Divison of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Waehringer Guertel 18-20, Vienna A-1090, Austria; Vienna Hepatic Hemodynamic Lab, Medical University of Vienna, Vienna, Austria.
Divison of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Waehringer Guertel 18-20, Vienna A-1090, Austria; Vienna Hepatic Hemodynamic Lab, Medical University of Vienna, Vienna, Austria; Christian Doppler Laboratory for Portal Hypertension and Liver Fibrosis, Medical University of Vienna, Vienna, Austria.
Dig Liver Dis. 2022 Apr;54(4):500-508. doi: 10.1016/j.dld.2021.09.009. Epub 2021 Nov 16.
Non-alcoholic steatohepatitis has become a leading cause of cirrhosis. The prognostic value of (HVPG)-guided NSBB prophylaxis remains to be investigated in the setting of NASH cirrhosis.
Patients with NASH cirrhosis and varices undergoing HVPG-guided NSBB therapy were included. HVPG-response to NSBBs was evaluated within a median 52 (IQR:28-71) days after baseline measurement. HVPG-Response was defined as a decrease of ≥10% from baseline or below <12 mmHg. The composite endpoint was defined as variceal bleeding, decompensation, and liver-related death.
Thirtyeight patients were included: Child-A/B:33(87%), Child-C:5(13%) median HVPG:19.7 ± 4.7 mmHg. 21(55.3%) patients achieved HVPG-response to NSBB. Presence of diabetes(aOR:0.16, p = 0.038) and arterial blood pressure (aOR:1.07, p = 0.044) were independently associated with NSBB-response. While NSBB-HVPG-responders showed fewer decompensations within 90 days (n = 1(5%) vs. n = 3(29%), p = 0.172), only Child-Pugh stage B/C (p = 0.001), MELD ≥ 15(p = 0.021) and HVPG ≥ 20 mmHg(p = 0.011) predicted the composite endpoint at 90 days. Similarly, after 2years of follow-up, only Child-Pugh stage (B:p = 0.001, C:p < 0.001), MELD ≥ 15 (p = 0.021), HVPG≥20 mmHg (p = 0.011) predicted the composite endpoint. Importantly, all bleeding events occurred in HVPG-NSBB non-responders.
HVPG-response to NSBB was achieved in 55.3% of NASH patients with varices and this seemed to protect from variceal bleeding. However, only baseline HVPG ≥ 20 mmHg, Child-Pugh stage B/C and MELD ≥ 15 were predictors of decompensation/death in patients with NASH cirrhosis and varices.
非酒精性脂肪性肝炎已成为肝硬化的主要病因。在 NASH 肝硬化患者中,HVPG 指导下的 NSBB 预防的预后价值仍有待研究。
纳入了接受 HVPG 指导的 NSBB 治疗的 NASH 肝硬化伴静脉曲张患者。在基线测量后中位 52(IQR:28-71)天内评估 NSBB 对 HVPG 的反应。HVPG 反应定义为从基线下降≥10%或低于<12mmHg。复合终点定义为静脉曲张出血、失代偿和与肝脏相关的死亡。
共纳入 38 例患者:Child-A/B:33(87%),Child-C:5(13%),HVPG 中位数:19.7±4.7mmHg。21 例(55.3%)患者对 NSBB 达到 HVPG 反应。存在糖尿病(OR:0.16,p=0.038)和动脉血压(OR:1.07,p=0.044)与 NSBB 反应独立相关。虽然 NSBB-HVPG 反应者在 90 天内失代偿的发生率较低(n=1(5%)比 n=3(29%),p=0.172),但只有 Child-Pugh 分期 B/C(p=0.001)、MELD≥15(p=0.021)和 HVPG≥20mmHg(p=0.011)可预测 90 天内的复合终点。同样,在 2 年的随访后,只有 Child-Pugh 分期(B:p=0.001,C:p<0.001)、MELD≥15(p=0.021)、HVPG≥20mmHg(p=0.011)可预测复合终点。重要的是,所有出血事件均发生在 HVPG-NSBB 无反应者中。
在接受 HVPG 指导的 NSBB 治疗的 NASH 静脉曲张患者中,有 55.3%的患者达到 HVPG 反应,这似乎可以预防静脉曲张出血。然而,只有基线 HVPG≥20mmHg、Child-Pugh 分期 B/C 和 MELD≥15 是 NASH 肝硬化伴静脉曲张患者失代偿/死亡的预测因素。