrhosis who underwent endoscopy of whom 63 had esophageal varices, our group found that a liver stiffness cutoff of 20 kPa by VCTE yielded PPV and NPV for varices of 80% and 75%, respectively. VCTE has been shown to be as effective as hepatic venous pressure gradient in predicting clinical decompensation in cirrhotic patients. In one study, hepatic venous pressure gradient ≥10 mm Hg and LSM ≥21.1 kPa had 100% NPV for portal hypertensive complications. In a group of 1000 Romanians with cirrhosis, a cutoff of 50.7 kPa had 82.71% PPV and 53.66% NPV for the prediction of esophageal bleeding.
Taken a step further, there may be a role for serial VCTE in patients with cirrhosis. Corpechot et al discovered that in cirrhotic patients with PBC who were followed with annual VCTE, increases in liver stiffness were powerfully associated with clinical outcomes such as decompensation, liver transplantation, or death. Similarly, in a cohort of 128 Korean patients with active HBV cirrhosis, a cutoff of 19 kPa yielded a hazard ratio of 7.176 for development of clinical decompensation including hepatocellular carcinoma.
VCTE is indeed a robust tool that reproducibly predicts hepatic decompensation. In a group of 667 patients with chronic viral hepatitis who were followed for 861 days, 57 patients died or developed ascites, encephalopathy, variceal bleeding, hepatocellular carcinoma, or listing for transplant. Overall, VCTE had AUROC of 0.87, and a cutoff of 10.5 kPa had NPV of 99.2% for the prediction of these important outcomes. Singh et al recently performed a meta-analysis of all studies examining the predictive power of VCTE for decompensation in chronic liver disease. For every kilopascal over the median LSM obtained, a given patient has an increased relative risk of an important clinical event: 1.07 for hepatic decompensation, 1.11 for hepatocellular carcinoma, and 1.22 for death.
A novel application for VCTE is spleen stiffness measurement, which also aims to predict portal hypertensive events. Spleen stiffness is an investigational technique where the measurements of spleen stiffness are considered reflective of splenic congestion. Further studies to delineate its limitations as well as the range of normal spleen stiffness are needed before clinicians should adopt this technique. First reported in 2011, Stefanescu et al found in their retrospective study that an optimal cutoff of 52.5 kPa rendered AUROC of 0.74 for predicting the presence of varices. The prospective study by Collecchia et al yielded similar results. In a prospective study of 174 Indian patients, among patients with varices, spleen stiffness was significantly higher in patients who had large varices (56 vs 49 kPa) and a history of variceal bleed (58 vs 50.2).
Vibration-Controlled Transient Elastography for Prediction of Liver-Related Outcomes
It is intuitive that increasing liver stiffness reflects increasing portal hypertension. VCTE can predict significant portal hypertension (hepatic venous pressure gradient ≥10 mm Hg), the presence of varices, and risk for variceal hemorrhage but is not recommended as a replacement for endoscopy. A recent meta-analysis found a pooled PPV and NPV of 88% for the ability of VCTE to predict the presence of significant portal hypertension. In the largest study to examine this question, Bureau et al prospectively studied 150 consecutive French patients undergoing transjugular liver biopsy and portal pressure measurement, 59% of whom were cirrhotic. Controlling for ALT, aspartate aminotransferase, albumin, international normalized ratio, and platelet count, LSM ≥21 kPa had OR of 120.4 for hepatic venous pressure gradient ≥10 mm Hg. A cutoff of 11.7 kPa had PPV and NPV of 77.4% and 93.1%, respectively, whereas 21.0 kPa had PPV and NPV of 92.5% and 90.7%, respectively. In a retrospective study of 124 Americans with cirrhosis who underwent endoscopy of whom 63 had esophageal varices, our group found that a liver stiffness cutoff of 20 kPa by VCTE yielded PPV and NPV for varices of 80% and 75%, respectively. VCTE has been shown to be as effective as hepatic venous pressure gradient in predicting clinical decompensation in cirrhotic patients. In one study, hepatic venous pressure gradient ≥10 mm Hg and LSM ≥21.1 kPa had 100% NPV for portal hypertensive complications. In a group of 1000 Romanians with cirrhosis, a cutoff of 50.7 kPa had 82.71% PPV and 53.66% NPV for the prediction of esophageal bleeding.
Taken a step further, there may be a role for serial VCTE in patients with cirrhosis. Corpechot et al discovered that in cirrhotic patients with PBC who were followed with annual VCTE, increases in liver stiffness were powerfully associated with clinical outcomes such as decompensation, liver transplantation, or death. Similarly, in a cohort of 128 Korean patients with active HBV cirrhosis, a cutoff of 19 kPa yielded a hazard ratio of 7.176 for development of clinical decompensation including hepatocellular carcinoma.
VCTE is indeed a robust tool that reproducibly predicts hepatic decompensation. In a group of 667 patients with chronic viral hepatitis who were followed for 861 days, 57 patients died or developed ascites, encephalopathy, variceal bleeding, hepatocellular carcinoma, or listing for transplant. Overall, VCTE had AUROC of 0.87, and a cutoff of 10.5 kPa had NPV of 99.2% for the prediction of these important outcomes. Singh et al recently performed a meta-analysis of all studies examining the predictive power of VCTE for decompensation in chronic liver disease. For every kilopascal over the median LSM obtained, a given patient has an increased relative risk of an important clinical event: 1.07 for hepatic decompensation, 1.11 for hepatocellular carcinoma, and 1.22 for death.
A novel application for VCTE is spleen stiffness measurement, which also aims to predict portal hypertensive events. Spleen stiffness is an investigational technique where the measurements of spleen stiffness are considered reflective of splenic congestion. Further studies to delineate its limitations as well as the range of normal spleen stiffness are needed before clinicians should adopt this technique. First reported in 2011, Stefanescu et al found in their retrospective study that an optimal cutoff of 52.5 kPa rendered AUROC of 0.74 for predicting the presence of varices. The prospective study by Collecchia et al yielded similar results. In a prospective study of 174 Indian patients, among patients with varices, spleen stiffness was significantly higher in patients who had large varices (56 vs 49 kPa) and a history of variceal bleed (58 vs 50.2).
