Risk stratification in primary biliary cholangitis (PBC) traditionally relies on biochemical response to ursodeoxycholic acid, but liver stiffness measurement (LSM) is increasingly used to assess fibrosis and portal hypertension. In everyday practice, clinicians often encounter a dilemma: biochemistry and LSM do not always move in the same direction, and it has been unclear how to interpret these discordant results.
Risk stratification in primary biliary cholangitis (PBC) traditionally relies on biochemical response to ursodeoxycholic acid, but liver stiffness measurement (LSM) is increasingly used to assess fibrosis and portal hypertension. In everyday practice, clinicians often encounter a dilemma: biochemistry and LSM do not always move in the same direction, and it has been unclear how to interpret these discordant results.
This large international multicenter study clarifies that uncertainty. The investigators evaluated patients with PBC who had serial LSM assessments and no prior hepatic decompensation, transplant, or liver cancer. They examined how biochemical response and changes in LSM relate to future liver-related outcomes, with a particular focus on discordant patterns.
The key finding is that discordance between biochemical response and LSM is common, occurring in more than half of patients. Importantly, when discordance exists, the most recent LSM value is the strongest predictor of future liver-related events, including first hepatic decompensation. Once the current LSM is known, earlier LSM trends and biochemical response add little additional prognostic information.
Patients who achieved biochemical response but had a persistently elevated current LSM remained at high risk of adverse liver outcomes. Conversely, patients with biochemical nonresponse but a low current LSM had a comparatively lower risk. This indicates that fibrosis burden and portal pressure—reflected by LSM—ultimately outweigh biochemical normalisation in determining prognosis.
From a practical standpoint, this study simplifies clinical decision-making. Rather than integrating complex trajectories of past LSM values and biochemical fluctuations, clinicians can focus on the latest reliable LSM to guide surveillance intensity, timing of second-line therapy, and transplant referral discussions.
In summary, while both biochemistry and LSM are important in PBC, the current LSM is the dominant prognostic marker. This finding supports routine, longitudinal elastography and emphasises that biochemical response alone does not guarantee low long-term risk in PBC.
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