Introduction

Baveno VII has suggested that a decrease in liver stiffness measurement (LSM) by ≥20% to <20kPa, or any LSM-decrease to a LSM <10kPa is “clinically significant” in compensated advanced chronic liver disease (cACLD). However, these LSM surrogates remain to be validated against direct clinical endpoints for the setting of etiological cure from hepatitis C virus (HCV).

Aims & Methods

We retrospectively analyzed HCV cACLD patients with paired liver stiffness measurement (LSM) before (BL, all LSM≥10kPa) and after (FU) HCV-cure by interferon-free therapies from 15 European centers. The cumulative incidence of hepatic decompensation was compared according to these criteria by competing risk regression analyses, considering hepatocellular carcinoma and non-liver-related death as competing risks.

Results

2314 patients followed for a median of 6 years were analyzed. Median BL-LSM was 16.6kPa with 37% showing BL-LSM ≥20kPa. After HCV-cure, FU-LSM decreased to a median of 11.0kPa (<10kPa: 990 [43%]; ≥20kPa: 462 [20%]) translating into a median LSM-change of -5.3 (-8.7-[-2.3])kPa corresponding to -33.7 (-47.8-[-15.6])%.
Patients meeting criteria for a clinically significant decrease in LSM (<10kPa: n=990 [43%], ≥20% and <20kPa: n=518 [22%]) had a 10-times lower risk of hepatic decompensation (subdistribution hazard ratio [SHR]: 0.10 [95%CI: 0.04-0.30], p<0.001). However, these risk differences were primarily driven by a negligible risk in patients with FU-LSM <10kPa (cumulative incidence at 6 years [6y-CI]: 0.3%; incidence rate [IR] 0.06/100 patient years [py]) compared to a high risk in patients with FU-LSM ≥20kPa (6y-CI: 12.2%; IR: 3.14/100py). Patients with FU-LSM of 10-19.9kPa (37%) also showed a rather low risk of hepatic decompensation (6y-CI:1.8%; IR: 0.30/100py), and importantly, their decompensation risk did not differ between those with/without an LSM-decrease ≥20% (p=0.370).

Conclusion

Dynamics in BL-LSM to FU-LSM provide limited incremental information over a single static FU-LSM for risk stratification after HCV-cure. The latter should guide clinical decision-making.

Introduction

The number of individuals who will be treated for and cured from HCV infection world-wide is expected to exceed 1 million per year for the next decade. In those with compensated advanced chronic liver disease (cACLD), the risks of de-novo hepatocellular carcinoma (HCC) and hepatic decompensation are decreased but not completely abolished by HCV-cure. Thus, risk stratification is key to decrease resource utilization by individualizing post-treatment management. We evaluated whether the incidences of HCC and hepatic decompensation decrease with time after HCV-cure and whether the discriminatory ability of a one-time post-treatment assessment is maintained during long-term follow-up.

Aims & Methods

We retrospectively analyzed cACLD patients with paired liver stiffness measurement (LSM) & platelet count (PLT) before and after HCV-cure by interferon-free therapies from 7 European regions. Cumulative incidence curves were used to estimate the incidence of hepatic decompensation/HCC over time in the overall group and throughout previously defined risk strata: Baveno VII criteria for clinically significant portal hypertension after HCV-cure (CSPH excluded: FU-LSM <12kPa & FU-PLT >150G/L; CSPH ruled-in: FU-LSM ≥25kPa), and Semmler et al., J Hepatol 2022 (algorithm based on age, LSM, albumin and alcohol consumption) for HCC.

Results

2347 patients (mean age 60±12 years, 60% male, 21% obese, 21% diabetes) with a median LSM of 16.3kPa (IQR: 12.1-24.5, 25% ≥25kPa) before HCV-cure were followed for a median of 6.0 years after treatment. Interestingly, the incidence of first hepatic decompensation was strictly linear with 65 patients (2.8%) developing hepatic decompensation before eventually being diagnosed with HCC (incidence rate 0.57/100 patient years, incidence at 6 years: 3.1%). Similarly, incidence of HCC was also linear with 184 patients (7.8%) developing HCC (incidence rate 1.60/100 patient years, incidence at 6 years: 8.3%). Stratifying the risks for hepatic decompensation according to Baveno VII identified patients with a distinct prognosis during long-term follow-up (incidence at 6 years: 0.3% [CSPH excluded] vs. 2.1% [Gray-zone] vs. 15.6% [CSPH ruled-in]). Similarly, cumulative HCC incidence at 6 years was 15.8% in the high-risk group vs. 5.4% in the low-risk group according to Semmler et al. Results were similar when limiting prediction to events occurring >3 years after HCV-cure.

Conclusion

In patients with cACLD, the risks of hepatic decompensation, and more importantly, HCC remain constant after HCV-cure, even in the long-term (>3 years). A one-time post-treatment risk stratification based on non-invasive criteria confers important prognostic information that is maintained during long-time follow-up, as the hazards over time remain proportional.

