目的:代谢功能障碍相关的脂肪变性肝病(MASLD)是晚期慢性肝病(ACLD)的主要原因。门静脉高压导致肝失代偿,最好通过肝静脉压力梯度(HVPG)测量来诊断。在这里,我们研究HVPG在代偿(cACLD)MASLD中的预后价值。
方法:这项欧洲多中心研究纳入了基线以HVPG为特征的MASLD-cACLD患者。肝功能失代偿(静脉曲张破裂出血/腹水/肝性脑病)和肝脏相关死亡率被认为是主要事件。
结果:包括340名MASLD-cACLD患者[56.2%男性;年龄:62(55-68)岁;MELD:8(7-9);71.2%糖尿病]。临床上显着的门静脉高压症(CSPH;即在209例患者中发现HVPG≥10mmHg)(61.5%)。在41.5(27.5-65.8)个月的中位随访期间,65例患者发生肝失代偿,2年(2Y)后累积发生率为10.0%,5年(5Y)后累积发生率为30.7%。在没有CSPH的患者中,2Y后为2.4%,5Y后为9.4%。没有CSPH不会发生静脉曲张出血。CSPH(子分布危险比,SHR:5.13;p<0.001)与失代偿风险增加相关,较高的HVPG仍然是多变量模型中的独立风险因素(每mmHgaSHR:1.12;p<0.001)。在CSPH中,37例患者发生与肝脏相关的死亡率,2Y后的累积发生率为3.3%,5Y后的累积发生率为21.4%。没有CSPH,5Y后发生率为0.8%。因此,较高的HVPG也与较高的肝脏相关死亡风险独立相关(aSHR/mmHg:1.20;p<0.001).
结论:HVPG测量在MASLD-cACLD中具有很高的预后价值。虽然没有CSPH的MASLD-cACLD患者表现出非常低的失代偿和肝脏相关死亡率的短期风险是罕见的,CSPH的存在大大增加了这两种风险。
虽然由于代谢功能障碍相关的脂肪变性肝病(MASLD)引起的代偿性晚期慢性肝病(cACLD)的发病率在全球范围内不断增加,在MASLD-cACLD中,关于临床显著门脉高压(CSPH)对肝脏相关事件风险的影响的见解仍然有限.根据这项欧洲多中心研究的结果,包括340MASLD-cACLD,我们可以证明,HVPG值升高,尤其是CSPH的存在与首次肝失代偿和肝脏相关死亡率的风险显著升高相关.相比之下,MASLD-cACLD无CSPH患者失代偿的短期发生率较低,肝脏死亡风险仍然可以忽略不计.因此,HVPG测量可以为MASLD-cACLD中的个性化风险分层提供重要的预后信息,并且可能有助于促进对MASLD的新颖和有希望的治疗可能性的研究。
OBJECTIVE: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a leading cause of advanced chronic liver disease (ACLD). Portal hypertension drives hepatic decompensation and is best diagnosed by hepatic venous pressure gradient (HVPG) measurement. Here, we investigate the prognostic value of HVPG in MASLD-related compensated ACLD (MASLD-cACLD).
METHODS: This European multicentre study included patients with MASLD-cACLD characterised by HVPG at baseline. Hepatic decompensation (variceal bleeding/ascites/hepatic encephalopathy) and liver-related mortality were considered the primary events of interest.
RESULTS: A total of 340 patients with MASLD-cACLD (56.2% male; median age 62 [55-68] years, median MELD 8 [7-9], 71.2% with diabetes) were included. Clinically significant portal hypertension (CSPH: i.e., HVPG ≥10 mmHg) was found in 209 patients (61.5%). During a median follow-up of 41.5 (27.5-65.8) months, 65 patients developed hepatic decompensation with a cumulative incidence of 10.0% after 2 years (2Y) and 30.7% after 5 years (5Y) in those with MASLD-cACLD with CSPH, compared to 2.4% after 2Y and 9.4% after 5Y in patients without CSPH. Variceal bleeding did not occur without CSPH. CSPH (subdistribution hazard ratio [SHR] 5.13; p <0.001) was associated with an increased decompensation risk and a higher HVPG remained an independent risk factor in the multivariable model (adjusted SHR per mmHg: 1.12, p <0.001). Liver-related mortality occurred in 37 patients at a cumulative incidence of 3.3% after 2Y and 21.4% after 5Y in CSPH. Without CSPH, the incidence after 5Y was 0.8%. Accordingly, a higher HVPG was also independently associated with a higher risk of liver-related death (adjusted SHR per mmHg: 1.20, p <0.001).
CONCLUSIONS: HVPG measurement is of high prognostic value in MASLD-cACLD. In patients with MASLD-cACLD without CSPH, the short-term risk of decompensation is very low and liver-related mortality is rare, while the presence of CSPH substantially increases the risk of both.
UNASSIGNED: While the incidence of compensated advanced chronic liver disease (cACLD) due to metabolic dysfunction-associated steatotic liver disease (MASLD) is increasing worldwide, insights into the impact of clinically significant portal hypertension (CSPH) on the risk of liver-related events in MASLD-cACLD remain limited. Based on the findings of this European multicentre study including 340 MASLD-cACLD patients, we could show that increasing HVPG values and the presence of CSPH in particular were associated with a significantly higher risk of first hepatic decompensation and liver-related mortality. In contrast, the short-term incidence of decompensation in patients with MASLD-cACLD without CSPH was low and the risk of liver-mortality remained negligible. Thus, HVPG measurements can provide important prognostic information for individualised risk stratification in MASLD-cACLD and may help facilitate the study of novel and promising treatment possibilities for MASLD.