CLNICAL and MOLECULAR HEPATOLOGY The forum for latest knowledge of hepatobiliary diseasses

Portal hypertension is the main driver of complications in compensated advanced chronic liver disease (cACLD). Par-ticularly, the presence of clinically significant portal hyper-tension (CSPH) identifies those at risk for hepatic decompen-sation.1 The recommendation of the recent Baveno VII consensus to treat CSPH upon diagnosis (i.e., prevention of hepatic de-compensation), instead of waiting for (high-risk) varices to develop to initiate primary bleeding prophylaxis, marked a paradigm shift in clinical hepatology.2 Specifically, endosco-pies to screen for high-risk varices or performance of endo-scopic band ligation have been a cornerstone in the manage-ment of cACLD patients (i.e., primary prophylaxis of variceal bleeding) until recently.3, 4 Following Baveno VII,2 the presence of CSPH should be investigated by non-invasive tests (NIT)5 or, where available, hepatic venous pressure gradi-ent-measurement6 upon the diagnosis of cACLD, to facilitate timely treatment initiation with non-selective betablockers (NSBB; preferably carvedilol) for preventing first hepatic de-compensation1,7, 8 -most commonly, the occurrence of as-cites.2 In a recent issue of Clinical and Molecular Hepatology, Wong and colleagues9 set out to validate the performance of NIT to exclude CSPH (liver stiffness measurement [LSM] <15 kPa and platelet count [PLT] >= 150x109/L), rule-in CSPH (LSM >= 25 kPa), and to identify those at high probability for CSPH (LSM 20-25 kPa and PLT <150x109/L, or LSM 15-20 kPa and PLT <110x109/L) for the prediction of first hepatic decompen-sation in a multicentre cohort, including 1,159 'cACLD' pa-tients from Italy, India, China, and Singapore. Notably, this multi-ethnic cohort included predominantly cured hepatitis C virus (HCV) (56%) or suppressed hepatitis B virus (HBV) (21%) patients; the median LSM was approximately 24 kPa at study inclusion, and the patients were followed for 40 months.

Automated summary

Portal hypertension is the main cause of complications in advanced chronic liver disease. Clinically significant portal hypertension identifies individuals at risk for liver decompensation. Recent consensus recommends treating clinically significant portal hypertension upon diagnosis to prevent liver decompensation, instead of waiting for high-risk varices to develop. Non-invasive tests should be used to investigate the presence of clinically significant portal hypertension and initiate timely treatment with non-selective beta blockers.