Hepatic venous pressure gradient: Inaccurately estimates portal venous pressure gradient in alcoholic cirrhosis and portal hypertension

BACKGROUND Portal hypertension(PHT)in patients with alcoholic cirrhosis causes a range of clinical symptoms,including gastroesophageal varices and ascites.The hepatic venous pressure gradient(HVPG),which is easier to measure,has replaced the portal venous pressure gradient(PPG)as the gold standard for diagnosing PHT in clinical practice.Therefore,attention should be paid to the correlation between HVPG and PPG.METHODS Between January 2017 and June 2020,134 patients with alcoholic cirrhosis and PHT who met the inclusion criteria underwent various pressure measurements during transjugular intrahepatic portosystemic shunt procedures.Correlations were assessed using Pearson’s correlation coefficient to estimate the correlation coefficient(r)and determination coefficient(R^(2)).Bland-Altman plots were constructed to further analyze the agreement between the measurements.Disagreements were analyzed using paired t tests,and P values<0.05 were considered statistically significant.RESULTS In this study,the correlation coefficient(r)and determination coefficient(R2)between HVPG and PPG were 0.201 and 0.040,respectively(P=0.020).In the 108 patients with no collateral branch,the average wedged hepatic venous pressure was lower than the average portal venous pressure(30.65±8.17 vs.33.25±6.60 mmHg,P=0.002).Hepatic collaterals were identified in 26 cases with balloon occlusion hepatic venography(19.4%),while the average PPG was significantly higher than the average HVPG(25.94±7.42 mmHg vs 9.86±7.44 mmHg;P<0.001).The differences between HVPG and PPG<5 mmHg in the collateral vs no collateral branch groups were three cases(11.54%)and 44 cases(40.74%),respectively.CONCLUSION In most patients,HVPG cannot accurately represent PPG.The formation of hepatic collaterals is a vital reason for the strong underestimation of HVPG.

Cirrhosis and portal hypertension: The importance of risk stratification, the role of hepatic venous pressure gradient measurement

Portal hypertension is the main prognostic factor in cirrhosis. The recent emergence of potent antiviral drugs and new algorithm of treatment for the management of complications due to portal hypertension have sensibly changed our perception of cirrhosis that can be now considered as a multistage liver disease whose mortality risk can be reduced by a tailored approachfor any stage of risk. Experts recommend to move toward a pathophysiological classification of cirrhosis that considers both structural and functional changes. The hepatic venous pressure gradient HVPG, is the reference gold standard to estimate the severity of portal hypertension in cirrhosis. It correlates with both structural and functional changes that occur in cirrhosis and carries valuable prognostic information to stratify the mortality risk. This article provides a general overview of the pathophysiology and natural course of cirrhosis and portal hypertension. We propose a simplified classification of cirrhosis based on low, intermediate and high mortality stage. The prognostic information provided by HVPG is presented according to each stage. A comparison with prognostic models based on clinical and endoscopic variables is discussed in order to evidence the additional contribute given by HVPG on top of other clinical and instrumental variables widely used in clinical practice.

Computed tomography perfusion in liver and spleen for hepatitis B virus-related portal hypertension:A correlation study with hepatic venous pressure gradient

