Dear Editor,
We read with great interest the recent study by Wang et al. published in
Clinical and Molecular Hepatology, which prospectively validated the Baveno VI-spleen stiffness measurement (SSM) model for stratifying portal hypertension-related risk in hepatitis B virus (HBV)-related compensated cirrhosis. The study provides timely insight into noninvasive strategies to guide esophagogastroduodenoscopy (EGD) decisions and longitudinal patient monitoring [
1]. However, as the field moves toward personalized and etiologyspecific cirrhosis management, we believe that several critical aspects of the study methodology and interpretation warrant further scrutiny and refinement.
The current study confirms that a single baseline Baveno VI-SSM assessment (liver stiffness measurement [LSM] <20 kPa, platelet count [PLT] >150×10
9/L, and SSM ≤40 kPa) reliably identifies low-risk patients who can avoid EGD. However, this binary stratification framework based on rigid thresholds may not adequately capture the progressive and dynamic nature of portal hypertension. Portal hypertension is not dichotomous—it progresses along a clinical continuum. Patients just above or just below a given cutoff (e.g., SSM 41 kPa vs. 39 kPa) may have overlapping clinical trajectories, yet be classified differently. In this study, the sharp binary design may have inflated perceived model accuracy. In addition, LSM and SSM values may fluctuate due to technical factors (probe pressure, variability in spleen size), transient inflammation, or hemodynamic shifts-especially in patients on active antiviral treatment. Recent studies have demonstrated the superiority of continuous risk prediction models over rule-based cutoffs. For example, Berzigotti et al. proposed the integration of LSM with albumin and bilirubin in continuous scales to predict hepatic decompensation in Asian cohorts [
2]. Similarly, recent machine learning approaches combining elastography, laboratory indices, and antiviral response markers have shown improved area under the curves over traditional Baveno criteria [
3]. We suggest that future iterations of the Baveno VI-SSM model consider a continuous, weighted risk score that integrates LSM, SSM, PLT, alanine aminotransferase (ALT) trends, and treatment response. This would provide greater granularity, reduce misclassification around cutoffs, and be consistent with the principles of precision hepatology.
The study adopts a uniform 6-month reassessment interval for transient elastography and SSM, consistent with the Baveno VII guidelines. However, longitudinal data from this cohort raise questions about the utility and cost-effectiveness of this approach. Of the 270 patients with favorable Baveno VI SSM status at baseline, only 28 (10.4%) transitioned to unfavorable status during follow-up, suggesting that the majority may not benefit from such frequent surveillance. Moreover, among these 28 patients, decompensation remained rare—raising the question of whether they were truly at high clinical risk or merely crossing an arbitrary threshold due to measurement noise. Rather than applying a one-size-fits-all reassessment interval, we advocate a risk-adapted monitoring strategy. Patients with SSM levels approaching 40 kPa, decreasing platelet trends, or intermittent ALT elevations (reflecting residual necroinflammation) may be candidates for more frequent monitoring (e.g., every 6 months), whereas those with robustly low LSM/SSM levels and stable labs could safely extend follow-up to 12 or even 18 months. Such staged follow-up, similar to current surveillance practices for hepatocellular carcinoma, could improve efficiency without compromising safety, especially in health systems with limited access to transient elastography.
The exclusive inclusion of HBV-related cirrhosis, while methodologically sound to minimize etiologic heterogeneity, limits the generalizability of the findings. HBV cirrhosis typically follows a different natural history than alcohol-related liver disease or metabolically associated steatotic liver disease, both of which are increasing worldwide and differ in their fibrotic architecture, hemodynamic profiles, and inflammatory patterns. Several studies have shown that portal hypertension may occur earlier and at lower LSM levels in metabolically associated steatotic liver disease-related cirrhosis than in viral etiologies.4 Similarly, SSM dynamics may vary with splenic congestion patterns unique to alcohol-related liver disease. Therefore, the Baveno VISSM thresholds validated in an HBV-specific cohort may not translate seamlessly to non-HBV populations. Prospective, multicenter validation studies including mixed etiologies— and ideally comparing the performance of etiologyspecific cutoffs—are urgently needed. This would allow adaptation of Baveno-based strategies to the changing epidemiology of cirrhosis and ensure equity of care across diverse patient populations.
