Non-invasive response prediction in prophylactic carvedilol therapy for cirrhotic patients with esophageal varices

Kim, Hwi Young; So, Young; Kim, Won; Ahn, Dong Won; Jung, Yong Jin; Woo, Hyunsik; Kim, Dong‐Hee; Kim, Moon Young; Baik, Soon Koo

doi:10.1016/j.jhep.2018.10.018

Cited by 70 publications

(51 citation statements)

References 49 publications

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“…Still, these noninvasive methods do not confer the same information as HVPG response, as they are incapable of monitoring the dynamics of PH with adequate accuracy. It would have been interesting to assess the diagnostic performance of spleen stiffness in this setting, because changes in spleen stiffness have recently shown some promise as a noninvasive marker of HVPG response to carvedilol . Future studies assessing clinical endpoints in larger cohorts should aim to refine the use of combinations and/or serial assessments of noninvasive tests for risk stratification.…”

Section: Discussionmentioning

confidence: 99%

“…It would have been interesting to assess the diagnostic performance of spleen stiffness in this setting, because changes in spleen stiffness have recently shown some promise as a noninvasive marker of HVPG response to carvedilol. (44) Future studies assessing clinical endpoints in larger cohorts should aim to refine the use of combinations and/or serial assessments of noninvasive tests for risk stratification. SVR to IFN-free therapy was associated with a decrease in LBP and tended to lower IL-6 levels.…”

Section: Discussionmentioning

confidence: 99%

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Changes in Hepatic Venous Pressure Gradient Predict Hepatic Decompensation in Patients Who Achieved Sustained Virologic Response to Interferon‐Free Therapy

et al. 2019

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Background and Aims Sustained virologic response (SVR) to interferon (IFN)‐free therapies ameliorates portal hypertension (PH); however, it remains unclear whether a decrease in hepatic venous pressure gradient (HVPG) after cure of hepatitis C translates into a clinical benefit. We assessed the impact of pretreatment HVPG, changes in HVPG, and posttreatment HVPG on the development of hepatic decompensation in patients with PH who achieved SVR to IFN‐free therapy. Moreover, we evaluated transient elastography (TE) and von Willebrand factor to platelet count ratio (VITRO) as noninvasive methods for monitoring the evolution of PH. Approach and Results The study comprised 90 patients with HVPG ≥ 6 mm Hg who underwent paired HVPG, TE, and VITRO assessments before (baseline [BL]) and after (follow‐up [FU]) IFN‐free therapy. FU HVPG but not BL HVPG predicted hepatic decompensation (per mm Hg, hazard ratio, 1.18; 95% confidence interval, 1.08‐1.28; P < 0.001). Patients with BL HVPG ≤ 9 mm Hg or patients who resolved clinically significant PH (CSPH) were protected from hepatic decompensation. In patients with CSPH, an HVPG decrease ≥ 10% was similarly protective (36 months, 2.5% vs. 40.5%; P < 0.001) but was observed in a substantially higher proportion of patients (60% vs. 24%; P < 0.001). Importantly, the performance of noninvasive methods such as TE/VITRO for diagnosing an HVPG reduction ≥ 10% was inadequate for clinical use (area under the receiver operating characteristic curve [AUROC], < 0.8), emphasizing the need for HVPG measurements. However, TE/VITRO were able to rule in or rule out FU CSPH (AUROC, 0.86‐0.92) in most patients, especially if assessed in a sequential manner. Conclusions Reassessment of HVPG after SVR improved prognostication in patients with pretreatment CSPH. An “immediate” HVPG decrease ≥ 10% was observed in the majority of these patients and was associated with a clinical benefit, as it prevented hepatic decompensation. These results support the use of HVPG as a surrogate endpoint for interventions that lower portal pressure by decreasing intrahepatic resistance.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Changes in Hepatic Venous Pressure Gradient Predict Hepatic Decompensation in Patients Who Achieved Sustained Virologic Response to Interferon‐Free Therapy

et al. 2019

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“…However, spleen stiffness measurement seems to be a suitable non-invasive tool for evaluation of response to NSBB. Two recent studies using pSWE [53]and VCTE [54] technique indicate promising results in noninvasive NSBB response evaluation but further data and standardization is needed in this field. Absence of spleen stiffness measurement could be considered a weak point of our study; nonetheless, based on the above-mentioned data, we could have not expected a breaking improvement of HVPG prediction using also spleen stiffness measurement.…”

