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高淑娟,许邵娴,崔仕元,王 萍,刘贵生.肝硬化食管胃静脉曲张患者门静脉血栓形成及内镜治疗后门脉高压性胃病加重的危险因素分析[J].现代生物医学进展英文版,2024,(15):2939-2944.
肝硬化食管胃静脉曲张患者门静脉血栓形成及内镜治疗后门脉高压性胃病加重的危险因素分析
Analysis of Risk Factors of Portal Vein Thrombosis and Endoscopic Treatment of Backdoor Hypertension Gastric Aggravation in Patients with Esophageal and Gastric Varices
Received:January 28, 2024  Revised:February 24, 2024
DOI:10.13241/j.cnki.pmb.2024.15.026
中文关键词: 肝硬化食管胃静脉曲张  门静脉血栓  食管胃静脉曲张内镜下治疗术  门脉高压性胃病加重  危险因素
英文关键词: Esophageal varices in cirrhosis  Portal vein thrombosis  Endoscopic treatment of oesophageal and gastric varices  Portal hypertensive gastropathy aggravated  Risk factor
基金项目:陕西省卫生健康委科研基金项目(2022D008)
Author NameAffiliationE-mail
高淑娟 陕西省人民医院消化内一科 陕西 西安 710068 ghx19782066@163.com 
许邵娴 陕西省人民医院消化内一科 陕西 西安 710068  
崔仕元 陕西省人民医院消化内一科 陕西 西安 710068  
王 萍 陕西省人民医院消化内一科 陕西 西安 710068  
刘贵生 陕西省人民医院消化内一科 陕西 西安 710068  
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中文摘要:
      摘要 目的:探讨肝硬化食管胃静脉曲张患者门静脉血栓形成及治疗后门脉高压性胃病加重的危险因素。方法:回顾性选择2019年1月至2023年12月来我院诊治的肝硬化食管胃静脉曲张患者102例,所有患者均行食管胃静脉曲张内镜下治疗,根据患者是否出现门静脉血栓将其分为两组,门静脉血栓组(n=48例)、非门静脉血栓者(54例),对比两组的实验室检查、一般临床资料、影像学检查结果,使用多因素Logistic回归分析确定肝硬化食管胃静脉曲张门静脉血栓的危险因素。根据治疗后患者是否出现门脉高压性胃病加重。将102例患者分为门脉高压性胃病加重组与无门脉高压性胃病加重组组,对比两组的一般资料、实验室检查结果。多因素Logistic回归分析确定内镜治疗后门脉高压性胃病加重的危险因素。结果:内镜下食管静脉曲张门静脉血栓形成比例为47.06%(48/102)。单因素分析结果表明,门静脉血栓形成组的脾切除史、胃底硬化剂注射史、PLT、FIB、D2、门静脉主干内径、脾脏长度、脾脏厚度、脾静脉内径明显较无门静脉血栓形成高(P<0.05);多因素Logistic回归分析表明,有脾切除史、D-二聚体、PLT、脾脏厚度、脾静脉内径增大是肝硬化食管胃静脉曲张患者门静脉血栓形成的危险因素(P<0.05)。肝硬化食管胃静脉曲张患者内镜治疗后门脉高压性胃病加重占比为29.41%(30/102),单因素分析结果表明,门脉高压性胃病加重组与无门脉高压性胃病加重组的食管静脉曲张分级、Child-Pugh分级、Hp感染、门奇静脉断流史、门静脉主干内径、脾静脉内径对比有统计学意义(P<0.05);多因素Logistic回归分析表明,食管静脉曲张分级重度、Child-Pugh分级C级、有Hp感染、有门奇静脉断流史是肝硬化食管胃静脉曲张内镜治疗后门脉高压性胃病加重的危险因素(P<0.05)。结论:有脾切除史、D-二聚体、PLT、脾脏厚度、脾静脉内径升高是肝硬化食管胃静脉曲张门静脉血栓形成的危险因素,食管静脉曲张分级重度、Child-Pugh分级C级、有Hp感染、有门奇静脉断流史是内镜治疗肝硬化食管静脉曲后张门脉高压性胃病加重的危险因素。
英文摘要:
      ABSTRACT Objective: To explore the risk factors of portal vein thrombosis and treatment of backdoor hypertension in patients with esophageal and gastric varices. Methods: In tively, 102 patients from January 2019, all patients underwent endoscopic treatment with oesophageal and gastric varices, with portal venous thrombosis group (n=48 cases) and non-portal vein thrombosis (54 cases), compared with the two groups of laboratory examination, general clinical data, imaging examination results, and multifactor Logistic regression analysis was used to determine the risk factors of esophageal and gastric venous thrombosis. According to whether the patient has portal hypertension gastric disease aggravation after treatment. 102 patients were divided into portal hypertension plus restructuring and no portal hypertension and aggravation, and the general data and laboratory examination results of the two groups were compared. Multivariate Logistic regression analysis identified the risk factors for endoscopic treatment of posterior artery hypertension gastric disease aggravation. Results: The proportion of endoscopic esophageal varicose portal vein thrombosis was 47.06% (48 / 102). Univariate analysis showed that splenectomy history of portal vein thrombosis, gastric sclerosis injection, PLT, FIB, D2, internal diameter of portal vein, spleen length, spleen thickness, and splenic vein diameter without portal vein thrombosis (P<0.05); multifactor Logistic regression analysis showed that the history of splenectomy, D-dimer, PLT, splenic thickness, and enlarged splenic vein diameter were the risk factors for portal vein thrombosis in patients with cirrhosis (P<0.05). The proportion of endoscopic treatment for backdoor hypertension gastric disease aggravation was 29.41% (30 / 102). The results of the univariate analysis showed that, Portal hypertensive gastric disease and esophageal gastric Pux grade, Child-Pugh grade, Hp infection, portal vein flow history, portal vein trunk diameter and splenic vein diameter (P<0.05); The multivariate Logistic regression analysis showed that, Severe esophageal varicose veins, Child-Pugh grade C, Hp infection, and history of portal vein disconnection were the risk factors for endoscopic treatment of posterior artery hypertension in cirrhosis (P<0.05). Conclusion: A history of splenectomy, D-dimer, PLT, splenic thickness, and elevated splenic vein diameter are the risk factors for portal vein thrombosis of esophageal and gastric varices, severe, Child-Pugh grade C, Hp infection, and a history of portal vein rupture are the risk factors for the aggravation of portal hypertensive gastric disease after endoscopic treatment of liver cirrhosis.
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