Introduction

According to Baveno VII, non-invasive-based criteria is useful to rule in or out for clinically significant portal hypertension (CSPH) in advanced chronic liver disease (ACLD). Liver stiffness measurement (LSM) and platelet count (PLT) are the two parameters considered in this field, particularly LSM≥25 kPa is highly predictive for CPSH, while LSM ≤15 kPa plus PLT ≥150 G/L exclude CSPH. Spleen Stiffness Measurement (SSM) can be used in ACLD patients, identifying patients with a low probability (SSM<40 kPa) of having high-risk varices.

Aims & Methods

The aim of our study is to explore the utility of SSM in predicting endoscopic signs of portal hypertension and its added value compared to LSM and platelet count. This retrospective study was conducted at the University of Naples “Federico II”. All patients with ACLD (for any etiologies) with at least LSM≥10 who underwent esophagogastroduodenoscopy (EGD) for portal hypertension assessment within one year before Spleen Stiffness measurement were enrolled. Exclusion criteria were patients < 18 yrs, PLT>150*10³/cc, liver transplantation, HCC patients, portal vein thrombosis and incomplete data. The study population was divided in three groups: the first includes patients with LSM≥25, the second patients with LSM≥15 and <25 and the third patients with LSM≥10 and <15.

Results

Sixty-nine patients (41 male, mean age 62.7±14.8 years old) were recruited. The main etiology was virus-related (30 patients, 43.4%) followed by metabolic (13 patients, 18.8%), alcohol (12 patients, 17.4%), autoimmune (7 patients, 10.1%) and other (7 patients, 10.1%). Fifty-five patients were Child A and 14 patients were Child B. Overall, mean LSM was 24.7±12.9 kPa, mean SSM was 59.8±23.5 kPa and mean PLT count was 102±50*10³/cc. The groups were composed by 25, 27 and 17 patients, respectively. Eighteen out of 25 patients (69.2%) belonging to the first group had endoscopic sign of PH and almost all of them (17/18, 94.4%) had SSM≥40kPa. In the second group a lower rate of endoscopic sign of PH was found (14/27, 51.8%), although SSM had a high diagnostic performance (100%). Finally, in the third group, in which according to Baveno VII the pre-test probability of CSPH is low, 5 out of 17 (29.4%) had endoscopic sign of PH and, among them, 60% of patients (3/5) had SSM>40kPa. Indeed, SSM demonstrated a better positive correlation with the presence of endoscopic sign of PH (Pearson coefficient r=0.4) then LSM (r=0.3).

Conclusion

SSM enhances the diagnostic performance of LSM and PLT assessment proposed by Baveno VII in predicting portal hypertension in patients with ACLD.

Introduction

Since the advent of the BAVENO VII consensus, Transient elastography (Fibroscan) has taken on a key role in the assessment of clinically significant portal hypertension (CSPH) and the prediction of decompensation and death. A liver stiffness measurement (LSM) ≤ 15 kPa associated with platelets ≥ 150 G/L excludes CSPH (NPV > 90%), while a LSM > 25 kPa is very much in favor of CSPH (PPV > 90%). CSPH remains possible in non-obese patients with LSM between 20 and 25 kPa with platelets < 150 G/L or LSM between 15 and 20 kPa with platelets < 110 G/L) but with a 40% risk of error.

Aims & Methods

We conducted this study to evaluate the reliability of transient elastography (TE) and platelet count in the diagnosis of CSPH, and to determine the extent of adherence to the consensus recommendations in our center.
This is a monocentric and retrospective study made in the gastroenterology and hepatology department of Mohamed Taher Maamouri Hospital in Nabeul, Tunisia, in which we collated reports of Fibroscans performed from March 2023 to March 2024.
We excluded patients with etiologies other than viral, alcoholic, or non-obese non-alcoholic steatohepatitis (NASH).
Platelet count and upper gastrointestinal endoscopy (EGD) data (if performed) were collected.
Data were entered and analyzed using SPSS version 27 software, with a significance level of 0.05.

Results

One hundred and fifty-nine Fibroscans were performed, of which 127 were included.
Women accounted for 64.6%, with a M/F sex ratio of 0.55. Mean age was 55.13 years [20-83].
The indications for Fibroscan were distributed as follows: 53.5% (68 patients) for non-obese NASH, 33.1% (42 patients) for HBV, 11.8% (15 patients) for HCV and only 2 cases for chronic ethylism.
The mean LSM value was 6.45 kPa [2-41.5], with thresholds distributed as follows; LSM <5 kPa in 70 patients (55.1%), LSM between 5 and 10 kPa in 44 patients (34.6%), LSM between 10 and 15 kPa in seven patients (5.5%), LSM between 15 and 20 kPa in two patients (1.6%), LSM between 20 and 25 kPa in a single patient, and LSM >25 kPa in three patients (2.4%).
The mean platelet count was 220 G/L [20-440], with a count > 150 G/L in 111 patients (87.4%), a count between 110 and 150 G/L in 13 patients (10.2%) and a count < 110 G/L in 3 patients.
Of all patients, 24 FOGDs were performed. Signs of Portal hypertension (PH) were noted in only 5 cases, represented by grade I esophageal varices.
In analytical study, hepatic elastography and platelet count were significantly correlated with the presence of endoscopic PH (p=0.009). Indeed, among patients with signs of endoscopic PH, 60% had a LSM > 25 kPa, 20% had a LSM between 15 and 20 kPa with a platelet count < 110 G/L and only 20% had a LSM < 10 kPa.
Furthermore, the consensus recommendations for the indication or not of EGD were not respected in our center (p=0.004); of all endoscopies performed 87.5% (21 EGD) were not indicated, and we noted one case where EGD was indicated but not performed.

