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研究进展

炎症性肠病并发结直肠息肉的机制及治疗研究进展

  • 段萌 ,
  • 王培 ,
  • 董钰婧 ,
  • 周鹏 ,
  • 陈伟杰 ,
  • 樊志敏
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  • 1.南京中医药大学附属南京中医院,江苏 南京 210022;
    2.江苏省中医肛肠疾病临床医学创新中心,江苏 南京 210022;
    3.南京中医肛肠疾病临床医学研究中心,江苏 南京 210022;
    4.南京中医药大学南通附属医院,江苏 南通 226000
段萌,男,在读硕士,研究方向:中西医结合治疗结直肠肛门外科疾病

收稿日期: 2025-09-29

  修回日期: 2025-12-16

  录用日期: 2026-03-18

  网络出版日期: 2026-04-21

基金资助

江苏省中医药科技发展项目(ZD202226):分段齿形结扎术治疗混合痔的真实世界队列研究;江苏省重点研发计划(社会发展)项目(BE2021611):基于气-液法类器官培养技术的“扶正”调节结直肠癌免疫微环境科学内涵及临床转化研究;江苏省研究生培养创新工程研究生实践创新计划(SJCX25_1048);南京市博士后优秀科研项目;江苏省自然科学基金青年基金项目(BK20230162);2024年度南京中医药大学自然科学基金项目—— 一般项目(XZR2024234);2024年度南通市中医医疗联盟课题-重点项目(TZYK202423)

Research Progress on the Mechanism and Treatment of Colorectal Polyps Complicated with Inflammatory Bowel Disease

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  • 1.Nanjing Hospital of Chinese Medicine Affiliated to Nanjing University of Chinese Medicine Jiangsu Nanjing 210022, China
    2.Jiangsu Provincial Clinical Medicine Innovation Center for Traditional Chinese Medicine Anorectal Diseases Jiangsu Nanjing 210022, China;3.Nanjing Clinical Medicine Research Center for Traditional Chinese Medicine Anorectal Diseases Jiangsu Nanjing 210022, China;4.Nantong Hospital Affiliated to Nanjing University of Chinese Medicine Jiangsu Nantong 226000, China

Received date: 2025-09-29

  Revised date: 2025-12-16

  Accepted date: 2026-03-18

  Online published: 2026-04-21

摘要

炎症性肠病(IBD)患者结直肠息肉发生风险显著升高,后者是IBD相关结直肠癌的关键癌前病变,阐明其发病机制、优化防控策略具有重要临床价值。慢性肠道炎症驱动Wnt/β-cateninSTAT3等信号通路异常激活,是息肉发生的核心机制,可直接导致肠上皮细胞增殖分化紊乱;而DNA甲基化模式失衡、TP53等基因突变引发的表观遗传异常,以及肠道菌群失调伴随的胆汁酸、短链脂肪酸代谢紊乱,与炎症反应相互作用形成恶性循环,进一步推动息肉发生发展。目前临床防控以规范内镜监测与微创干预为核心,辅以5-氨基水杨酸等药物及生活方式、微生态调节手段,也已筛选出SATB2ATF6等潜在诊断标志物。但现有研究仍存在机制阐释碎片化、标志物多中心验证不足以及缺乏特异性防治药物等问题,未来需依托多组学技术解析关键分子靶点,构建个体化精准防控体系。


本文引用格式

段萌 , 王培 , 董钰婧 , 周鹏 , 陈伟杰 , 樊志敏 .

炎症性肠病并发结直肠息肉的机制及治疗研究进展

[J]. 中国医药导刊, 2026 , 28(3) : 276 -283 . DOI: magtech.2025.09.29-00001

Abstract

Patients with inflammatory bowel disease IBD have a significantly increased risk of developing colorectal polyps which represent a critical precancerous lesion for IBD‑associated colorectal cancer. Elucidating the underlying mechanisms and optimizing preventive and therapeutic strategies therefore hold substantial clinical value. Chronic intestinal inflammation drives aberrant activation of key signaling pathways including Wnt/β‑catenin and STAT3 which serves as the core mechanism of polyp formation and directly leads to dysregulated proliferation and differentiation of intestinal epithelial cells. In addition epigenetic abnormalities caused by imbalanced DNA methylation patterns and mutations in genes such as TP53 together with disturbances in the gut microbiota accompanied by metabolic alterations in bile acids and short‑chain fatty acids interact with inflammatory responses to form a vicious cycle that further promotes the development and progression of colorectal polyps. Current clinical management centers on standardized endoscopic surveillance and minimally invasive interventions supplemented by pharmacologic agents such as 5‑aminosalicylic acid along with lifestyle modifications and microecological modulation. Potential diagnostic biomarkers including SATB2 and ATF6 have also been identified. However existing research still faces challenges such as fragmented mechanistic insights insufficient multicenter validation of biomarkers and a lack of specific preventive and therapeutic agents. Future efforts should focus on deciphering key molecular targets using multi‑omics technologies and establishing individualized precision prevention and treatment strategies.


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