肝脏 ›› 2021, Vol. 26 ›› Issue (5): 490-493.

• 肝纤维化及肝硬化 • 上一篇    下一篇

食管胃底静脉曲张出血患者低肝脏弹性值原因分析

白艳锋, 何玲玲, 魏红山   

  1. 101400 首都医科大学附属北京朝阳医院怀柔医院消化内科(白艳锋);
    首都医科大学附属北京地坛医院消化内科(何玲玲,魏红山)
  • 收稿日期:2020-12-03 出版日期:2021-05-31 发布日期:2021-06-17
  • 通讯作者: 魏红山,Email: drwei@ccmu.edu.cn
  • 基金资助:
    首都特色临床研究(Z141107002514132);首都医学发展科研基金(2014-2-2171)

An analysis of the possible causes of low liver stiffness measurement in patients with esophageal and gastric varices bleeding

BAI Yan-feng1, HE Ling-ling2, WEI Hong-shan2   

  1. 1. Department of gastroenterology, Beijing Chaoyang Hospital Beijing Huairou Hospital, Capital Medical University, No.9, Yongtai North Street, Huairou District, Beijing 101400, China;
    2.Department of gastroenterology, Beijing Ditan Hospital, Capital Medical University,No.8, Jingshun East Street, Chaoyang District, Beijing 100069, China
  • Received:2020-12-03 Online:2021-05-31 Published:2021-06-17
  • Contact: WEI Hong-shan,Email: drwei@ccmu.edu.cn

摘要: 目的 探讨食管胃底静脉曲张出血患者肝脏弹性值(LSM)低的可能原因。方法 回顾性分析2017年1月至2019年10月因食管胃底静脉曲张出血就诊于北京地坛医院患者的临床资料,其中LSM<12 kpa的患者29例,LSM>17.5 kpa的患者37例。比较两组患者的肝功能及门静脉血流动力学指标,病因学以及合并症。结果 与LSM≤12 kpa组相比,LSM≥17.5 kpa组患者Alb(Z=-3.05, P=0.002)、CHE(Z=-3.81,P=0.000)、PTA(Z=-2.34, P=0.019)、PLT(Z=-2.29, P=0.022)均显著降低,CHILD评分(Z=-2.41, P=0.016)、AST(Z=-2.33, P=0.020)、Cr(Z=-1.97, P=0.048)、PT(Z=-2.88,P=0.004)、INR(Z=-2.15, P=0.031)均显著升高,差异有统计学意义(P<0.05)。LSM≤12 kpa组病因以特发性门静脉高压[10/29(34.4%)]及感染HBV[13/29(44.8%)]为主,LSM≥17.5 kpa组以感染HBV[15/37(40.5%)]及饮酒[12/37(32.4%)]为主,病因构成比差异有统计学意义(χ2=11.3,P=0.023)。两组患者的合并疾病和发生腹水率(χ2=0.695,P=0.405,χ2 =2.363,P=0.124)差异均无统计学意义。结论 食管胃底静脉曲张出血并非均为肝硬化引起,可能为特发性门静脉高压。临床中不能单凭肝弹性值大小来预测门静脉高压程度及出血风险。

关键词: 肝脏硬度检测, 肝硬化, 食管胃底静脉曲张破裂出血, 病因学, 门静脉高压

Abstract: Objective To investigate the possible causes of low liver stiffness measurement in patients with esophageal and gastric varices bleeding.Methods The clinical data of 29 patients with liver stiffness measurement less than 12kPa and 37 patients with liver stiffness measurement greater than 17.5kpa who visited Beijing Ditan Hospital due to esophageal and gastric varices rupture bleeding from January 2017 to October 2019 were retrospectively analyzed. The differences of liver function, portal hemodynamic indicators, etiology and complications between these two groups of patients were compared. Results Compared with the patients in the group of liver stiffness measurement ≤ 12kPa, patients in the group of liver stiffness measurement≥ 17.5kPa had significantly lower levels of albumin (Alb)(Z=-3.05, P=0.002), cholinesterase (CHE)(Z=-3.81, P=0.000), Prothrombin activity (PTA)(Z=-2.34, P=0.019), platelet (PLT) count(Z=-2.29, P=0.022), and significantly higher Child-Puch (CHILD) scores (Z=-2.41, P=0.016), levels of aspartate aminotransferase(AST)(Z=-2.33, P=0.020)and aspartate aminotransferase(Cr)(Z=-1.97, P=0.048), prolongation of prothrombin time(PT)(Z=-2.88 ,P=0.004)and International Normalized Ratio(INR)(Z=-2.15, P=0.031). The etiologies of patients in the LSM≤ 12kPa group was mainly idiopathic portal hypertension (34.4%) and hepatitis B viral infection (44.8%), while in the LSM≥ 17.5kPa group were mainly hepatitis B virus infection (40.5%) and alcoholic (32.4%). The difference of etiological composition ratio was statistically significant (χ2=11.3, P=0.023). The difference in developing complications and the rate of ascites between these two groups had no statistical significance (χ2=0.695, P=0.405, χ2 = 2.363, P=0.124).Conclusion Esophageal and gastric varices bleeding is not always caused by cirrhosis. It may also be due to idiopathic portal hypertension. The degree of portal hypertension and the risk of bleeding cannot be predicted by liver stiffness measurement alone.

Key words: Liver stiffness measurement, Liver cirrhosis, Esophageal and gastric varices rupture bleeding, Etiology, Portal hypertension