Conclusion

Our study highlighted the recommendations of the latest BAVENO VII consensus regarding the reliability of transient elastography and platelet count in the evaluation of CSPH (p=0.009). This must be taken into consideration by practitioners in order to implement adequate preventive measures and to rationalize the indication of EGD which remains an inconvenient procedure for our patients.

Introduction

Portal hypertension is a major complication of advanced chronic liver disease (ACLD) and is associated with gastro-oesophageal varices, a leading cause of morbidity and mortality. The British Society of Gastroenterology (BSG) recommends oesophagogastroduodenoscopy (OGD) for variceal screening in all patients with cirrhosis, which could result in a high volume of unnecessary procedures. Given increasing demands on NHS services and the need for cost-effective resource allocation, strategies to reduce unnecessary endoscopy are critical.
The Baveno VI and VII consensus workshops propose non-invasive criteria to optimise variceal screening. Baveno VI suggests that patients with a liver stiffness measurement (LSM) less than 20 kPa and a platelet count greater than 150×10⁹/L can safely avoid OGD. Baveno VII further refines this by recommending non-selective beta-blocker (NSBB) therapy in patients with clinically significant portal hypertension (CSPH), defined as LSM greater than 25 kPa, thereby eliminating the need for screening endoscopy in this group. For patients not clearly stratified by Baveno VI or VII criteria, splenic stiffness measurement (SSM) offers an additional non-invasive tool to refine risk assessment. Incorporating SSM in this intermediate-risk group may further reduce the need for OGD, with recent data showing a high negative predictive value for ​ruling out high-risk varices.

Aims & Methods

We aim to quantify the reduction in endoscopy burden achieved by applying Baveno VI and VII criteria in ACLD patients.
A retrospective analysis was conducted on 1,703 patients who underwent 1,802 FibroScans between January 1, 2024, and December 31, 2024. Patients were stratified based on LSM and platelet counts into the following categories:
1. BSG Criteria: All patients with LSM ≥10 kPa requiring OGD.
2. Baveno VI Criteria: Patients with LSM <20 kPa and platelet count ≥150×10⁹/L, for whom OGD could be safely avoided.
3. Baveno VII Criteria: Patients with CSPH (LSM ≥25 kPa) recommended for NSBB therapy without the need for screening OGD.
4. Patients requiring OGD: Those not meeting Baveno VI criteria and without CSPH.

Results

Liver stiffness distribution:
• <10 kPa: 1,534 patients
• 10–14.9 kPa: 136 patients
• 15–19.9 kPa: 44 patients
• 20–24.9 kPa: 31 patients
• ≥25 kPa: 57 patients
Impact of Adopting Baveno VI and VII:
• BSG Guidelines: 274 patients (LSM ≥10 kPa) would require OGD.
• Baveno VI: 149 patients (LSM <20 kPa, platelets ≥150) could avoid OGD.
• Baveno VII: 57 patients (LSM ≥25 kPa) would be managed with NSBB, avoiding OGD.
• Total Reduction: 206 out of 274 patients (~75%) could avoid OGD.

Conclusion

Adopting Baveno VI and VII criteria would significantly reduce the need for variceal screening endoscopy in ACLD patients. By applying these thresholds, up to 75% of OGDs could be avoided, optimising NHS resources and reducing patient burden. These findings support the routine use of non-invasive risk stratification in ACLD management.

References

1. Tripathi D, Stanley AJ, Hayes PC, et al. UK guidelines on the management of variceal haemorrhage in cirrhotic patients. Gut. 2015;64(11):1680–1704. doi:10.1136/gutjnl-2015-309262
2. de Franchis R, Bosch J, Garcia-Tsao G, et al. Baveno VI Consensus Workshop: Stratifying risk and individualizing care for portal hypertension. J Hepatol. 2015;63(3):743–752. doi:10.1016/j.jhep.2015.05.022
3. de Franchis R, Bosch J, Garcia-Tsao G, et al. Baveno VII – Renewing consensus in portal hypertension. J Hepatol. 2022;76(4):959–974. doi:10.1016/j.jhep.2021.12.022