Discussion
death, non-cirrhotic ACLF, end-stage liver disease, inflammation, cirrhosis, sarcopenia, abrupt hepatic deterioration, liver disease, organ failure, NAFLD, hepatic fibrosis, CLD, cirrhosis in non-cirrhotic HBV-ACLF
INFLAMMATION, CIRRHOSIS, SARCOPENIA, LIVER FIBROSIS, LIVER DISEASE, MALNUTRITION, OXIDATIVE STRESS, CLD
To our knowledge, this is the first research to exam how PMI could affect non-cirrhotic HBV-ACLF patients' long-term (1 year) progression to cirrhosis. Our research suggests that a higher PMI at L3 may prevent the development of cirrhosis. We have also developed a PMI-based nomogram for cirrhosis risk stratification in HBV-ACLF patients. This nomogram demonstrated good predictive performance for the occurrence of cirrhosis in non-cirrhotic HBV-ACLF patients at baseline. By weighing the likelihood of cirrhosis occurrence, these patients can be identified in advance and individualized clinical management could be optimized during the recovery.Despite the fact that there is no consensus definition for ACLF, it is widely acknowledged to be a complicated clinical condition marked by abrupt hepatic deterioration in CLD, along with organ failure and substantial short-term death ratesSarcopenia, a form of malnutrition, can affect up to 70% of advanced liver disease patientsThe underlying biological mechanism linking sarcopenia to ACLF progression remains incompletely understood. However, evidence suggests that ACLF is accompanied by intense systemic inflammation and oxidative stress, which can disrupt the delicate equilibrium between protein synthesis and breakdownAge is a primary and immutable risk factor for the advancement of CLD, such as NAFLD, hepatic fibrosis, cirrhosis, and liver cancerIn this study, we discovered that PMI-based nomograms outperformed MELD and MELD-Na scores at predicting the long-term risk of cirrhosis in patients with non-cirrhotic HBV-ACLF. This may be explained by the fact that MELD and MELD-Na scores are designed for those with severe end-stage liver disease, while our study included non-cirrhotic ACLF patients. This could also be due to the strong association reported between sarcopenia and cirrhosis, which was neglected by MELD and MELD-Na scores. The nomogram can effectively guide the frequency of the follow-up and the decision related to initiation of nutritional intervention. Higher nomogram scores might lead to recommendations for more frequent follow-up and more aggressive nutritional intervention for greater benefit. Our DCA results indicated that more patients with HBV-ACLF could benefit from the timely and appropriate treatment when the threshold probability of the nomogram was > 3%.The current study has certain limitations. First, it was retrospective in nature, thus resulting in inherent bias in the results. Second, all the subjects and their clinical information were obtained from a single center and external validation was lacking. Third, this study only analyzed the possible effect of baseline PMI on outcome, but the dynamic alterations of PMI were not taken into consideration. Lastly, the liver status prior to ACLF, particularly the extent of liver fibrosis, affects the risk of cirrhosis during the recovery period. Unfortunately, this study lacks data on this aspect. Therefore, the impact of PMI on the prognosis of ACLF lacks adequate assessment. Hence, multicenter prospective studies could be performed in future to further verify the robustness and applicability of our conclusions.In summary, our study revealed that among non-cirrhotic HBV-ACLF patients, a lower PMI is independently correlated with the development of cirrhosis. The PMI-based nomogram can be a useful tool for assessing the likelihood of cirrhosis in non-cirrhotic HBV-ACLF patients at 1 year.