The study shows that patients with unfavorable Baveno VI-SSM status—particularly those with high-risk varices identified by follow-up EGD—have a significantly increased risk of decompensation (up to 42.8 per 1,000 personyears). However, the study stops short of proposing a management pathway for these high-risk individuals. While nonselective beta blockers (NSBBs) remain the mainstay of high-risk varices prophylaxis, real-world data show that adherence is often suboptimal due to contraindications, intolerance, or physician inertia [
5]. Furthermore, not all highrisk patients develop decompensation, and the “treat all” approach may not be efficient or safe. We suggest that future research prioritize the integration of Baveno risk stratification with tailored intervention algorithms, including NSBB initiation thresholds based on longitudinal Baveno VI-SSM status, not just static esophageal varices grade; assessment of response to NSBB using serial transient elastography or SSM, similar to the concept of “functional response” used in hemodynamic monitoring; development of additional risk modifiers, such as sarcopenia or systemic inflammation scores, to refine treatment decisions. By embedding the Baveno VI-SSM model into a dynamic, actionoriented management pathway, clinicians could shift from reactive to preventive strategies, improving patient outcomes while conserving resources.
The study by Wang et al. provides compelling prospective evidence for the utility of the Baveno VI-SSM model in HBV-related cirrhosis. However, the current approach, although methodologically sound, is not without limitations. We advocate: moving from fixed thresholds to continuous, multivariable risk models; implementing risk-adapted surveillance intervals rather than uniform reassessment; extending validation to non-HBV cirrhosis populations; integrating high-risk identification with evidence-based, individualized treatment pathways. These refinements are not merely academic-they are essential to elevating the Baveno VI-SSM model from a stratification tool to a clinically actionable decision framework, ultimately advancing the quality and personalization of cirrhosis care.
FOOTNOTES
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Authors’ contributions
Bo Zheng wrote the manuscript, Lizhou Wang provided methodological and revised the manuscript.
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Conflicts of Interest
The authors have no conflicts to disclose.
Abbreviations
esophagogastroduodenoscopy
liver stiffness measurement
nonselective beta blockers
spleen stiffness measurement
REFERENCES
- 1. Wang H, Liang W, Zhou L, Song J, Wen B, Wu Q, et al. Baveno VI-SSM stratifies the risk of portal hypertension-related events in patients with HBV-related cirrhosis. Clin Mol Hepatol 2025;31:866-880.
- 2. Berzigotti A, Gilabert R, Abraldes JG, Nicolau C, Bru C, Bosch J, et al. Noninvasive prediction of clinically significant portal hypertension and esophageal varices in patients with compensated liver cirrhosis. Am J Gastroenterol 2008;103:1159-1167.
- 3. Singh Y, Faghani S, Eaton JE, Venkatesh SK, Erickson BJ. Deep learning-based prediction of hepatic decompensation in patients with primary sclerosing cholangitis with computed tomography. Mayo Clin Proc Digit Health 2024;2:470-476.
- 4. Berzigotti A, Seijo S, Arena U, Abraldes JG, Vizzutti F, García-Pagán JC, et al. Elastography, spleen size, and platelet count identify portal hypertension in patients with compensated cirrhosis. Gastroenterology 2013;144:102-111.e1.
- 5. Villanueva C, Torres F, Sarin SK, Shah HA, Tripathi D, Brujats A, et al. Carvedilol reduces the risk of decompensation and mortality in patients with compensated cirrhosis in a competingrisk meta-analysis. J Hepatol 2022;77:1014-1025.
Citations
Citations to this article as recorded by
- Correspondence to letter to the editor on “Baveno VI-SSM stratifies the risk of portal hypertension-related events in patients with HBV-related cirrhosis”
Haiyu Wang, Jinjun Chen
Clinical and Molecular Hepatology.2026; 32(2): e238. CrossRef
