肝硬化急性失代偿患者的临床特征及预后

摘要/Abstract

摘要： 目的分析肝硬化急性失代偿患者的临床特征,研究影响其预后的因素。方法收集2016年1月1日—2022年12月31日在昆明市第三人民医院诊断为失代偿期乙型肝炎、丙型肝炎、酒精性肝炎及自身免疫性肝炎肝硬化的患者。收集相关临床资料,将其分为急性失代偿组和非急性失代偿组,对两组患者的临床特征进行分析。在研究结束时发生肝癌(HCC)或死亡的患者为不良预后组,未发生则为对照组。对可能影响肝硬化失代偿患者不良预后的因素进行单因素及多因素logistic回归分析,利用Kaplan-Meier法估算生存率并绘制不同代偿状态的生存曲线,log -rank检验生存曲线。结果共863例失代偿期肝硬化患者入组,急性失代偿组624例,非急性失代偿组239例,急性失代偿的发生率为72.3%。其中116例死亡(急性失代偿组97例,非急性失代偿组19例),109例发生HCC(急性失代偿组83例,非急性失代偿组26例),以及558例实现再代偿(急性失代偿组428例,非急性失代偿组130例)。Log-rank检验显示,两组在再代偿率(χ²=15.509,P<0.001)和肝病相关死亡率(χ²=7.359,P=0.007)方面差异具有统计学意义,Kaplan-Meier曲线明显分离,而HCC发生率差异无统计学意义(χ²=0.757,P=0.384)。单因素logistic回归分析显示,不良预后组急性失代偿159例(79.5%)、Child-Pugh分级[A级23例(11.5%)、B级88例(44.0%)、C级89例(44.5%)]、年龄53.0(46.0,60.0)岁、总胆红素(TBil) 40.05(24.95,80.25)μmol/L、γ-谷氨酰基转移酶 81.50(40.55,149.00)U/L、碱性磷酸酶 143.80(108.00,210.00)U/L、白蛋白(Alb) 28.65(24.40,32.80)g/L、IL-6 20.11(10.28,41.35)pg/mL、PT 17.50(15.70,19.75)s;对照组:急性失代偿468例(70.1%)、Child-Pugh分级[A级106例(16.0%)、B级338例(46.5%)、C级219例(33.0%)]、年龄50.0(44.0,57.0)岁、TBil 31.80(21.10,57.75)μmol/L、γ-谷氨酰基转移酶 63.00(35.00,134.50)U/L、碱性磷酸酶132.00(98.50,179.00)U/L、Alb 30.00(26.15,34.80)g/L、IL-6 15.27(9.00,28.51)pg/mL、PT 17.00(15.40,18.83)s,两组相比,差异有统计学意义(χ²=6.728,χ²=9.249,Z=-2.652、-0.331、-2.057、-2.140、-3.229、-3.465、-2.240,P均<0.05),多因素分析结果显示:年龄[OR 95%CI:1.024(1.008~1.041),P=0.003]、TBil[OR 95%CI:1.003(1.001~1.005),P=0.010]及Alb[OR 95%CI:0.962(0.929~0.996),P=0.030]是失代偿患者不良预后发生的独立影响因素。结论 TBil升高、Alb降低及年龄增长是提示肝硬化失代偿期患者不良预后的关键风险因素。肝硬化急性失代偿事件与肝病相关死亡率升高及再代偿率降低显著相关。

