Rethinking sustained recompensation in MASLD cirrhosis: The value of pharmacological maintenance

To the editor, We read with great interest the highly valuable study by Jiménez-Masip et al1 evaluating hepatic recompensation in decompensated metabolic dysfunction–associated steatotic liver disease (MASLD) cirrhosis. Among their critical findings, one observation prompts a necessary re-evaluation of how we define clinical success: sustained recompensation was uniquely associated with the complete absence of liver transplantation and liver-related mortality. At its core, portal hypertension is the fundamental mechanistic engine driving all primary decompensation phenotypes, including portal hypertension-related bleeding (PHB), ascites, and hepatic encephalopathy (HE). While PHB is an acute hemodynamic event driven by critically elevated portal pressure, recurrent ascites and HE frequently signal an additional transition into advanced liver dysfunction, marked by the severe exhaustion of synthetic capacity and detoxification mechanisms. Therefore, when patients achieve the sustained recompensation observed by the authors to universally prevent mortality and transplantation, this clinical state essentially reflects controlled portal pressure without advanced liver dysfunction—a state where the clinical manifestations of decompensation are effectively suppressed, even if the underlying fibrotic architecture remains largely intact. For this reason, we strongly endorse the authors’ proposition—echoing the expanded criteria proposed by Tonon et al2—to challenge the rigidly strict approach of the Baveno VII consensus.3 As the authors astutely note, the positive prognostic effects of recompensation occur even with low-dose treatment. From a pathophysiological standpoint, this observation is entirely sound. Clinicians may safely maintain patients in a hemodynamically stable state using non-selective beta-blockers, while concurrently managing fluid balance with low-dose diuretics and supporting nutritional and synthetic reserves with branched-chain amino acids. Because this pharmacological maintenance effectively controls the hemodynamic drivers and prevents recurrent decompensation, mandating strict medication withdrawal lacks a sound pathophysiological rationale. The continuous need for these baseline medications should indeed not disqualify a patient from being considered sustainably recompensated. The authors’ data strongly suggest that the absence of recurrent decompensation events is the true prognostic marker of survival. While emerging metabolic therapies—such as glucagon-like peptide-1 receptor agonists or targeted agents like resmetirom—hold future promise, there is currently no established evidence proving their disease-modifying efficacy specifically in MASLD cirrhosis.4,5 Until robust prospective trials validate these novel agents in this population, clinical management must pragmatically rely on sustained pharmacological stabilization. We commend Jiménez-Masip et al for highlighting the paramount importance of sustained recompensation in MASLD cirrhosis. Their findings strongly support refining future criteria. Rather than demanding complete medication withdrawal as a prerequisite, the definition must pragmatically embrace pharmacologically sustained clinical stability as the most essential and meaningful prognostic endpoint for these vulnerable patients.