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

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 as- sessed the i...

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Detalles Bibliográficos
Autores: Mandorfer, Mattias, Kozbial, Karin, Schwabl, Philipp, Chromy, David, Semmler, Georg, Stättermayer, Albert F., Pinter, Matthias, Hernández Gea, Virginia, Fritzer-Szekere, Monika, Steindl-Munda, Petra, Trauner, Michael, Peck-Radosavljevic, Markus, García Pagán, Juan Carlos, Ferenci, Peter, Reiberger, Thomas
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2020
País:España
Institución:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
Repositorio:Recercat. Dipósit de la Recerca de Catalunya
OAI Identifier:oai:recercat.cat:2445/160312
Acceso en línea:https://hdl.handle.net/2445/160312
Access Level:acceso abierto
Palabra clave:Cirrosi hepàtica
Hipertensió
Interferó
Hepatic cirrhosis
Hypertension
Interferon
Descripción
Sumario: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 as- sessed 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 elastogra- phy (TE) and von Willebrand factor to platelet count ratio (VITRO) as noninvasive methods for monitoring the evolu- tion 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 noninva- sive 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 im- proved 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 inter- ventions that lower portal pressure by decreasing intrahepatic resistance.