BACKGROUND Hepatic venous pressure gradient(HVPG)is the gold standard for diagnosis of portal hypertension(PH).However,its use can be limited because it is an invasive procedure.Therefore,it is necessary to explore a non-invasive method to assess PH.AIM To investigate the correlation of computed tomography(CT)perfusion of the liver with HVPG and Child-Pugh score in hepatitis B virus(HBV)-related PH.METHODS Twenty-eight patients(4 female,24 male)with gastroesophageal variceal bleeding induced by HBV-related PH were recruited in our study.All patients received CT perfusion of the liver before transjugular intrahepatic portosystemic stent-shunt(TIPS)therapy.Quantitative parameters of CT perfusion of the liver,including liver blood flow(LBF),liver blood volume(LBV),hepatic artery fraction,splenic blood flow and splenic blood volume were measured.HVPG was recorded during TIPS therapy.Correlation of liver perfusion with Child-Pugh score and HVPG were analyzed,and the receiver operating characteristic curve was analyzed.Based on HVPG(>12 mmHg vs≤12 mmHg),patients were divided into moderate and severe groups,and all parameters were compared.RESULTS Based on HVPG,18 patients were classified into the moderate group and 10 patients were classified into the severe group.The Child-Pugh score,HVPG,LBF and LBV were significantly higher in the moderate group compared to the severe group(all P<0.05).LBF and LBV were negatively associated with HVPG(r=-0.473,P<0.05 and r=-0.503,P<0.01,respectively),whereas splenic blood flow was positively associated with hepatic artery fraction(r=0.434,P<0.05).LBV was negatively correlated with Child-Pugh score.Child-Pugh score was not related to HVPG.Using a cutoff value of 17.85 mL/min/100 g for LBV,the sensitivity and specificity of HVPG≥12 mmHg for diagnosis were 80%and 89%,respectively.CONCLUSION LBV and LBF were negatively correlated with HVPG and Child-Pugh scores.CT perfusion imaging is a potential non-invasive quantitative predictor for PH in HBV-related liver cirrhosis.

Sildenafil does not influence hepatic venous pressure gradient in patients with cirrhosis

AIM: To investigate if sildenafil increases splanchnic blood flow and changes the hepatic venous pressure gradient (HVPG) in patients with cirrhosis.Phosphodiesterase type-5 inhibitors are valuable in the treatment of erectile dysfunction and pulmonary hypertension in patients with end-stage liver disease.However,the effect of phosphodiesterase type-5 inhibitors on splanchnic blood flow and portal hypertension remains essentially unknown.METHODS: Ten patients with biopsy proven cirrhosis (five females/five males,mean age 54 ± 8 years) and an HVPG above 12 mmHg were studied after informed consent.Measurement of splanchnic blood flow and the HVPG during liver vein catheterization were done before and 80 min after oral administration of 50 mg sildenafil.Blood flow was estimated by use of indocyanine green clearance technique and Fick's principle,with correction for non-steady state.RESULTS: The plasma concentration of sildenafil was 222 ± 136 ng/mL 80 min after administration.Mean arterial blood pressure decreased from 77 ± 7 mmHg to 66 ± 12 mmHg,P = 0.003,while the splanchnic blood flow and oxygen consumption remained unchanged at 1.14 ± 0.71 L/min and 2.3 ± 0.6 mmol/ min,respectively.Also the HVPG remained unchanged (18 ± 2 mmHg vs 16 ± 2 mmHg) with individual changes ranging from -8 mmHg to +2 mmHg.In seven patients,HVPG decreased and in three it increased.CONCLUSION: In spite of arterial blood pressure decreases 80 min after administration of the phosphodiesterase type-5 inhibitor sildenafil,the present study could not demonstrate any clinical relevant influence on splanichnic blood flow,oxygen consumption or the HVPG.

Osteopontin: A non-invasive parameter of portal hypertension and prognostic marker of cirrhosis

