Liver stiffness measurement: Is it a non-invasive substitution for HVPG?

Cirrhosis, the end stage of any chronic liver disease, can lead to portal hypertension (PHT), which can lead to fatal complications. Therefore, the prognosis and management of chronic liver diseases strongly depend on the severity of PHT. The best method to diagnose PHT is the direct measurement of portal pressure, and hepatic venous pressure gradient (HVPG) has been suggested as a reliable gold standard for the assessment of PHT. HVPG measures a hemodynamic change of portal blood flow derived from the fibrotic transformation of liver tissue and reflects the disease progression in chronic liver disease without sampling error as in the case of liver biopsy. Clinically significant portal hypertension (CSPH) is defined as HVPG ≥10 mmHg and severe PHT is defined as HVPG ≥12 mmHg. Esophageal varices (EVs), ascites, and all other complications of PHT may develop when the HVPG increases above 10 mmHg. However, HVPG measurement is invasive, relatively expensive, and available only in specialized centers with well trained operators, it needs reliable, non-invasive, and widely available methods. Transient elastography is a rapid and non-invasive technique that allows the measurement of liver stiffness. Liver stiffness measurement (LSM) has been shown to be correlated to fibrosis stage in various chronic liver diseases with a high sensitivity and specificity for the diagnosis of cirrhosis. Recently, several studies demonstrated the correlation between LSM and HVPG (Table 1). Although the characteristics of patients and the causes of chronic liver disease were heterogenous, there was a good correlation between LSM and HVPG in whole patient population. However, the level of correlation differed between LSM and HVPG according to the value of the HVPG. The liver stiffness was very well correlated with HVPG up to values of 10-12 mmHg, whereas it hardly reaches statistical significance for HVPG values ≥12 mmHg. This suggests that beyond a certain degree of portal pressure gradiet (≥10 to 12 mmHg), PHT develops partially independent from the tissue fibrosis responsible for liver tissue stiffness. Also, several extrahepatic factors including the hyperdynamic circulation, the splanchnic vasodilatation, and the resistance opposed to portal blood flow by the portosystemic collaterals become the cause of rise in portal pressure. These factors make structural variables that have an independent impact on portal pressure in individual patients. LSM cut-off values for HVPG ≥10 mmHg were also variable, ranging from 13.6 kPa to 34.9 kPa. These differences may be due to the heterogeneity of studied population and different causes of disease. Optimal LSM cut-off values for HVPG ≥10 mmHg were different between alcohol and Liver stiffness measurement: Is it a non-invasive substitution for HVPG?