Explainable Retinal Imaging for Prediction of Multi-Organ Dysfunction in Type 2 Diabetes
可解释的视网膜成像用于预测2型糖尿病多器官功能障碍
Mini Han Wang, Liting Huang, Wei Hong, Boonthawan Wingwon
AI总结 本研究利用常规实验室生物标志物构建系统级异常指数,通过梯度提升模型预测2型糖尿病多系统失调,并采用SHAP实现可解释性,揭示了高血糖、肾功能障碍、血脂异常和炎症是主要驱动因素。
Comments 15 pages, 8 figures
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背景:2型糖尿病(T2DM)日益被认为是一种以代谢、肾脏、脂质和炎症通路协调功能障碍为特征的系统性疾病。现有的临床评估往往无法捕捉这种多维度负担。方法:我们对1,195名患者进行了回顾性研究,使用了常规收集的实验室生物标志物。构建了系统级异常指数以量化器官特异性功能障碍,并将多系统受累定义为两个或以上系统异常。训练了包括逻辑回归、随机森林和梯度提升在内的监督机器学习模型来预测多系统失调。使用SHapley Additive exPlanations(SHAP)实现模型可解释性。结果:梯度提升模型表现出近乎完美的区分能力(AUC = 1.000),显著优于逻辑回归(AUC = 0.925)。特征归因分析显示,高血糖、肾功能障碍、血脂异常和炎症是多系统风险的主要驱动因素。部分依赖分析中观察到的剂量-反应关系进一步支持了模型预测的生物学合理性。结论:本研究提出了一个可解释的、数据驱动的框架,用于量化T2DM的系统性疾病负担。通过将常规生物标志物与多器官功能障碍联系起来,我们的方法提供了预测准确性和机制洞察,为糖尿病护理中的风险分层和精准医学提供了潜力。本研究中使用的数据和代码可在GitHub上公开获取:https://github.com/MiniHanWang/Type-2-Diabetes-1.git
Background: Type 2 diabetes mellitus (T2DM) is increasingly recognised as a systemic disease characterised by coordinated dysfunction across metabolic, renal, lipid, and inflammatory pathways. Existing clinical assessments often fail to capture this multi-dimensional burden. Methods: We conducted a retrospective study of 1,195 patients using routinely collected laboratory biomarkers. System-level abnormality indices were constructed to quantify organ-specific dysfunction, and multi-system involvement was defined as abnormalities in two or more systems. Supervised machine learning models, including logistic regression, random forest, and gradient boosting, were trained to predict multi-system dysregulation. Model interpretability was achieved using SHapley Additive exPlanations (SHAP). Results: The gradient boosting model demonstrated near-perfect discrimination (AUC = 1.000), significantly outperforming logistic regression (AUC = 0.925). Feature attribution analysis revealed that hyperglycaemia, renal impairment, dyslipidaemia, and inflammation were the dominant drivers of multi-system risk. Dose-response relationships observed in partial dependence analyses further supported the biological plausibility of model predictions. Conclusion: This study presents an interpretable, data-driven framework for quantifying systemic disease burden in T2DM. By linking routine biomarkers to multi-organ dysfunction, our approach provides both predictive accuracy and mechanistic insight, offering potential for improved risk stratification and precision medicine in diabetes care. The data and code used in this study are openly available on GitHub at: https://github.com/MiniHanWang/Type-2-Diabetes-1.git