自发性门体分流对乙型肝炎肝硬化患者预后的影响

摘要/Abstract

摘要： 目的分析自发性门体分流对乙型肝炎肝硬化患者预后的影响。方法收集2020年1月至2021年1月邯郸市传染病医院收治的乙型肝炎硬化患者72例,其中门静脉压力升高(高压组)35例,门静脉压正常(正常组)37例。比较两组患者的血清生化学指标、门静脉内径、腹水、并发症以及纤维化程度。统计学处理采用t检验和卡方检验。结果高压组患者Alb、ALT、AST、TBil、PT及PLT分别为(23.5±4.3)g/L、(223.2±21.6)U/L、(189.6±30.9)U/L、(78.2±9.3)μmol/L、(18.3±4.3)s及(61.3±9.3)×10⁹/L,正常组分别为(32.0±5.6)g/L、(51.7±11.4)U/L、(45.8±22.3)U/L、(52.1±6.1)μmol/L、(11.9±3.9)s及(95.9±9.6)×10⁹/L,差异有统计学意义(t=10.142,-56.358,37.445,-11.208,-17.569,12.120,P<0.05)。高压组、正常组患者门静脉内径分别为(12.3±2.3)cm、(14.6±3.0)cm,腹水深度分别为(79.6±12.3)cm、(53.2±9.6)cm,差异有统计学意义(t=-11.269,P<0.05);消化道出血分别为14例(40.0%)、1例(3.1%),肝性脑病分别为17例(48.6%)、1例(3.1%),死亡分别为10例(28.6%)、2例(5.4%),差异均有统计学意义(χ²=-30.504,均P<0.05)。高压组患者PCⅢ、IV-C、LN及HA分别为(42.1±11.1)ng/mL、(192.2±18.6)ng/mL、(156.0±14.5)ng/mL及(285.3±23.9)ng/mL,正常组分别为(21.8±9.7)ng/mL、(143.9±10.6)ng/mL、(131.2±15.2)ng/mL及(176.9±22.3)ng/mL,差异均有统计学意义(t=-16.800,-11.602,-9.786,-13.612,均P<0.05)。结论乙型肝炎肝硬化导致门静脉压力升高出现代偿性自发性门体分流,导致肝功能进一步恶化,加重肝硬化的进展,容易引起消化道出血和肝性脑病的发生,对患者的预后产生不利的影响。

关键词: 自发性门体分流, 乙型肝炎后肝硬化, 门静脉高压, 肝性脑病, 消化道出血

Abstract: Objective To analyze the effect of spontaneous portosystemic shunt on the prognosis of chronic hepatitis B patients with liver cirrhosis, and to provide theoretical basis for the clinical treatment and prognostic evaluation of such patients. Methods A total of 72 patients (40 males and 32 females) with an average age of (46.3±8.7) years were enrolled in this study from January 2020 to January 2021. The measured value of portal vein pressure as represented by hepatic venous pressure gradient (HVPG) >10mmHg is defined as portal hypertension, and HVPG <10mmHg is defined as normal portal pressure. The measurement data are expressed as (±s), and compared using t-test between these two groups, while the counting data are expressed as (%) and analyzed with chi-square test. Results There were 35 patients (20 males and 15 females) with portal hypertension, with an average age of (46.0±8.9) years. There were 37 cases (20 males and 17 females) with normal portal vein pressure, with an average age of (46.6±8.4) years. The levels of ALB, ALT, AST, TBIL, PT and PLT in the hypertension group were (23.5±4.3)g/L, (223.2±21.6)U/L, (189.6±30.9)U/L, (78.2±9.3) μmol/L, (18.3±4.3)s and (61.39.3)×10⁹/L, respectively. Compared with those of [(32.0±5.6) g/L, (51.7±11.4) U/L, (45.8±22.3) U/L, (52.1±6.1) μmol/L, (11.9±3.9) s and (95.9±9.6)×10⁹/L] in the normal group, respectively, and the differences were statistically significant (t=10.142, -56.358, 37.445, -11.208, -17.569, 12.120, P<0.05). The internal diameters of portal vein in hypertension group and normal group were (12.3±2.3)cm and (14.6±3.0)cm, respectively, the difference was statistically significant (t=9.126, P<0.05). The depth of ascites in high pressure group and normal group was (79.6±12.3) cm and (53.2±9.6)cm, respectively, and the difference was statistically significant (t=-11.269, P<0.05). There were 14 cases (40.0%) in high pressure group and 1 case (3.1%) in normal pressure group developed gastrointestinal bleeding, with statistical significant difference (χ²=-68.104, P<0.05). Hepatic encephalopathy occurred in 17 cases (48.6%) of high pressure group and 1 case (3.1%) in normal pressure group, and the difference was statistically significant (χ²=-78.345, P<0.05). Ten patients (28.6%) died in high pressure group, which was statistically significant when compared to that of two patients (5.4%) in the normal pressure group (χ²=-30.504, P<0.05). The levels of PCⅢ, IV-C, LN and HA in the hypertension group were (42.1±11.1) ng/mL, (192.2±18.6) ng/mL, (156.0±14.5) ng/mL and (285.3±23.9) ng/mL, respectively, which were significantly higher than those of [(21.8±9.7) ng/mL, (143.9±10.6) ng/mL, (131.2±15.2) ng/mL and (176.9±22.3) ng/mL in the normal pressure group, respectively [t=-16.800, -11.602, -9.786, -13.612, P<0.05]. Conclusion Liver cirrhosis in chronic hepatitis B patients leads to increased portal pressure and compensatory spontaneous portosystemic shunt that may further deteriorate liver function, aggravate liver cirrhosis progression, cause gastrointestinal bleeding and hepatic encephalopathy, and impose adverse effect on the prognosis of patients.

