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Liver stiffness measurement improves prediction of liver disease outcomes

19th July 2023

Repeating liver stiffness measurements (LSM) allows for an individual and updated risk assessment for decompensation and mortality in patients with advanced chronic liver disease (CLD), a study has found.

LSM provide an opportunity for clinicians to non-invasively monitor liver disease progression and even regression. But is there a prognostic value in measurement of liver stiffness dynamics over time for liver-related events and death in patients with CLD?

This was the question posed in a recent retrospective study, published in the journal Gastroenterology by a team of researchers from the Department of Internal Medicine III at the Medical University of Vienna and University Hospital Vienna in Austria. They showed that the dynamics of LSM are directly linked to either an increased or decreased risk for hepatic decompensation in compensated and decompensated advanced CLD.

Researchers focused on patients with CLD undergoing more than two reliable LSM at least 180 days apart. For the purposes of the analysis, patients were categorised as having non-advanced CDL (nonACLD), compensated advanced CLD (cACLD) and decompensated advanced CLD (dACLD). 

The primary objective to assess the association of longitudinal changes in LSM with clinical events of hepatic decompensation in nonACLD and cACLD patients. A range of secondary objectives included a comparison of LSM dynamics between different disease severity groups and an exploratory analysis of the impact of dynamics of LSM on liver-related mortality in dACLD.

LSM and patient outcomes

A total of 2,508 patients with 8,561 reliable LSM (a median of three per patient) were included in the analysis. This comprised 65.7% with non-ACLD, 30.2% with cACLD and 4.1% with dACLD. In addition, 83 patients with cACLD developed hepatic decompensation after a median follow-up of 71 months.

The researchers found that a 20% increase in LSM at any time was associated with an increased risk for hepatic decompensation (Hazard ratio, HR = 1.58, 95% CI 1.41 – 1.79, p < 0.001) as well as hepatic-related mortality (HR = 1.45, 95% CI 1.28 – 1.68, p < 0.001) in cACLD patients.

In addition, LSM dynamics yielded a high accuracy to predict hepatic decompensation in the following 12 months (area under the curve, AUC = 0.933). This performance was numerically superior to dynamics in FIB-4 (AUC = 0.873), MELD (AUC = 0.835) and single time-point LSM.

Any LSM decrease to less than 20 kPa identified cACLD patients with a substantially lower risk of hepatic decompensation (HR = 0.13, 95% CI 0.07 – 0.24).

Commenting on these findings, the study’s principal investigator Thomas Reiberger said: ‘An understanding of the individual patient’s personal risk profile means that it is possible to initiate optimised, personalised treatment.‘

Indeed, taken together, the findings of the study reveal how regular measurements of liver stiffness indicate a personalised patient risk profile, which enables the initiation of individualised treatment strategies.