Section: Plos Onementioning

confidence: 99%

Liver stiffness measured by two-dimensional shear-wave elastography predicts hepatic vein pressure gradient at high values in liver transplant candidates with advanced liver cirrhosis

et al. 2021

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Liver stiffness is a reliable non-invasive predictor of Hepatic Venous Pressure Gradient (HVPG) above 10 mm Hg. However, it failed to predict higher thresholds of HVPG. Our aim was to investigate whether liver stiffness and selected previously published non-invasive blood biomarkers could predict higher HVPG thresholds in liver transplant candidates without ongoing alcohol use. One hundred and nine liver transplant candidates with liver cirrhosis of various aetiologies underwent direct HVPG measurement, liver stiffness measurement by 2D shear-wave elastography (Aixplorer Multiwave, Supersonic Imagine, France) and assessment of blood HVPG biomarkers (osteopontin, VCAM-1, IL-6, TNF-α, IL-1ra/IL-1F3 and ELF score). The correlation between liver stiffness and HVPG was linear up to 30 mm Hg of HVPG (r = 0.765, p < 0.0001). The regression lines had similar slopes for HVPG values below and above 16 mm Hg (p > 0.05) and the correlation in patients with HVPG <16 mm Hg (r = 0.456, p = 0.01) was similar to patients with HVPG ≥ 16 mm Hg (r = 0.499, p < 0.0001). The correlation was similar in the subgroup patients with alcoholic (r = 0.718, p < 0.0001), NASH (r = 0.740, p = 0.008), cryptogenic (r = 0.648, p = 0,0377), cholestatic and autoimmune (r = 0.706, p < 0.0001) and viral cirrhosis (r = 0.756, p < 0.0001). Liver stiffness distinguished patients with HVPG above 16, and 20 mm Hg with AUROCs 0.90243, and 0.86824, sensitivity 0.7656, and 0.7027, and specificity 0.9333, and 0.8750. All studied blood biomarkers correlated better with liver stiffness than with HVPG and their AUROCs did not exceed 0.8 at both HVPG thresholds. Therefore, a composite predictor superior to liver stiffness could not be established. We conclude that liver stiffness is a clinically reliable predictor of higher HVPG thresholds in non-drinking subjects with advanced liver cirrhosis.

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“…In a single‐center prospective proof‐of‐concept cohort study, Kim et al 99 estimated a prediction model for hemodynamic response to prophylactic carvedilol therapy in cirrhotic patients with esophageal varices: ModelΔspleen stiffness = 0.0490 − 2.8345 × Δspleen stiffness with score = (exp(ModelΔspleen stiffness))/(1 + exp(ModelΔspleen stiffness)). If the threshold value of 0.530 was used, the model had an area under the receiver operating characteristic curve of 0.803.…”

Section: Primary Prevention Of Variceal Hemorrhagementioning

confidence: 99%

Primary prevention of bleeding from esophageal varices in patients with liver cirrhosis: An update and review of the literature

Garbuzenko

Arefyev

2020

J Evidence Based Medicine

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All patients with liver cirrhosis and portal hypertension should be stratified by risk groups to individualize different therapeutic strategies to increase the effectiveness of treatment. In this regard, the development of primary prophylaxis of variceal bleeding and its management according to the severity of portal hypertension may be promising. This paper is to describe the modern principles of primary prophylaxis of esophageal variceal bleeding in patients with liver cirrhosis. The PubMed and EMbase databases, Web of Science, Google Scholar, and the Cochrane Database of Systematic Reviews were used to search for relevant publications from 1999 to 2019. The results suggested that depending on the severity of portal hypertension, patients with cirrhosis should be divided into those who need preprimary prophylaxis, which aims to prevent the formation of esophageal varices, and those who require measures that aim to prevent esophageal variceal bleeding. In subclinical portal hypertension, therapy should be etiological and pathogenetic. Cirrhosis with clinically significant portal hypertension should receive nonselective β‐blockers if they have small esophageal varices and risk factors for variceal bleeding. Nonselective β‐blockers are the first‐line drugs for the primary prevention of bleeding from medium to large‐sized esophageal varices. Endoscopic band ligation is indicated for the patients who are intolerant to nonselective β‐blockers or in the case of contraindications to pharmacological therapy. In summary, the stratification of cirrhotic patients by the severity of portal hypertension and an individual approach to the choice of treatment may increase the effectiveness of therapy as well as improve survival rate of these patients.

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Non-invasive response prediction in prophylactic carvedilol therapy for cirrhotic patients with esophageal varices

Cited by 70 publications

References 49 publications

Changes in Hepatic Venous Pressure Gradient Predict Hepatic Decompensation in Patients Who Achieved Sustained Virologic Response to Interferon‐Free Therapy

Changes in Hepatic Venous Pressure Gradient Predict Hepatic Decompensation in Patients Who Achieved Sustained Virologic Response to Interferon‐Free Therapy

Liver stiffness measured by two-dimensional shear-wave elastography predicts hepatic vein pressure gradient at high values in liver transplant candidates with advanced liver cirrhosis

Primary prevention of bleeding from esophageal varices in patients with liver cirrhosis: An update and review of the literature

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