AIM: To investigate the relationship between osteopontin plasma concentrations and the severity of portal hypertension and to assess osteopontin prognostic value.METHODS: A cohort of 154 patients with confirmed liver cirrhosis(112 ethylic, 108 men, age 34-72 years)were enrolled in the study. Hepatic venous pressure gradient(HVPG) measurement and laboratory and ultrasound examinations were carried out for all patients. HVPG was measured using a standard catheterization method with the balloon wedge technique. Osteopontin was measured using the enzyme-linked immunosorbent assay(ELISA) method in plasma. Patients were followed up with a specific focus on mortality. The control group consisted of 137 healthy age- and sex- matched individuals.RESULTS: The mean value of HVPG was 16.18 ± 5.6 mm Hg. Compared to controls, the plasma levels of osteopontin in cirrhotic patients were significantly higher(P < 0.001). The plasma levels of osteopontin were positively related to HVPG(P = 0.0022, r = 0.25) and differed among the individual Child-Pugh groups of patients. The cut-off value of 80 ng/m L osteopontin distinguished patients with significant portal hypertension(HVPG above 10 mm Hg) at 75% sensitivity and 63% specificity. The mean follow-up of patients was 3.7 ± 2.6 years. The probability of cumulative survival was 39% for patients with HVPG > 10 mm Hg and 65% for those with HVPG ≤ 10 mm Hg(P = 0.0086, odds ratio(OR), 2.92, 95% confidence interval(CI): 1.09-7.76). Osteopontin showed a similar prognostic value to HVPG. Patients with osteopontin values above 80 ng/m L had significantly lower cumulative survival compared to those with osteopontin ≤ 80 ng/m L(37% vs 56%, P = 0.00035; OR = 2.23, 95%CI: 1.06-4.68).CONCLUSION: Osteopontin is a non-invasive parameter of portal hypertension that distinguishes patients with clinically significant portal hypertension. It is a strong prognostic factor for survival.

Plasma Nogo-A and placental growth factor levels are associated with portal hypertension in patients with liver cirrhosis

BACKGROUND Clinically significant portal hypertension(CSPH) and severe portal hypertension(SPH) increase the risk for decompensation and life-threatening complications in liver cirrhosis. Pathologic angiogenesis might contribute to the formation of these conditions. Placental growth factor(PlGF) and Nogo-A protein are biomarkers of pathological angiogenesis, but data on their role in liver cirrhosis and portal hypertension is scarce.AIM To determine plasma levels of PlGF and Nogo-A in patients with liver cirrhosis,CSPH, SPH and potential to predict portal hypertension.METHODS A cohort of 122 patients with hepatitis C virus and/or alcohol-induced liver cirrhosis with characterized hepatic venous pressure gradient(HVPG) were included in the study. Demographic data, medical history, Child-Turcotte-Pugh and Model of End Stage liver disease score, clinical chemistry, liver stiffnessvalues were recorded on the day of the procedure prior HVPG measurement. The degree of portal hypertension was determined by the invasive HVPG measurement. Nogo-A and PlGF plasma levels were evaluated using enzyme linked immunosorbent assay. The control group consisted of 30 healthy age-and sex-matched individuals.RESULTS Peripheral PlGF levels were higher and Nogo-A levels were lower in patients with liver cirrhosis(23.20 vs 9.85;P < 0.0001 and 2.19 vs 3.12;P = 0.004 respectively). There was a positive linear correlation between peripheral levels of PlGF and HVPG(r = 0.338, P = 0.001) and negative linear correlation between the peripheral Nogo-A levels and HVPG(r =-0.267, P = 0.007). PlGF levels were higher in CSPH and SPH(P = 0.006;P < 0.0001) whereas Nogo-A levels were lower(P = 0.01;P < 0.033). Area under the curve for the diagnosis of CSPH for PlGF was 0.68(P = 0.003) and for Nogo-A-0.67(P = 0.01);for SPH 0.714(P <0.0001) and 0.65(P = 0.014) respectively. PlGF levels were higher and Nogo-A levels were lower in patients with esophageal varices(P < 0.05). PlGF cut-off value of 25 pg/mL distinguished patients with CSPH at 55.7% sensitivity and76.7% specificity;whereas Nogo-A cut-off value of 1.12 ng/mL was highly specific(93.1%) for the diagnosis of CSPH.CONCLUSION Plasma PlGF levels were higher while Nogo-A levels were lower in patients with liver cirrhosis and portal hypertension. Biomarkers showed moderate predictive value in determining CSPH and SPH.

Subharmonic aided pressure estimation in portal hypertension:A noninvasive ultrasound-based technique to assess portal pressure gradient

Portal hypertension(PH)is a clinical syndrome,characterized by elevated pressure gradient between portal vein and inferior vena cava.These elevated pressures gradient due to increased vascular resistance and/or increased volume of blood flowing through the portal vein circulation,results in blood outflow difficulty from portal vein to hepatic veins and inferior vena cava.