Key words: Spontaneous portosystemic shunt, Cirrhosis after hepatitis B, Portal hypertension, Hepatic encephalopathy, Gastrointestinal bleeding

叶东, 张俊霞, 李洁, 张丹, 刘颖, 郭永泽. 自发性门体分流对乙型肝炎肝硬化患者预后的影响[J]. 肝脏, 2021, 26(11): 1246-1249.

YE Dong, ZHANG Jun-xia, LI Jie, ZHANG Dan, LIU Ying, GUO Yong-ze. Effect of spontaneous portal-systemic shunt on the prognosis of patients with hepatitis B-related liver cirrhosis[J]. Chinese Hepatolgy, 2021, 26(11): 1246-1249.

参考文献

[1] Schweitzer A, Horn J, Mikolajczyk RT, et al. Estimations of worldwide prevalence of chronic hepatitis B virus infection: a systematic review of data published between 1965 and 2013. Lancet, 2015, 386:1546-1555.
[2] Lo GH. The use of transjugular intrahepatic portosystemic stent shunt (TIPS) in the management of portal hypertensive bleeding. J Chin Med Assoc, 2014, 77:395-402.
[3] Villanueva C, Albillos A, Genescà J, et al. β blockers to prevent decompensation of cirrhosis in patients with clinically significant portal hypertension (PREDESCI): a randomised, double-blind, placebo-controlled, multicentre trial. Lancet, 2019, 393:1597-1608.
[4] 中华医学会感染病学分会, 中华医学会肝病学分会. 慢性乙型肝炎防治指南(2019年版).中华肝脏病杂志, 2019, 27:938-961.
[5] Garcia-Tsao G, Abraldes JG, Berzigotti A, et al. Portal hypertensive bleeding in cirrhosis: risk stratification, diagnosis, and management: 2016 practice guidance by the American Association for the study of liver diseases. Hepatology, 2017, 65: 310-335.
[6] Cifuentes LI, Gattini D, Torres-Robles R, et al. Beta-blockers versus placebo or no intervention for primary prophylaxis of oesophageal variceal bleeding in children with chronic liver disease or portal vein thrombosis. Cochrane Database Syst Rev, 2021, 1:CD011973.
[7] Qi X, Berzigotti A, Cardenas A, et al. Emerging non-invasive approaches for diagnosis and monitoring of portal hypertension. Lancet Gastroenterol Hepatol, 2018, 3:708-719.
[8] Hoffman DH, Ayoola A, Nickel D, et al. MR elastography, T1 and T2 relaxometry of liver: role in noninvasive assessment of liver function and portal hypertension. Abdom Radiol (NY), 2020, 45:2680-2687.
[9] Guillaume M, Bureau C. Should the presence of spontaneous portosystemic shunts be implemented to the model for end-stage liver disease score for a better prediction of outcome. Gastroenterology, 2018, 154:1569-1571.
[10] Gouya H, Grabar S, Vignaux O, et al. Portal hypertension in patients with cirrhosis: indirect assessment of hepatic venous pressure gradient by measuring azygos flow with 2D-cine phase-contrast magnetic resonance imaging. Eur Radiol, 2016, 26:1981-1990.
[11] Lin JY, Zhang CH, Zheng L, et al. Establishment and assessment of the hepatic venous pressure gradient using biofluid mechanics (HVPGBFM): protocol for a prospective, randomised, non-controlled, multicentre study. BMJ Open, 2019, 9:e028518.
[12] Leng X, Zhang F, Zhang M, et al. Comparison of transjugular intrahepatic portosystemic shunt for treatment of variceal bleeding in patients with cirrhosis with or without spontaneous portosystemic shunt. Eur J Gastroenterol Hepatol, 2019, 31:853-858.
[13] Li LN, Sun XY, Wang GC, et al. Transjugular intrahepatic portosystemic shunt prevents rebleeding in cirrhotic patients having cavernous transformation of the portal vein without improving their survival. J Dig Dis, 2019, 20:89-96.
[14] Li ZP, Wang SS, Wang GC, et al. Transjugular intrahepatic portosystemic shunt for the prevention of recurrent esophageal variceal bleeding in patients with cavernous transformation of portal vein. Hepatobiliary Pancreat Dis Int, 2018, 17:517-523.
[15] 杨金凤, 张秉强. 经颈静脉肝内门体分流术后肝性脑病诊治进展. 中华肝脏病杂志, 2016, 24:545-548.