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高脂血症性胰腺炎的病理机制与综合管理研究进展
Advances in Pathological Mechanisms and Comprehensive Management of Hyperlipidemic Pancreatitis

DOI: 10.12677/acm.2025.153827, PP. 1975-1983

Keywords: 高脂血症性胰腺炎,游离脂肪酸,血液净化,靶向治疗,精准管理
Hyperlipidemic Pancreatitis
, Free Fatty Acids, Plasmapheresis, Targeted Therapy, Precision Management

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Abstract:

高脂血症性胰腺炎(HLP)是急性胰腺炎的重要亚型,占所有病例的12%~20%,以血清甘油三酯(TG)急剧升高(≥11.3 mmol/L)为特征,病死率高达20%~30%。其核心机制涉及脂质代谢异常、游离脂肪酸(FFA)介导的线粒体损伤、炎症级联反应及微循环障碍,遗传因素(如LPL、APOC2基因突变)与代谢性疾病(糖尿病、肥胖)显著增加复发风险。急性期治疗以胰岛素联合低分子肝素降脂为主,血液净化技术(血浆置换、双重滤过)可快速清除TG及炎症介质;长期管理需强化血脂控制(TG < 2.3 mmol/L),结合贝特类药物、靶向治疗(ApoC3抑制剂、ANGPTL3单抗)及生活方式干预。本文系统阐述HLP的病理生理机制、治疗策略及复发防控,强调个体化精准管理的重要性,为临床实践提供理论依据。
Hyperlipidemic pancreatitis (HLP), accounting for 12%~20% of acute pancreatitis cases, is characterized by a rapid increase in serum triglycerides (TG ≥ 11.3 mmol/L) with a mortality rate of 20%~30%. Its pathogenesis involves lipid metabolism disorders, free fatty acid (FFA)-mediated mitochondrial dysfunction, inflammatory cascades, and microcirculatory disturbances, while genetic factors (e.g., LPL and APOC2 mutations) and metabolic diseases (diabetes, obesity) significantly increase recurrence risk. Acute-phase management focuses on insulin combined with low molecular weight heparin for lipid reduction, supplemented by plasmapheresis or double-filtration plasmapheresis to rapidly clear TG and inflammatory mediators. Long-term strategies require strict lipid control (TG < 2.3 mmol/L) through fibrates, targeted therapies (ApoC3 inhibitors, ANGPTL3 monoclonal antibodies), and lifestyle modifications. This review systematically outlines the pathophysiological mechanisms, therapeutic approaches, and recurrence prevention of HLP, highlighting the importance of personalized precision management to guide clinical practice.

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