内镜超声在肝硬化门脉高压症诊治中的研究进展

内镜超声(endoscopic ultrasound,EUS)的发展及创新扩大了其在肝脏疾病诊治中的作用,EUS不仅被广泛应用于胆胰疾病的诊治,其在肝实质和门脉系统疾病中的应用也在迅速发展。本文回顾相关文献,概述了EUS在肝硬化门脉高压症的诊断及其并发症治疗中的研究现状及前景,重点介绍EUS引导下肝活检、EUS引导下门静脉压力梯度测量及EUS引导下胃静脉曲张治疗的研究进展。目前的数据表明:EUS引导下肝活检安全有效,在取样充分性上可与传统活检方式相媲美,而且术后恢复更快、疼痛程度更低。EUS引导下门静脉压力梯度测量较肝静脉压力梯度更准确地反映以窦前性门脉高压为主疾病的门静脉压力的程度,适用疾病更广。与常规内镜相比,EUS引导下血管介入术治疗胃静脉曲张优势众多,其中EUS引导弹簧圈联合组织胶治疗比单独使用弹簧圈或组织胶治疗更有效、并发症更少。

普萘洛尔与卡维地洛预防肝硬化患者并发食管胃静脉曲张破裂出血临床疗效比较

目的 比较普萘洛尔与卡维地洛预防肝硬化患者并发食管胃静脉曲张破裂出血的临床疗效和安全性。方法 2013年4月~2020年9月南京鼓楼医院消化科收治的连续肝硬化并发食管胃静脉曲张患者377例,符合纳入和排除标准患者312例,分别接受普萘洛尔(n=122)或卡维地洛(n=190)预防治疗。常规行肝静脉楔压(WHVP)和肝静脉游离压(FHVP)测定,计算肝静脉压力梯度(HVPG)。随访。结果 在随访期间,普萘洛尔处理组食管胃静脉曲张破裂出血(EVB)发生率为34.4%,显著高于卡维地洛处理组的13.2%(P<0.05);病死率分别为5.7%和1.6%(P>0.05);治疗后,66例普萘洛尔组WHVP、FHVP和HVPG分别为(22.7±5.1)mmHg、9.0(6.0~11.0)mmHg和(13.7±3.5)mmHg,与32例卡维地洛治疗组[(22.5±4.5)mmHg、(8.0(6.0~10.0))mmHg和(14.5±3.8)mmHg]比,差异无统计学意义(P>0.05)。结论 尽管在降低HVPG方面无显著性差异,应用卡维地洛预防肝硬化患者EVB的效果比普萘洛尔更优,值得进一步研究。

肝静脉压力梯度对肝移植受者术前评估及预后预测的价值

肝静脉压力梯度(HVPG)是诊断门静脉高压的“金标准”,可用于肝硬化的评估,与终末期肝病模型(MELD)评分系统联合应用能更精准地匹配肝硬化肝移植供受者,选择合适的手术时机,并为患者在等待肝移植期间的桥接治疗提供指导。除此之外,HVPG也能预测肝移植受者的预后,并为可能出现的并发症提供早发现、早干预的依据。因此,本文通过对HVPG在肝移植受者术前评估及预后预测的价值进行综述,以期为临床肝移植受者术前和术后的诊疗提供指导。

