00106360

March 16, 2026, 18:54

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Reader’s code: 00106360 Commentary on the Article Impact of metabolic dysfunction-associated steatotic liver disease on liver metastasis and survival in pancreatic cancer The study by Chon HY et al. examines the impact of metabolic dysfunction-associated steatotic liver disease (MASLD) on liver metastasis and survival in patients with Pancreatic Ductal Adenocarcinoma. Using a large retrospective cohort of 2123 patients, the authors assessed hepatic steatosis primarily through the hepatic steatosis index (HSI) and additionally validated findings using CT-based measurements of liver fat. The study found no significant association between MASLD and the presence of liver metastasis at diagnosis or during follow-up, suggesting that hepatic steatosis may not be a key determinant of metastatic spread in pancreatic cancer (Chon et al., 2026). The findings contrast with previous research in other malignancies, such as colorectal and breast cancers, where hepatic steatosis has been reported to influence liver metastasis risk or metastasis-free survival (van Saane et al., 2019; Wu et al., 2020). In the present study, tumor size and elevated CA19-9 levels were the main predictors of liver metastasis, while diabetes mellitus was associated with improved survival outcomes, possibly reflecting earlier detection among diabetic patients (Chon et al., 2026). Critical Appraisal of the Study The study by Chon HY and colleagues evaluates the relationship between metabolic dysfunction-associated steatotic liver disease (MASLD) and liver metastasis in patients with Pancreatic Ductal Adenocarcinoma. Using a large retrospective cohort of 2123 patients, the authors investigated whether hepatic steatosis, measured by the hepatic steatosis index (HSI), influences the development of liver metastasis and overall survival. Strengths One of the major strengths of this study is its large sample size and long study period (2006–2021), which enhances the statistical power and reliability of the findings. The authors used robust statistical methods, including logistic regression and Cox proportional hazards models, to analyze risk factors for both baseline and newly developed liver metastases. Another notable strength is the additional CT-based validation in a subgroup of patients, which helps corroborate the HSI-based assessment of hepatic steatosis. The study also carefully adjusted for multiple potential confounders such as age, BMI, diabetes, lipid profile, tumor size, and CA19-9 levels. Limitations Despite these strengths, several limitations should be considered. First, the retrospective design limits the ability to establish causal relationships. Second, the primary assessment of hepatic steatosis relied on the HSI, an indirect surrogate marker derived from BMI and liver enzyme ratios, which may be influenced by cancer-related factors such as cachexia, inflammation, or biliary obstruction. Third, important pathological variables (e.g., lymph node status, lymphovascular invasion, and perineural invasion) were not consistently available and therefore could not be included in the multivariate models. Additionally, the CT-based validation was limited to a subset of patients, which may introduce selection bias. Clinical Implications Clinically, the findings suggest that MASLD may not be a significant determinant of liver metastasis in pancreatic cancer, contrasting with observations in other malignancies. Instead, established markers such as tumor size and elevated CA19-9 levels appear to remain more reliable predictors of metastatic risk and mortality. These results highlight the aggressive biological behavior of pancreatic cancer, where tumor-driven mechanisms may outweigh the influence of underlying hepatic metabolic conditions. Future prospective studies incorporating advanced imaging, histologic confirmation, and molecular analysis of the tumor–liver microenvironment are needed to further clarify the role of MASLD in pancreatic cancer progression. Despite its strengths, including a large sample size and robust statistical modeling, the retrospective design and reliance on HSI rather than histologic confirmation limit the ability to establish causality. Nevertheless, this study contributes important evidence suggesting that the relationship between MASLD and metastasis may be cancer-specific and biologically complex. Reference Chon HY, Rhee H, Kim J, et al. Impact of metabolic dysfunction-associated steatotic liver disease on liver metastasis and survival in pancreatic cancer. World Journal of Gastroenterology. 2026;32(11):115488. van Saane AM, et al. Non-alcoholic fatty liver disease and colorectal liver metastasis risk. Liver International. 2019. Wu W, et al. Hepatic steatosis and liver metastasis-free survival in breast cancer. Cancer Medicine. 2020.