Sustained virologic response to interferon-free therapies ameliorates HCV-induced portal hypertension

Background & Aims We aimed to investigate the impact of sustained virologic response (SVR) to interferon (IFN)-free therapies on portal hypertension in patients with paired hepatic venous pressure gradient (HVPG) measurements. Methods One hundred and four patients with portal hypertension (HVPG ⩾6 mmHg) who underwent HVPG and liver stiffness measurement before IFN-free therapy (baseline [BL]) were retrospectively studied. Among 100 patients who achieved SVR, 60 patients underwent HVPG and transient elastography (TE) after antiviral therapy (follow-up [FU]). Results SVR to IFN-free therapies significantly decreased HVPG across all BL HVPG strata: 6–9 mmHg (BL: 7.37 ± 0.28 vs. FU: 5.11 ± 0.38 mmHg; −2.26 ± 0.42 mmHg; p <0.001), 10–15 mmHg (BL: 12.2 ± 0.4 vs. FU: 8.91 ± 0.62 mmHg; −3.29 ± 0.59 mmHg; p <0.001) and ⩾16 mmHg (BL: 19.4 ± 0.73 vs. FU: 17.1 ± 1.21 mmHg; −2.3 ± 0.89 mmHg; p = 0.018). In the subgroup of patients with BL HVPG of 6–9 mmHg, HVPG normalized (<6 mmHg) in 63% (12/19) of patients, while no patient progressed to ⩾10 mmHg. Among patients with BL HVPG ⩾10 mmHg, a clinically relevant HVPG decrease ⩾10% was observed in 63% (26/41); 24% (10/41) had a FU HVPG <10 mmHg. Patients with Child-Pugh stage B were less likely to have a HVPG decrease (hazard ratio [HR]: 0.103; 95% confidence interval [CI]: 0.02–0.514; p = 0.006), when compared to Child-Pugh A patients. In the subgroup of patients with BL CSPH, the relative change in liver stiffness (per %; HR: 0.972; 95% CI: 0.945–0.999; p = 0.044) was a predictor of a HVPG decrease ⩾10%. The area under the receiver operating characteristic curve for the diagnosis of FU CSPH by FU liver stiffness was 0.931 (95% CI: 0.865–0.997). Conclusions SVR to IFN-free therapies might ameliorate portal hypertension across all BL HVPG strata. However, changes in HVPG seemed to be more heterogeneous among patients with BL HVPG of ⩾16 mmHg and a HVPG decrease was less likely in patients with more advanced liver dysfunction. TE might be useful for the non-invasive evaluation of portal hypertension after SVR. Lay summary We investigated the impact of curing hepatitis C using novel interferon-free treatments on portal hypertension, which drives the development of liver-related complications and mortality. Cure of hepatitis C decreased portal pressure, but a decrease was less likely among patients with more pronounced hepatic dysfunction. Transient elastography, which is commonly used for the non-invasive staging of liver disease, might identify patients without clinically significant portal hypertension after successful treatment. We aimed to investigate the impact of sustained virologic response (SVR) to interferon (IFN)-free therapies on portal hypertension in patients with paired hepatic venous pressure gradient (HVPG) measurements. One hundred and four patients with portal hypertension (HVPG ⩾6 mmHg) who underwent HVPG and liver stiffness measurement before IFN-free therapy (baseline [BL]) were retrospectively studied. Among 100 patients who achieved SVR, 60 patients underwent HVPG and transient elastography (TE) after antiviral therapy (follow-up [FU]). SVR to IFN-free therapies significantly decreased HVPG across all BL HVPG strata: 6–9 mmHg (BL: 7.37 ± 0.28 vs. FU: 5.11 ± 0.38 mmHg; −2.26 ± 0.42 mmHg; p <0.001), 10–15 mmHg (BL: 12.2 ± 0.4 vs. FU: 8.91 ± 0.62 mmHg; −3.29 ± 0.59 mmHg; p <0.001) and ⩾16 mmHg (BL: 19.4 ± 0.73 vs. FU: 17.1 ± 1.21 mmHg; −2.3 ± 0.89 mmHg; p = 0.018). In the subgroup of patients with BL HVPG of 6–9 mmHg, HVPG normalized (<6 mmHg) in 63% (12/19) of patients, while no patient progressed to ⩾10 mmHg. Among patients with BL HVPG ⩾10 mmHg, a clinically relevant HVPG decrease ⩾10% was observed in 63% (26/41); 24% (10/41) had a FU HVPG <10 mmHg. Patients with Child-Pugh stage B were less likely to have a HVPG decrease (hazard ratio [HR]: 0.103; 95% confidence interval [CI]: 0.02–0.514; p = 0.006), when compared to Child-Pugh A patients. In the subgroup of patients with BL CSPH, the relative change in liver stiffness (per %; HR: 0.972; 95% CI: 0.945–0.999; p = 0.044) was a predictor of a HVPG decrease ⩾10%. The area under the receiver operating characteristic curve for the diagnosis of FU CSPH by FU liver stiffness was 0.931 (95% CI: 0.865–0.997). SVR to IFN-free therapies might ameliorate portal hypertension across all BL HVPG strata. However, changes in HVPG seemed to be more heterogeneous among patients with BL HVPG of ⩾16 mmHg and a HVPG decrease was less likely in patients with more advanced liver dysfunction. TE might be useful for the non-invasive evaluation of portal hypertension after SVR.