乙肝肝硬化门静脉高压患者磁共振肝脏T1弛豫时间与肝静脉压力梯度的相关性分析

目的 探讨MRI肝脏T1弛豫时间在乙肝肝硬化门静脉高压患者中与肝静脉压力梯度(HVPG)相关性。方法 选取本院接治的92例乙肝肝硬化患者的临床资料,以HVPG值划分为高压组和对照组。其中以HVPG>5 mmHg为高压组(n=60),以HVPG<5 mmHg为对照组(n=32)。分析两组一般临床资料、生化指标、凝血酶原时间、肝脏T1弛豫时间、肝脏硬度检测(LSM)及增强肝纤维化(ELF)评分,分析肝硬化门静脉高压患者肝脏T1弛豫时间与HVPG的关系。结果 高压组患者凝血酶原时间、肝脏T1弛豫时间长于对照组,差异均有统计学意义(P<0.05);此外,高压组患者LSM、ELF评分及HVPG均明显高于对照组,差异均有统计学意义(P<0.05);高压组肝脏T1弛豫时间与HVPG均呈正相关(r=0.533,P<0.05)。结论 乙肝肝硬化门静脉高压患者肝脏T1弛豫时间联合其他指标可代替HVPG,用于无创检测乙肝肝硬化门静脉高压,适合临床推广。

肝脏普美显增强MRI联合CT门静脉成像评估肝静脉压力梯度

目的探讨肝脏普美显增强MRI联合CT门静脉成像评估肝静脉压力梯度(HVPG)应用价值。方法回顾性分析40例行肝脏普美显增强MRI及腹部增强CT并在1周内完成HVPG测量的资料。分析门静脉、脾静脉管径、肝脾体积及其比值、肝胆期相对强化程度(RE)值与HVPG相关性,按照HVPG>12 mmHg及HVPG≤12 mmHg分为两组,使用多因素二元逻辑回归建立联合模型,绘制单一参数及延迟20 min RE20 min与肝脏体积/脾脏体积联合诊断指标受试者工作特征曲线(ROC),计算曲线下面积(AUC)。结果延迟10 min RE10 min及延迟20 min RE20 min与HVPG呈中度负相关(r值分别为-0.632、-0.688,P<0.05)。门静脉管径及脾脏体积与HVPG呈中度正相关(r值分别为0.690、0.592,P值<0.05),肝脏体积/脾脏体积与HVPG呈高度负相关(r=-0.794,P<0.05)。脾体积、肝脏体积/脾脏体积、门静脉管径、RE10 min及RE20 min、联合诊断模型(RE20 min与肝脏体积/脾脏体积)预测HVPG>12 mmHg AUC值分别为0.826、0.791、0.848、0.759、0.721、0.880。结论肝脏普美显增强MRI联合CTPV可较精确预测门静脉压力,RE20 min与肝脏/脾脏体积联合诊断模型可有效预测食管胃静脉曲张破裂出血,在门静脉高压无创诊断中有一定价值。

门静脉高压的无创指标及预测模型研究

目的:探讨肝静脉压力梯度(HVPG)的无创预测指标,并构建精准预测HVPG的无创预测模型。方法:选取2019年9月至2021年12月于十堰市太和医院感染科住院并行HVPG的肝硬化患者135例,收集一般临床资料、WBC、Hb、PLT、ALT、AST、总胆红素(TBil)、白蛋白(Alb)、国际标准化比值(INR)、门静脉宽度(PV)、胆囊壁厚度(GBWT)、脾直径(SD)及Fibroscan测量的肝硬度(LS)结果。比较HVPG在不同Child-pugh分级中的差异。根据HVPG结果将患者分为3组,分别为5~12 mmHg组、12~20 mmHg组、≥20 mmHg组。分析无创指标在不同HVPG分组中的差异,筛选有差异的指标进行多因素分析并构建HVPG的无创预测模型。通过受试者工作特征曲线(ROC)评价无创预测模型对HVPG的预测价值,并绘制列线图。结果:不同Child-pugh等级中,HVPG随着肝功能受损程度的加重而加重(P<0.05)。随着HVPG的升高,年龄、AST、TBil、INR、SD、LS呈升高趋势,而WBC、PLT、Hb、Alb呈下降趋势。多因素分析显示,PLT、Alb、LS是肝硬化患者HVPG加重的独立危险因素,构建了BPL评分模型:0.067×LS-0.051×PLT-0.122×Alb。对该模型行ROC曲线分析,BPL模型预测HVPG≥12 mmHg和HVPG≥20 mmHg的AUC分别为0.95、0.87,cutoff值分别为-6.50、-4.31,灵敏度、特异度分别为92.70%、88.46%和89.10%、73.75%。结论:无创指标PLT、Alb、LS是肝硬化患者HVPG升高的独立危险因素,基于上述指标构建的BPL评分预测模型可精准预测HVPG。

