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Liver Stiffness-Based Risk Prediction Model for Hepatocellular Carcinoma in Patients with Nonalcoholic Fatty Liver Disease.

ABSTRACT: Non-alcoholic fatty liver disease (NAFLD) is associated with an increased hepatocellular carcinoma (HCC) risk. We established and validated a liver stiffness (LS)-based risk prediction model for HCC development in patients with NAFLD. A total of 2666 and 467 patients with NAFLD were recruited in the training and validation cohorts, respectively. NAFLD was defined as controlled attenuated parameter ≥238 dB/m by transient elastography. Over a median of 64.6 months, HCC developed in 22 (0.8%) subjects in the training cohort. Subjects who developed HCC were older and had higher prevalence of diabetes and cirrhosis, lower platelet count, and higher AST levels compared to those who did not develop HCC (all p < 0.05). In multivariate analysis, age ≥60 years (hazard ratio (HR) = 9.1), platelet count <150 × 10³/μL (HR = 3.7), and LS ≥9.3 kPa (HR = 13.8) were independent predictors (all p < 0.05) that were used to develop a risk prediction model for HCC development, together with AST ≥34 IU/L. AUCs for predicting HCC development at 2, 3, and 5 years were 0.948, 0.947, and 0.939, respectively. This model was validated in the validation cohort (AUC 0.777, 0.781, and 0.784 at 2, 3, and 5 years, respectively). The new risk prediction model for NAFLD-related HCC development showed acceptable performance in the training and validation cohorts.

SUBMITTER: Lee JS

PROVIDER: S-EPMC8472221 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Non-alcoholic liver disease (NAFLD) defines liver abnormalities ranging from simple steatosis to nonalcoholic steatohepatitis with or without cirrhosis development, occurring in the absence of significant alcohol consumption, use of teratogenic medication, or hereditary disorders. The association between NAFLD and metabolic syndrome is well documented and widely recognized. Obesity, type 2 diabetes mellitus (T2DM), and dyslipidemia are the most common metabolic risk factors associated with NAFLD. Among the components of metabolic syndrome, current evidence strongly indicates obesity and diabetes as hepatocellular carcinoma (HCC) risk factors. There is also growing evidence that suggests an increased risk of HCC in NAFLD patients, even surpassing other etiologies in some high-income countries. Epidemiologic data demonstrate a parallel rise in prevalence of obesity, diabetes, NAFLD, and HCC. As obesity and its related diseases have steadily afflicted larger populations, HCC incidence is expected to increase in the future. Pathophysiologic mechanisms that underlie NAFLD development and subsequent progression to nonalcoholic steatohepatitis and cirrhosis (insulin resistance and hyperinsulinemia, oxidative stress, hepatic stellate cell activation, cytokine/adipocytokine signaling pathways, and genetic and environmental factors) appear to play a significant role in the development of NAFLD-related HCC. However, a comprehensive view of molecular mechanisms linking obesity, T2DM, and NAFLD-related HCC, as well as the exact sequence of molecular events, is still not understood in its entirety. Good-quality data are still necessary, and efforts should continue towards better understanding the underlying carcinogenic mechanisms of NAFLD-related HCC. In this paper, we aimed to centralize the most important links supporting these relationships, focusing on obesity, T2DM, and NAFLD-related HCC, as well as point out the major gaps in knowledge regarding the underlying molecular mechanisms behind them.

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Liver Stiffness-Based Risk Prediction Model for Hepatocellular Carcinoma in Patients with Nonalcoholic Fatty Liver Disease.

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