关键词: 肝硬化失代偿期, 急性失代偿, 临床特征, 影响因素

Abstract: Objective To analyze the clinical characteristics of cirrhotic patients with acute decompensation events and to investigate the factors influencing their prognosis. Methods Patients diagnosed with decompensated cirrhosis due to HBV, HCV, alcoholic hepatitis, and autoimmune hepatitis who visited the Third People's Hospital of Kunming from January 1, 2016 to December 31, 2022 were collected. Relevant clinical data of all patients were collected and they were divided into an acute de-compensation group and a non-acute de-compensation group. The clinical characteristics of the two groups were analyzed. At the end of the study, patients who developed hepatocellular carcinoma (HCC) or died were classified as the poor prognosis group, while those who did not were classified as the control group. Univariate and multivariate logistic regression analyses were conducted to identify the factors that might affect the poor prognosis of patients with decompensated cirrhosis. Kaplan-Meier method was used to estimate survival rates and draw survival curves for patients with different compensation status. Log-rank test was used to compare their survival curves. Results A total of 863 patients with decompensated cirrhosis were included, with 624 in the acute decompensation group and 239 in the non-acute decompensation group. The incidence of acute decompensation was 72.3%. Among them, 116 patients died (97 in the acute decompensation group and 19 in the non-acute decompensation group), 109 patients developed HCC (83 in the acute decompensation group and 26 in the non-acute decompensation group), and 558 achieved recompensation (428 in the acute decompensation group and 130 in the non-acute decompensation group). The result of log-rank test showed that there were statistically significant differences between the two groups in recompensation rate (χ²=15.509, P<0.001) and liver disease-related mortality (χ²=7.359, P=0.007), with Kaplan-Meier curves clearly separated. However, there was no statistically significant difference in the incidence of HCC (χ²=0.757, P=0.384). Univariate Logistic regression analysis showed that in the poor prognosis group, there were 159 cases of acute decompensation (79.5%), Child classification [A grade 23 cases (11.5%), B grade 88 cases (44.0%), C grade 89 cases (44.5%)], age 53.0 (46.0, 60.0) years, TBil 40.05 (24.95,80.25) μmol/L, GGT 81.50 (40.55,149.00) U/L, ALP 143.80 (108.00,210.00) U/L, Alb 28.65 (24.40,32.80) g/L, IL-6 20.11 (10.28,41.35) pg/mL, PT 17.50 (15.70,19.75) s, compared with the control group with 468 cases of acute decompensation (70.1%), Child-Pugh classification [A grade 106 cases (16.0%), B grade 338 cases (46.5%), C grade 219 cases (33.0%)], age 50.0 (44.0, 57.0) years, TBil 31.80 (21.10,57.75) μmol/L, GGT 40.55 (28.00,68.00) U/L, ALP 108.00 (80.00,148.00) U/L, Alb 29.00 (25.00, 32.00) g/L, IL-6 10.28 (5.28, 19.35) pg/mL, PT 15.70 (14.00,17.40) s. The differences in 63.00 (35.00,134.50) U/L, ALP 132.00 (98.50,179.00) U/L, Alb 30.00 (26.15,34.80) g/L, IL-6 15.27 (9.00,28.51) pg/mL, and PT 17.00 (15.40,18.83) S were statistically significant (χ²=6.728, χ²=9.249, Z=-2.652, -0.331, -2.057, -2.140, -3.229, -3.465, -2.240, all P<0.05). The results of the multivariate analysis showed that age [OR 95% CI:1.024 (1.008~1.041), P=0.003], TBil [OR 95% CI:1.003 (1.001~1.005), P=0.010], and Alb [OR 95% CI:0.962 (0.929~0.996), P=0.030] were independent influencing factors for poor prognosis in decompensated patients. Conclusion Elevated total bilirubin, decreased albumin, and increasing age are key risk factors for poor prognosis in patients with decompensated liver cirrhosis. Acute decompensated cirrhosis events are significantly associated with increased liver disease-related mortality and decreased re-compensation rate.

Key words: Decompensated liver cirrhosis, Acute decompensation, Clinical features, Influencing factors

许丹青, 木唤, 张映媛, 牟春燕, 撒采芬, 刘立, 李卫昆. 肝硬化急性失代偿患者的临床特征及预后[J]. 肝脏, 2026, 31(8): 1084-1090.

Xu Danqing, Mu Huan, Zhang Yingyuan, Mou Chunyan, Sa Caifen, Liu Li, Li Weikun. The clinical characteristics and prognosis of liver cirrhotic patients with acute decompensation[J]. Chinese Hepatolgy, 2026, 31(8): 1084-1090.