肝硬化食管胃静脉曲张内镜特征与肝静脉压力梯度相关性研究

目的探讨肝硬化食管胃静脉曲张内镜特征和分型与肝静脉压力梯度(hepatic venous pressure gradient,HVPG)的相关性。方法 45例肝硬化食管胃静脉曲张患者,通过颈静脉或股静脉途径插管球囊测压法进行HVPG测定。分别采用LDRf分型、Mc Cormick分度、丰永分型评估内镜下食管胃静脉曲张严重程度。同时收集患者人口学资料、临床表现、肝功能分级等。应用单因素和多因素统计方法分析临床和内镜特征与HVPG的相关性。结果单因素分析显示,食管胃静脉曲张的直径、危险度分级、丰永分型、Child-Pugh评分和分级与HVPG呈正相关(P<0.05)。多因素回归分析显示,仅有丰永分型(β=0.537)和LDRf分型中的危险度分级(Rf,β=0.368)是HVPG的独立预测因素(P<0.05),其预测模型为HVPG=丰永分型(Grade1,2,3)×3.97+Rf(0,1,2)×4.51+4.19。结论内镜下门脉高压性胃病严重程度和食管胃静脉曲张破裂出血危险度能较好地预测肝硬化门脉高压严重程度。

卡维地洛与普萘洛尔降低肝硬化门静脉高压效果的对照研究

目的探讨卡维地洛与普萘洛尔降低肝硬化门静脉高压患者肝静脉压力梯度（HVPG）的疗效。方法将72例肝硬化合并门静脉高压患者随机分为卡维地洛组、普萘洛尔组及安慰剂组，每组24例，分别服用卡维地洛、普萘洛尔及安慰剂，对比服药前及服药1个月后的血流动力学指标。结果卡维地洛及普萘洛尔均能显著降低肝硬化合并门静脉高压患者的HVPG（均P〈0．05），且卡维地洛降低HVPG及平均动脉压的幅度大于普萘洛尔（均P〈005）。卡维地洛组HVPG降至基线值20％以下或12mmHg以下患者比例亦明显多于普萘洛尔组（P〈0．05）。而普萘洛尔降低心率及心排出量的幅度均大于卡维地洛（均P〈0．05）。结论卡维地洛在降低肝硬化门静脉高压患者的门静脉压力方面较普萘洛尔更具优势。

乙型肝炎肝硬化患者肝静脉压力梯度与门静脉压力梯度相关性及临床价值

目的探讨乙型肝炎肝硬化患者门静脉压力梯度(PPG)与肝静脉压力梯度(HVPG)间相关性及其临床价值。方法收集2016年6月至2017年12月在南方医科大学南方医院接受经颈静脉肝内门体分流术(TIPS)乙型肝炎肝硬化患者肝静脉楔入压(WHVP)、肝静脉游离压(FHVP)、下腔静脉压(IVCP)、门静脉压(PVP)资料,同时计算HVPG和PPG,Spearman秩和检验分析WHVP与PVP、FHVP与IVCP、HVPG与PPG相关性。结果 17例患者符合入组条件,平均WHVP、PVP分别为(25.88±6.40) mmHg、(27.65±6.20) mmHg,两者呈正相关(r=0.914,P<0.01),斜率为0.883;平均FHVP、IVCP分别为(7.24±2.80) mmHg、(7.76±2.90) mmHg,两者呈正相关(r=0.815,P<0.01),斜率为0.847;平均HVPG、PPG分别为(18.65±6.60) mmHg、(19.94±6.56) mmHg,两者呈正相关(r=0.875,P<0.01),斜率为0.868。结论乙肝后肝硬化患者HVPG与PPG、WHVP与PVP、FHVP与IVCP有较好相关性,临床上可用HVPG反映乙肝后肝硬化患者PPG。

