Presence of varices in patients after hepatitis C virus eradication predicts deterioration in the FIB‐4 index

Aim Factors associated with improvement of liver fibrosis after successful hepatitis C virus (HCV) eradication by interferon (IFN)‐free direct‐acting antiviral agents (DAAs) have been not clarified well. Angiopoietin‐2 (Ang2) is reported to be associated with vascular leak and inflammation observed in patients with advanced liver fibrosis. Methods In this retrospective study, patients treated with IFN‐free DAAs who underwent transient elastography before and at 24‐weeks post‐treatment and achieved sustained viral response were enrolled. Baseline serum Ang2 was measured, and its relationship with other clinical factors was analyzed. Liver fibrosis stage was defined based on liver stiffness according to a previous report. Predictive factors for regression of liver fibrosis stage after DAA therapy were evaluated. Results Overall, 116 patients were analyzed. Baseline serum Ang2 levels were significantly associated with liver stiffness, spleen index, and liver stiffness‐based liver fibrosis stage. Moreover, 75% of patients experienced regression of liver fibrosis stage after DAA therapy. Multivariate analysis revealed that advanced liver fibrosis stage and Ang2 levels were significantly associated with regression of liver fibrosis stage after DAA therapy. In patients with advanced liver fibrosis (F3/4), baseline Ang2 level alone could predict regression of liver fibrosis stage. A baseline Ang2 cut‐off value (354 pg/ML) could predict regression of liver fibrosis stage after DAA therapy with high accuracy (sensitivity 0.882, specificity 0.733). Conclusions Evaluation of serum Ang2 levels before DAA therapy is important. Our results provide a novel mechanistic insight into non‐regression of liver stiffness after DAA therapy. Long‐term and larger studies are required.

Section: Discussionmentioning

confidence: 95%

High serum angiopoietin‐2 level predicts non‐regression of liver stiffness measurement‐based liver fibrosis stage after direct‐acting antiviral therapy for hepatitis C

Kawagishi

Suda

Kimura

et al. 2020

“…Thus, the shunts are also responsible for ascites formation through impaired improvement of liver dysfunction, as well as underling portal hypertension. Similar results were reported by Seko et al ., in that in patients who showed SVR after DAA therapy, the presence of varices was an independent predictor of deterioration of the FIB‐4 index . In contrast, El‐Sherif et al .…”

Section: Discussionmentioning

confidence: 99%

Involvement of portosystemic shunts in impaired improvement of liver function after direct‐acting antiviral therapies in cirrhotic patients with hepatitis C virus

Tsuji

Uchida

Uemura

et al. 2020

Aim: Factors responsible for impaired improvement of liver function despite sustained viral response after direct-acting antiviral agents therapies in cirrhotic patients with hepatitis C virus need to be elucidated.Methods: Liver function and the extent of portosystemic shunting were evaluated for 79 patients with compensated cirrhosis, in whom sustained viral response had been achieved after direct-acting antiviral agents therapies for hepatitis C virus at least 3 years earlier. Conclusions:A large size of portosystemic shunts was found to be a crucial determinant of impaired improvement of liver function, as well as of the development of portal hypertensionrelated events, even after sustained viral response in patients with compensated cirrhosis.

“…Improvements of hepatic function and prognosis are expected by viral eradication in HCV-infected patients. [8][9][10][11] Therefore, effective and safe antiviral therapies for patients with HCV-related decompensated cirrhosis are needed.…”

Section: Introductionmentioning

confidence: 99%

“…Patients with decompensated cirrhosis are at high risk for development of HCC, bleeding diatheses, and fulminant infections. Improvements of hepatic function and prognosis are expected by viral eradication in HCV‐infected patients 8–11 . Therefore, effective and safe antiviral therapies for patients with HCV‐related decompensated cirrhosis are needed.…”

Section: Introductionmentioning

confidence: 99%

Real‐world efficacy of sofosbuvir plus velpatasvir therapy for patients with hepatitis C virus‐related decompensated cirrhosis

Ohya

Imamura

Teraoka

et al. 2020

Aim: Combination therapy with sofosbuvir (SOF) plus velpatasvir (VEL) is approved for patients with hepatitis C virus (HCV)-related decompensated cirrhosis. We analyzed the real-world efficacy of SOF/VEL therapy. Methods: Thirty-three patients with HCV-related decompensated cirrhosis (25 and eight patients with Child B and C, respectively) were treated with SOF/VEL for 12 weeks. The HCV non-structural protein (NS)5A and NS5B drug resistance-associated substitutions (RASs) were determined by direct sequencing. Result: Thirty-two of 33 patients completed the treatment, but the remaining patient discontinued the therapy during third week of the treatment due to aggravation of hepatic encephalopathy. Serum HCV-RNA became negative during the treatment in all patients but relapsed after the end of therapy in five patients. In total, 28 out of 33 patients (85%) achieved sustained vi-rological response 12 weeks following completion of treatment (SVR12). The SVR12 rate was 96% in patients with Child B, but significantly lower, at 50%, in patients with Child C (P<0.05). In genotype 1b HCV-infected patients, all eight patients without baseline NS5A RASs, but only three of seven patients with RASs, achieved SVR12. Multivariate analysis identified Child B (odds ratio, 35.8 for Child C; P=0.045) as an independent predictor of SVR12. Median serum albumin levels significantly increased only in patients who achieved SVR12. Child-Pugh scores improved in 16 of 28 patients (57%) following achievement of SVR12. Conclusion: The effect of SOF/VEL therapy is lower for patients with Child C. Improvement of hepatic function is expected after viral eradication with SOF/VEL therapy in patients with decompensated cirrhosis.