急性胆管炎患炎症因子的研究进展

Research Progress on Inflammatory Cytokines in Acute Cholangitis

摘要: 急性胆管炎因胆道梗阻伴细菌感染引发强烈炎症反应，临床进展快、并发症多，仍为危及生命的急腹症。炎症因子反映机体免疫激活与损伤程度，是疾病分层、疗效评估与预后判断的重要生物标志物。随着检测技术与炎症免疫学研究的发展，探讨急性胆管炎中关键炎症因子的动态变化及其临床意义，有助于优化早期诊断、制定个体化治疗策略并降低病死率。急性胆管炎是一种起病急、进展快、可迅速引发全身炎症反应及多器官功能损害的严重胆道感染性疾病，若未能及时识别与干预，患者病死率显著升高。近年来，炎症因子作为反映机体感染应答与炎症损伤程度的重要生物标志物，在急性胆管炎的诊疗研究中受到广泛关注。炎症因子不仅可用于揭示胆道梗阻、细菌感染及内毒素释放后机体免疫激活的病理过程，还可能在疾病严重程度评估、疗效监测以及预后判断中发挥重要作用。本文围绕急性胆管炎炎症因子的研究进展进行综述，重点阐述其生物学基础、常见炎症介质的类型及功能特征，以及相关临床研究的主要发现。研究表明，胆道梗阻有助于细菌移位和毒素积聚，进而激活先天免疫反应并诱导多种细胞因子、趋化因子和急性期蛋白释放，其中C反应蛋白、降钙素原、白细胞介素-6、白细胞介素-8、肿瘤坏死因子-α等指标研究最为深入。现有证据提示，上述炎症因子的升高与感染程度加重、全身炎症负荷增加、脓毒症发生风险上升以及急诊胆道引流需求密切相关；其动态变化还可为抗菌治疗和内镜或介入性胆道减压疗效评价提供参考。然而，目前相关研究仍存在入组标准不统一、采样时间差异较大、检测指标组合不一致以及截断值缺乏标准化等问题，导致研究结果之间可比性有限。总体而言，炎症因子在急性胆管炎中具有较好的临床应用前景，但其真正用于精准分层和个体化治疗决策仍需高质量前瞻性研究进一步验证。未来应结合临床评分、影像学表现及病原学结果，构建更加全面的风险评估体系，以提升急性胆管炎的早期识别与精准干预水平。

Abstract: Acute cholangitis, caused by biliary obstruction complicated by bacterial infection, triggers a strong inflammatory response; it progresses rapidly, has multiple complications, and remains a life-threatening surgical emergency. Inflammatory mediators reflect the degree of immune activation and tissue injury and are important biomarkers for disease stratification, therapeutic evaluation, and prognosis. With advances in detection techniques and research in inflammation and immunology, investigating the dynamic changes of key inflammatory mediators in acute cholangitis and their clinical significance can help optimize early diagnosis, guide individualized treatment strategies, and reduce mortality. Acute cholangitis is a severe biliary tract infection characterized by rapid disease progression, systemic inflammatory response, and a substantial risk of organ dysfunction if diagnosis and treatment are delayed. In recent years, inflammatory factors have become an important focus in the study of acute cholangitis because they not only reflect the host immune response to biliary obstruction and infection, but also provide potential clues for disease severity assessment, treatment monitoring, and prognosis prediction. This review summarizes the biological basis of inflammatory factor involvement in acute cholangitis, the main categories of commonly studied mediators, and the current progress in clinical research. Mechanistically, biliary obstruction facilitates bacterial translocation and toxin accumulation, which activate innate immune signaling pathways and trigger the release of cytokines, chemokines, and acute-phase proteins. Among these, C-reactive protein, procalcitonin, interleukin-6, interleukin-8, tumor necrosis factor-α, and other related markers have been widely investigated. Existing studies suggest that elevated inflammatory factors are closely associated with infection severity, systemic inflammatory burden, the occurrence of sepsis, and the need for urgent biliary drainage. In addition, dynamic changes in inflammatory factors may help evaluate the effectiveness of antibiotic therapy and endoscopic or interventional biliary decompression. However, current evidence remains limited by differences in patient populations, diagnostic criteria, sampling time points, and marker combinations, resulting in inconsistent cutoff values and limited comparability across studies. Therefore, while inflammatory factors have promising clinical value in acute cholangitis, their application still requires standardized testing strategies and high-quality prospective validation. Future research should integrate inflammatory biomarkers with clinical scoring systems, imaging findings, and microbiological data to improve individualized risk stratification and treatment decision-making in acute cholangitis.