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The manuscript is generally well written and follows a standard structure. The background is comprehensive, with appropriate references establishing the rationale for incorporating pancreatic steatosis (PS) into predictive modeling. Figures and tables are clear, and raw data are provided. However, there are several areas where clarification and refinement would improve clarity:
The definition of “severe chronic organ dysfunction” as an exclusion criterion is vague. Please specify whether this was based on standard scoring systems (e.g., Child–Pugh for liver, NYHA for cardiac function, CKD staging) or on clinician judgment.
The term “mental abnormalities (MAs)” is not adequately defined. Were specific psychiatric/neurological scales used, or was this based on subjective physician assessment?
There are errors in the unit labeling of hematological variables (Tables 1–2, pages 35–39). For example, cell counts are reported with inconsistent unit notation (e.g., ×10⁹/L vs. L/L). These should be standardized.
The study addresses a clinically important problem and introduces a novel PS-based predictive model. The inclusion of over 300 retrospectively collected patients plus a prospective validation cohort strengthens the design. However, methodological details require clarification:
Inter-rater reliability of PS assessment: Two radiologists independently assessed PS using CT attenuation ratios, but the manuscript does not report reliability metrics. Kappa statistics or intraclass correlation coefficients (ICC) should be presented to ensure reproducibility.
CT standardization: The retrospective cohort spans five years. Please clarify whether CT scan acquisition parameters (e.g., slice thickness, machine type, HU calibration) were standardized across time. Inconsistencies may bias PS quantification and model accuracy.
Modeling approach: The multivariate regression method is not described in detail. Please specify whether backward/forward stepwise selection, LASSO, or another approach was used to arrive at the eight final predictors. Clarify why variables significant in univariate analysis (e.g., creatinine, abdominal effusion) were excluded.
The predictive model demonstrates strong discriminative ability (AUC = 0.937 in training; 0.922 in validation) and calibration. Nonetheless, some points should be addressed to support robustness:
AUC comparisons: You state that AUCs were compared with MCTSI, BISAP, and SOFA using a “web tool” (VassarStats). Please specify the statistical test (e.g., DeLong’s test) and report exact p-values.
Therapeutic confounders: Post-admission treatments (lipid-lowering therapy, fluid resuscitation volume, nutritional support) may influence progression to HTG-SAP. These were not adjusted for in the model, which could limit its generalizability. Please discuss.
Practicability: For an acute condition like pancreatitis, model usability depends not only on accuracy but also on the speed of variable acquisition. Please indicate how quickly each included variable (RR, D-dimer, BUN, Ca²⁺, pH, imaging findings) can be obtained in clinical practice, compared with other scoring systems. A table summarizing “time to availability” would be valuable.
The discussion provides a solid overview of pathophysiology, but would benefit from refinement:
Expand on the mechanistic links between PS and pancreatic injury. While you reference lipid toxicity and inflammation, a deeper discussion of how PS sensitizes the pancreas to HTG-related injury (e.g., impaired microcirculation, enhanced lipotoxicity, stellate cell activation) would strengthen the biological plausibility.
The discussion could be more coherent by organizing findings around: (a) epidemiology of HTG-AP, (b) rationale for PS as a predictor, (c) performance of the model vs. existing scores, and (d) clinical application and limitations. This will improve logical flow and clinical impact.
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The conclusion of the article is not completely consistent with the title and purpose of the research article. The title overly emphasizes the role of pancreatic steatosis, while in the conclusion, pancreatic steatosis is only one of the risk factors. I suggest modifying the title of the article.
1. In the Methods, Assessment of PS by CT, "The round ROIs were placed away from necrotic or tumorous areas to minimize bias."(Line 162). Does the case of pancreatitis in the article include pancreatic cancer?
2. The relationship between pancreatic steatosis and the severity of pancreatitis is not discussed enough.
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