Divison of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Vienna Hepatic Hemodynamic Laboratory, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Aliment Pharmacol Ther. 2023 Oct;58(8):805-813. doi: 10.1111/apt.17653. Epub 2023 Jul 31.
Non-selective betablockers (NSBBs) reduce the risk of hepatic decompensation in patients with compensated advanced chronic liver disease (cACLD). Metabolic co-morbidities (MetC) are increasingly observed in cACLD patients.
To investigate the impact of MetC on the haemodynamic effects of NSBB and hepatic decompensation in cACLD.
cACLD patients undergoing paired hepatic venous pressure gradient (HVPG) measurements before/under NSBB therapy were retrospectively considered for this study. We recorded baseline characteristics on MetC (obesity, dyslipidaemia and diabetes), as well as hepatic decompensation and liver-related mortality during follow-up.
We included 92 patients (Child-A n = 80, 87%; Child-B n = 12, 13%). MetC were found in 34 (37%) patients: 19 (20.7%) with obesity, 14 (15.2%) with dyslipidaemia and 23 (34.8%) with diabetes. The median baseline HVPG of 18 (IQR:15-21) mmHg decreased to 15 (IQR:9-12) mmHg under NSBB. HVPG-response (decrease ≥10% or to ≤12 mmHg) was achieved in 60 (65.2.%) patients. Patients with diabetes (OR: 0.35, p = 0.021) and higher BMI (OR: 0.89 per kg/m , p = 0.031) were less likely to achieve HVPG-response. During a median follow-up of 2.3 (0.5-4.2) years, 18 (19.5%) patients experienced hepatic decompensation. Child-B (adjusted subdistribution hazard ratio, aSHR: 4.3 [95% CI:1.5-12.2], p = 0.006), HVPG-response (aSHR: 0.3 [95% CI:0.1-0.9], p = 0.037) and diabetes (aSHR: 2.8 [95% CI:1.1-7.2], p = 0.036) were independently associated with hepatic decompensation.
In patients with cACLD, diabetes and a higher BMI impair the HVPG-response to NSBB. Furthermore, diabetes-independently from Child B and lack of HVPG-response-increases the risk of hepatic decompensation.
非选择性β受体阻滞剂(NSBB)可降低代偿性晚期慢性肝病(cACLD)患者肝失代偿的风险。代谢合并症(MetC)在 cACLD 患者中越来越常见。
研究 MetC 对 cACLD 患者 NSBB 血流动力学效应和肝失代偿的影响。
回顾性分析了接受 NSBB 治疗前后行配对肝静脉压力梯度(HVPG)测量的 cACLD 患者。我们记录了基线时 MetC(肥胖、血脂异常和糖尿病)的特征,以及随访期间的肝失代偿和与肝脏相关的死亡率。
共纳入 92 例患者(Child-Pugh A 级 n=80,87%;Child-Pugh B 级 n=12,13%)。34 例(37%)患者存在 MetC:肥胖 19 例(20.7%),血脂异常 14 例(15.2%),糖尿病 23 例(34.8%)。基线 HVPG 中位数为 18(IQR:15-21)mmHg,在 NSBB 治疗下降至 15(IQR:9-12)mmHg。60 例(65.2%)患者达到 HVPG 反应(降低≥10%或降至≤12mmHg)。糖尿病患者(OR:0.35,p=0.021)和 BMI 较高的患者(OR:每公斤体重增加 0.89,p=0.031)HVPG 反应的可能性较小。在中位随访 2.3(0.5-4.2)年期间,18 例(19.5%)患者发生肝失代偿。Child-Pugh B 级(调整后的亚分布风险比,aSHR:4.3 [95%CI:1.5-12.2],p=0.006)、HVPG 反应(aSHR:0.3 [95%CI:0.1-0.9],p=0.037)和糖尿病(aSHR:2.8 [95%CI:1.1-7.2],p=0.036)与肝失代偿独立相关。
在 cACLD 患者中,糖尿病和较高的 BMI 会损害 NSBB 对 HVPG 的反应。此外,糖尿病独立于 Child B 级和缺乏 HVPG 反应增加了肝失代偿的风险。