目的:慢性丙型肝炎(CHC)相关的失代偿期肝硬化与较低的SVR-12发生率和直接作用抗病毒药物(DAA)后疾病严重程度的变量回归相关。我们评估了SVR-12、再补偿率(BavenoVII标准)、以及这些患者的生存。
方法:在2018年7月至2023年7月之间,DAAs治疗后失代偿性CHC相关性肝硬化患者,对SVR-12进行评估,然后进行6个月的随访。
结果:在6516例肝硬化患者中,1152例失代偿期肝硬化(年龄53.2±11.5岁,63%的男性,MELD-Na:16.5±4.6,87%基因型3)入组。一个疗程后SVR-12为81.8%;额外治疗后最终SVR为90.8%。失代偿事件包括腹水(1098,95.3%),肝性脑病(191,16.6%),静脉曲张出血(284,24.7%)。86%的腹水消退(24%的患者实现利尿剂戒断)。再补偿发生在284(24.7%),中位时间为16.5(IQR-14.5-20.5)个月。关于多变量Cox比例风险分析,低胆红素(aHR-0.6,95CI-0.5-0.8,P<0.001),INR(aHR-0.2,95CI:0.1-0.3,P<0.001),没有大的食管静脉曲张(aHR-0.4,95CI:0.2-0.9,P=0.048),或胃静脉曲张(aHR-0.5,95CI:0.3-0.7,P=0.022)可预测再补偿。门脉高压症(PHT)进展158例(13.7%),4%的患者再出血。既往代偿失调伴静脉曲张破裂出血(aHR-1.6,95CI:1.2-2.8,P=0.042),大静脉曲张的存在(aHR-2.9,95CI:1.3-6.5,P<0.001)与PHT进展相关。在221例(19%)中发现了进一步的代偿失调;145例患者死亡,6例接受了肝移植。MELDNa下降≥3的是409(35.5%),最终MELDNa评分<10的是335(29%),但尽管有SVR-12,但仍有2.9%的人发展为HCC。
结论:SVR-12在HCV相关的失代偿期肝硬化中占主导地位的基因型3人群中,在公共卫生环境中,在4年的随访中,24.7%的患者获得了再补偿。尽管SVR-12,新的肝失代偿发展在19%和HCC发展在2.9%的患者。
OBJECTIVE: Chronic hepatitis C-related decompensated cirrhosis is associated with lower sustained virologic response (SVR)-12 rates and variable regression of disease severity after direct-acting antiviral agents. We assessed rates of SVR-12, recompensation (Baveno VII criteria), and survival in such patients.
METHODS: Between July 2018 and July 2023, patients with decompensated chronic hepatitis C-related cirrhosis after direct-acting antiviral agents treatment were evaluated for SVR-12 and then had 6-monthly follow-up.
RESULTS: Of 6516 patients with cirrhosis, 1152 with decompensated cirrhosis (age 53.2 ± 11.5 years; 63% men; Model for End-stage Liver Disease-Sodium [MELD-Na]: 16.5 ± 4.6; 87% genotype 3) were enrolled. SVR-12 was 81.8% after 1 course; ultimately SVR was 90.8% after additional treatment. Decompensation events included ascites (1098; 95.3%), hepatic encephalopathy (191; 16.6%), and variceal bleeding (284; 24.7%). Ascites resolved in 86% (diuretic withdrawal achieved in 24% patients). Recompensation occurred in 284 (24.7%) at a median time of 16.5 (interquartile range, 14.5-20.5) months. On multivariable Cox proportional hazards analysis, low bilirubin (aHR, 0.6; 95% confidence interval [CI], 0.5-0.8; P < 0.001), INR (aHR, 0.2; 95% CI, 0.1-0.3; P < 0.001), absence of large esophageal varices (aHR, 0.4; 95% CI, 0.2-0.9; P = 0.048), or gastric varices (aHR, 0.5; 95% CI, 0.3-0.7; P = 0.022) predicted recompensation. Portal hypertension progressed in 158 (13.7%) patients, with rebleed in 4%. Prior decompensation with variceal bleeding (aHR, 1.6; 95% CI, 1.2-2.8; P = 0.042), and presence of large varices (aHR, 2.9; 95% CI, 1.3-6.5; P < 0.001) were associated with portal hypertension progression. Further decompensation was seen in 221 (19%); 145 patients died and 6 underwent liver transplantation. A decrease in MELDNa of ≥3 was seen in 409 (35.5%) and a final MELDNa score of <10 was seen in 335 (29%), but 2.9% developed hepatocellular carcinoma despite SVR-12.
CONCLUSIONS: SVR-12 in hepatitis C virus-related decompensated cirrhosis in a predominant genotype 3 population led to recompensation in 24.7% of patients over a follow-up of 4 years in a public health setting. Despite SVR-12, new hepatic decompensation evolved in 19% and hepatocellular carcinoma developed in 2.9% of patients. (ClinicalTrials.gov, Number: NCT03488485).