/ 推荐

参考文献

[1] 中华医学会消化病学分会. 中国肝硬化临床诊治共识意见[J]. 临床肝胆病杂志, 2023, 39(9) : 2057-2073.
[2] Jalan R, D′amico G, Trebicka J, et al. New clinical and pathophysiological perspectives defining the trajectory of cirrhosis[J]. J Hepatol, 2021, 75 Suppl 1: S14-S26.
[3] Moreau R, Jalan R, Gines P, et al. Acute-on-chronic liver failure is a distinct syndrome that develops in patients with acute decompensation of cirrhosis[J]. Gastroenterology, 2013, 144(7): 1426-1437.e9.
[4] Arroyo V, Angel P, Moreau R,et al. The systemic inflammation hypothesis:towards a new paradigm of acute decompensation and multiorgan failure in cirrhosis[J].J Hepatol,2021,74(3):670-685.
[5] 许晓梅, 秦波. 急性失代偿期肝硬化诊治及其预后的研究进展[J].中华肝脏病杂志, 2023, 31(7) : 756-759.
[6] 中华医学会肝病学分会, 中华医学会感染病学分会. 丙型肝炎防治指南 (2022年版)[J]. 中华临床感染病杂志, 2022, 15(6): 428-447.
[7] 中华医学会肝病学分会, 中华医学会感染病学分会. 慢性乙型肝炎防治指南(2022年版)[J]. 中华肝脏病杂志, 2022, 30(12): 1309-1331.
[8] 中华医学会肝病学分会脂肪肝和酒精性肝病学组,中国医师协会脂肪性肝病专家委员会.酒精性肝病防治指南(2018年更新版)[J].临床肝胆病杂志.2018,34(5):939-946.
[9] 中华医学会肝病学分会. 自身免疫性肝炎诊断和治疗指南(2021)[J]. 临床肝胆病杂志, 2022,38(1):42-49.
[10] 中华医学会肝病学分会. 肝硬化腹水诊疗指南(2023年版)[J]. 中华肝脏病杂志, 2023, 31(8): 813-826.
[11] 中华人民共和国国家卫生健康委员会医政司. 原发性肝癌诊疗指南(2024年版)[J]. 中华肝脏病杂志, 2024, 32(7): 581-630.
[12] Tonon M, D′Ambrosio R, Calvino V,et al. A new clinical and prognostic characterization of the patterns of decompensation of cirrhosis[J]. J Hepatol. 2024,(80)4:603-609.
[13] Trebicka J, Fernandez J, Papp M, et al. PREDICT identifies precipitating events associated with the clinical course of acutely decompensated cirrhosis[J]. J Hepatol.2021,74(5):1097-1108.
[14] 方青青,李锋,陈世耀,等.肝硬化急性失代偿的机制研究与争议[J].肝脏,2024,29(7):766-769.
[15] Kumar R,Kumar S,Prakash S S.Compensated liver cirrhosis: natural course and disease-modifying strategies[J].World J Methodol,2023,13(4):179-193.
[16] Al Kaabi H,Al Alawi A M, Al Falahi Z, et al, Clinical characteristics, etiology, and prognostic scores in patients with acute decompensated liver cirrhosis[J]. J Clin Med. 2023, 12(17):5756.
[17] Wang T,Tan W,Wang X,et,al.Role of precipitants in transition of acute decompensation to acute-on-chronic liver failure in patients with HBV-related cirrhosis[J].JHEP Rep, 2022,4(10):100529.
[18] Tsochatzis E A,Bosch J,Burroughs A K. Liver cirrhosis[J]. Lancet,2014,383(9930):1749-1761.
[19] de Franchis R, Bosch J, Garcia-Tsao G, et al. Baveno VII-renewing consensus in portal hypertension.[J]. J Hepatol, 2022,76(4) :959-974.
[20] Margarit C, Lázaro J L,Charco R, et al.Liver transplantation in patients with splenorenal shunts: intraoperative flow measurements to indicate shunt occlusion[J]. Liver Transpl Surg. 1999,5(1):35-39.
[21] Simbrunner B, Villesen I F, Königshofer P, et al. Systemic inflammation is linked to liver fibrogenesis in patients with advanced chronic liver disease[J]. Liver Int, 2022,42(11):2501-2512.
[22] Garbuzenko D V. Therapeutic possibilities of gut microbiota modulation in acute decompensation of liver cirrhosis[J]. World J Hepatol,2023,15(4):525-537.
[23] 杨玲玲,李君.乙型肝炎相关慢加急性肝衰竭诊断与预后评估的中国标准[J].中华临床感染病杂志,2019,12(1):22-23.
[24] Qiao L, Tan W, Wang X, et al. Different effects of total bilirubin on 90-day mortality in hospitalized patients with cirrhosis and advanced fibrosis: a quantitative analysis[J]. Front Med(Lausanne), 2021, 8:704452.
[25] Xu X,Tan J,Wang H,et al.Risk stratification score to predict readmission of patients with acute decompensated cirrhosis within 90 days[J].Front Med(Lausanne),2021,8:646875.
[26] Oliver M,Fran N C,Scott R, et al.Dynamic changes in bilirubin predict 90-day mortality in patients with hepatocellular carcinoma and acute decompensations of cirrhosis: the HCC-AD score.[J].Mayo Clin Proc Innov Qual Outcomes,2025,9(5):100661.
[27] Gao F, Li X, Wan G, et al. Development and external validation of a prognostic nomogram for acute decompensation of chronic hepatitis B cirrhosis[J].BMC Gastro, 2018, 18(1): 179.
[28] Iloeje U H, Yang H I, Su J, et al. Predicting cirrhosis risk based on the level of circulating hepatitis B viral load[J].Gastroenterology, 2006, 130(3): 678-686.
[29] 李敏,苏健婷,武珊珊,等.乙型肝炎肝硬化患者年龄和性别与肝病相关死亡风险的关系[J].中华肝脏病杂志,2021,29(5):403-408.
[30] Chang X J,Li Y Y,Sun C,et al. High-risk population of progressive hepatic fibrosis in chronic hepatitis B patients on antiviral therapy[J].J Gastro,2023,58(5):481-493.