肝静脉压力梯度在肝硬化门静脉高压症患者中的临床应用

测量肝静脉压力梯度(HVPG)是评估门静脉高压症最常用的方法。大量研究表明,HVPG可作为食管静脉曲张出血的预测因子,此外,HVPG还可作为一个预后指标,可方便临床医生以其做参考为静脉曲张出血的一级预防和二级预防来制定合适的治疗策略。现阶段的治疗目标是使HVPG下降到12 mm Hg以下或比基线值下降20%,达到此目标的患者其食管静脉曲张的首次出血和再出血的风险均大大降低。对于一级预防,非选择性的β受体阻滞剂,如心得安,临床已广泛应用;然而,再出血的发生率仍然很高,临床上常用包括非选择性β受体阻滞剂在内的药物联合治疗和内镜干预,如经颈静脉肝内门体静脉分流术(TIPS)、内镜下硬化剂注射和内镜下套扎。主要探讨目前HVPG的测量方法及其临床应用,并重点对在肝硬化中HVPG对食管静脉曲张出血和再出血及治疗反应的预测作用做详细阐述。

肝静脉压梯度对食管曲张静脉出血的预测价值

目的探讨肝静脉压梯度(HVPG)对预测肝硬化食管曲张静脉出血(EVB)的临床价值。方法对26例有出血史和20例无出血史的肝硬化食管静脉曲张患者进行了HVPG测量,平均随访18个月观察HVPG值与EVB发生率之相关性。结果出血组HVPG值平均为15.13±3.57mmHg,明显高于非出血组11.07±2.21mmHg,两组相比差异显著(P<0.05);HVPG值>12mmHg者EVB或EVB再发率为73％,而HVPG值<12mmHg者EVB发生率为10％(P<0.01)。结论HVPG测定有预测首次EVB或EVB再发的价值。

无创诊断肝硬化门静脉高压症:血清标志物还是影像学检查?

门静脉高压症(portal hypertension,PH)是由不同因素引起的门静脉血液回流受阻而导致的门静脉系统压力增高,肝硬化是最常见的病因。压力持久升高会出现一系列相关的临床表现,如腹水、脾功能亢进症、食管胃静脉曲张破裂出血、肝肾综合征和肝性脑病等。肝静脉压力梯度(hepatic venous pressure gradient,HVPG)是肝静脉楔压与肝静脉自由压之间的差值,为目前临床诊断PH的“金标准”。不同分期的肝硬化患者,其发生PH并发症的风险、预后和治疗目标不同,这一观念已得到广泛的认同。HVPG测定不仅有助于PH类型的诊断和鉴别诊断,还能预测肝硬化失代偿事件的发生风险、进展程度和临床预后,指导治疗方案的选择并评估药物的疗效,近几年来在临床应用日益得到重视。2015年BavenoⅥ共识根据HVPG(≥10 mmHg)制订了临床显著性PH(clinically significant portal hypertension,CSPH)的概念,将代偿期肝硬化患者分为无CSPH和伴有CSPH两类。CSPH是肝硬化PH患者病程进展中的关键阶段,提示代偿期肝硬化患者发生静脉曲张、腹水、肝癌和失代偿事件的风险增加。

门静脉压力无创评估的研究进展

门静脉高压是慢性肝病的常见并发症,也是导致肝硬化多数临床后果的主要原因。正确评估门静脉压力对肝硬化治疗决策的制定和预后判断十分重要。肝静脉压力梯度(HVPG)是评估门静脉压力的金标准,但其是一种有创检测方法,难以在临床上常规开展,故迫切需要探索门静脉压力的无创评估方法。近年发现血清学指标、瞬时弹力超声、CT、MRI和多参数联合诊断模型具有诊断价值。本文就门静脉压力的无创评估进展作一综述。