Introduction Although steatotic liver disease (SLD) is a dynamic condition, the prognostic impact of subtype transitions over time remains unclear. We investigated the association between SLD subtype transitions and the risk of long-term liver-related events (LREs).
Methods From the Korean National Health Insurance Service database, adults who underwent national health checkups in both 2015 and 2017 were recruited. SLD subtypes included metabolic dysfunction–associated SLD, metabolic and alcohol-related SLD, and alcohol-related liver disease. Transitions were classified into no transitions, transitions to more advanced subtypes, and transitions to less advanced subtypes. LREs included incident cirrhosis, hepatocellular carcinoma, liver transplantation, and liver-related mortality. Subdistribution hazard ratios (sHRs) were estimated using Fine–Gray competing-risk models.
Results Among 1,988,878 individuals, 21.7% transitioned over two years: 11.3% transitioned to more advanced subtypes, whereas 10.4% transitioned to less advanced subtypes. In each SLD subtype, transitions to more advanced subtypes showed a higher risk of LREs, whereas transitions to less advanced subtypes showed a lower risk of LREs. In SLD, the transitions to more advanced subtypes showed a higher risk of LREs (sHR, 1.34; 95% confidence interval [CI], 1.28–1.40), whereas transitions to less advanced subtypes showed a lower risk (sHR, 0.86; 95% CI, 0.83–0.88). Sensitivity analyses stratified by sex, BMI, and a fatty liver index threshold of >60 demonstrated comparable findings.
Conclusion We found that transitions to more advanced SLD subtypes showed increased risks of LREs, whereas transitions to less advanced subtypes showed risk reduction. The findings highlight the need for management schemes considering SLD subtype changes over time.
Hepatitis B flare is a common complication of chronic hepatitis B and is defined as an increase in HBV viral load associated with abnormal alanine aminotransferases (ALT), the consensus being an ALT level ≥5 times the upper limit of normal. The immunopathogenesis is related to induction of inflammatory cells and cytokines by the rise in HBV DNA. There are multiple causes of flares, and they carry the risk of progression to hepatic decompensation and acute-on-chronic liver failure (ACLF) with associated mortality, potentially requiring liver transplantation. Initial assessment should exclude other causes of liver dysfunction and determine severity and prognosis. General prognostic models of ACLF are useful but the COSSH-ACLF II score is specific to HBV. Early initiation of nucleos(t)ide analogues is crucial, even in severe HBV flares; it can reduce mortality by 73.6%. Once jaundice and coagulopathy occur, salvage by antivirals is challenging, and liver transplantation should be considered. However, many patients may not be suitable candidates for transplant or donor livers may not be available, as is common in Asia. Recently, there has been increasing evidence of the benefits of adjunctive therapies such as corticosteroids and plasma exchange, but there are associated risks and these approaches should be considered rescue therapies in severe HBV flares or ACLF. Liver transplant is the ultimate intervention when these other strategies fail. In summary, HBV flares are clinically serious events that can lead to hepatic decompensation, ACLF, and the need for a donor liver; however, strategies for rescue should be considered before liver transplantation.
Prediction Model for Familial Aggregated HBV‐Associated Hepatocellular Carcinoma Based on Serum Biomarkers Linmei Zhong, Guole Nie, Qiaoping Wu, Honglong Zhang, Haiping Wang, Jun Yan Cancer Reports.2025;[Epub] CrossRef
Reply to correspondence on “Hepatocellular carcinoma prediction model performance decreases with long-term antiviral therapy in chronic hepatitis B patients” Beom Kyung Kim Clinical and Molecular Hepatology.2024; 30(4): 1044. CrossRef
Correspondence to editorial on “Hepatocellular carcinoma prediction model performance decreases with long-term antiviral therapy in chronic hepatitis B patients” Xiaoqian Xu, Hong You, Jidong Jia, Yuanyuan Kong Clinical and Molecular Hepatology.2024; 30(4): 994. CrossRef
Acute-on-chronic liver failure is an acute deterioration of liver function manifesting as jaundice and coagulopathy with the development of ascites, with a high probability of extrahepatic organ involvement and high 28-day mortality. The pathogenesis involves extensive hepatic necrosis, which is associated with severe systemic inflammation and subsequently causes the cytokine storm, leading to portal hypertension, organ dysfunction, and organ failure. These patients have increased gut permeability, releasing lipopolysaccharide (LPS) and damage-associated molecular patterns (DAMPS) in the blood, leading to hyper-immune activation and the secretion of cytokines, followed by immune paralysis, causing the development of infections and organ failure in a proportion of patients. Early detection and the institution of treatment, especially in the "Golden Window" period of 7 days, gives an opportunity for reversal of the syndrome. Scores like the Asian Pacific Association for the Study of the Liver (APASL) ACLF research consortium (AARC) score, a model for end stage liver disease (MELD), and the CLIF Consortium acute-on-chronic liver failure (CLIF-C ACLF) score can help in the prediction of mortality. Treatment strategy includes treatment of acute insult. Patients should be considered for early transplant with MELD score >28, AARC score >10, high-grade hepatic encephalopathy, and in the absence of >2 organ failure or overt sepsis to improve survival of up to 80% at five years. Patients, with no option of transplant, can be treated with emerging therapies like faecal microbial transplant, plasma exchange, etc., which need further evaluation.
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