Spleen stiffness measurement predicts decompensation and rules out high-risk oesophageal varices in primary biliary cholangitis

Cristina Rigamonti; Micol Giulia Cittone; Giulia Francesca Manfredi; Carla De Benedittis; Noemi Paggi; Francesca Baorda; Davide Di Benedetto; Rosalba Minisini; Mario Pirisi

doi:10.1016/j.jhepr.2023.100952

Spleen stiffness measurement predicts decompensation and rules out high-risk oesophageal varices in primary biliary cholangitis

JHEP Rep. 2023 Oct 31;6(1):100952. doi: 10.1016/j.jhepr.2023.100952. eCollection 2024 Jan.

Authors

Cristina Rigamonti^{1

2}, Micol Giulia Cittone^{1

2}, Giulia Francesca Manfredi^{1

2}, Carla De Benedittis^{1

2}, Noemi Paggi^{1

2}, Francesca Baorda^{1

2}, Davide Di Benedetto^{1

2}, Rosalba Minisini^{1

2}, Mario Pirisi^{1

2}

Affiliations

¹ Department of Translational Medicine, Università del Piemonte Orientale, Novara, Italy.
² Division of Internal Medicine, AOU Maggiore della Carità, Novara, Italy.

Abstract

Background & aims: Primary biliary cholangitis (PBC) may lead to portal hypertension (PH). Spleen stiffness measurement (SSM) by vibration-controlled transient elastography accurately predicts PH. We aimed to assess SSM role in stratifying the risk of liver decompensation in PBC.

Methods: In this monocentric, prospective, cross-sectional study, we included 114 patients with PBC who underwent liver stiffness measurement (LSM) and SSM. In total, 78 and 33 patients underwent two and three sequential vibration-controlled transient elastography examinations, respectively (longitudinal study). Screening for high-risk oesophageal varices by oesophagogastroduodenoscopy was performed according to guidelines and proposed to all patients with SSM >40 kPa.

Results: Among the 114 patients, 20 (17%) had LSM ≥10 kPa, whereas 17 (15%) had SSM >40 kPa. None of the patients with SSM ≤40 kPa had high-risk oesophageal varices, compared with three of 14 patients with SSM >40 kPa (21%; three refused endoscopy); any-size oesophageal varices were found in nine of 14 patients (64%). During a median follow-up of 15 months (IQR 10-31 months), five (4%) patients developed liver decompensation. The probability of liver decompensation was significantly higher among patients with both LSM ≥10 kPa and SSM >40 kPa: 41% at 24 months vs. 0% in other patient groups (i.e. LSM <10 kPa and SSM ≤40 kPa, or LSM ≥10 kPa and SSM ≤40 kPa, or LSM <10 kPa and SSM >40 kPa) (p <0.0001). Among the 78 patients undergoing longitudinal evaluation, four of nine patients (44%) with SSM increase during follow-up experienced liver decompensation, whereas none of those with stable LSM and SSM had liver decompensation.

Conclusions: Both LSM and SSM predict liver decompensation in patients with PBC. SSM ≤40 kPa rules out high-risk oesophageal varices and might be used in combination with LSM to improve the prediction of PH-related complications.

Impact and implications: Spleen stiffness measurement by vibration-controlled transient elastography accurately predicts portal hypertension in patients with chronic viral hepatitis. The present study is the first to demonstrate that in primary biliary cholangitis the combination of liver stiffness and spleen stiffness measurement can significantly improve risk stratification by predicting liver decompensation. Moreover, when spleen stiffness is combined with liver stiffness measurement and platelet count, it aids in identifying individuals with a low probability of having high-risk oesophageal varices, thereby allowing the avoidance of unnecessary endoscopy examinations. Further validation of our results in larger cohorts of patients with primary biliary cholangitis is needed to implement spleen stiffness measurement in clinical practice.

Keywords: Liver stiffness; Outcome; Portal hypertension; Vibration-controlled transient elastography.