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

Mandorfer, Mattias; Kozbial, K; Schwabl, Philipp; Freissmuth, C; Schwarzer, R; Stern, R; Chromy, David; Stättermayer, Albert Friedrich; Reiberger, Thomas; Beinhardt, Sandra; Sieghart, Wolfgang; Trauner, Michael; Hofer, Harald; Ferlitsch, Arnulf; Ferenci, Péter; Peck‐Radosavljevic, Markus

doi:10.1016/j.jhep.2016.05.027

Cited by 272 publications

(236 citation statements)

References 34 publications

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“…Although the overall liver stiffness significantly decreased at SVR12, a high percentage of patients still had a TE >20kPa and remained exposed to a high risk of developing liver-related complications. Our study is in concordance with the Mandorfer et al study [25], suggesting that TE might be useful for the noninvasive evaluation of portal hypertension after SVR.…”

Section: Discussionsupporting

confidence: 92%

Real-Life Use of 3 Direct-Acting Antiviral Regimen in a Large Cohort of Patients with Genotype-1b HCV Compensated Cirrhosis

Gheorghe

Iacob

Curescu

et al. 2017

JGLD

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Background & Aims: Ombitasvir/Paritaprevir/ritonavir/Dasabuvir (OBV/PTV/r+DSV) is one of the elective direct-acting antivirals (DAAs) recommended by international guidelines and the only one covered by the National Insurance System in Romania until November 2016. Our aim was to present the first prospective Romanian cohort evaluating the effectiveness and safety in clinical practice of this 3DAA combination in patients with HCV genotype-1b Child A liver cirrhosis.Methods: 681 patients received OBV/PTV/r+DSV+RBV for 12 weeks and were assessed clinically and biologically at baseline, week 4, 8, 12 (end of treatment, EOT), and 12 weeks after therapy (sustained viral response, SVR).Results: Per protocol, EOT virological response was 99.8% and SVR12 rate was 99.4%. Adverse events were present in 36.4% of patients. Permanent discontinuation of 3DAA regimen due to side effects was reported in 11 patients (1.6%). In 47.6% (185/389) of patients, Transient Elastography values were >20kPa (defined as clinically significant portal hypertension, CSPH) at baseline. Independent variables associated with CSPH were: baseline cholesterol level (p=0.003), platelet count <120,000/mm³ (p=0.02), MELD score (p=0.01).Liver stiffness measurement has significantly improved between baseline (26.6±12.7kPa) and SVR12 (21.6±11.8kPa) (p<0.0001). The same was true for APRI score (2.66±0.15 at baseline vs 0.85±0.02 at SVR12, p<0.0001) and FIB4 score (5.53±0.28 vs 3.24±0.08, p<0.0001), but not for Lok score (0.57±0.01 vs 0.63±0.01, p<0.0001).Conclusions: We report a high efficacy of the 3DAA regimen in a homogeneous compensated HCV genotype-1b liver cirrhosis population, in a real-life setting. Noninvasive fibrosis scores significantly improved at SVR12.Abbreviations: AE: adverse effect; AFP: alpha feto-protein; CSPH: clinically significant portal hypertension; DAA: direct-acting antiviral; EOT: end of treatment; GT: genotype; HCV: hepatitis C virus; HCC: hepatocellular carcinoma; LSM: liver stiffness measurement; MELD: Model of end stage liver disease; NHIA: National Health Insurance Agency; OBV/PTV/r+DSV: Ombitasvir/Paritaprevir/ritonavir/Dasabuvir; RBV: ribavirin; SAE: serious adverse effect; SVR: sustained viral response; TE: transient elastography.

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Section: Discussionsupporting

confidence: 92%

Real-Life Use of 3 Direct-Acting Antiviral Regimen in a Large Cohort of Patients with Genotype-1b HCV Compensated Cirrhosis

Gheorghe

Iacob

Curescu

et al. 2017

JGLD

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“…Liver fibrosis has been proven to be regressive in some patients who eliminated the virus; [18] hence post treatment transient elastography would be beneficial in defining patients within the surveillance program. Moreover, surveillance programs had to be strengthened by predictive genetic as well as angiogenic HCC bio-markers.…”

Section: Discussionmentioning

confidence: 99%

Hepatocellular carcinoma following direct anti-viral for hepatitis C treatment: a report of an Egyptian case series

Rewisha¹,

Elsabaawy²,

Elshaarawy³

et al. 2017

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How to cite this article: Rewisha EA, Elsabaawy MM, Elshaarawy O, Abdallah A, Elsabaawy DM, Alhaddad OM. Hepatocellular carcinoma following direct anti-viral for hepatitis C treatment: a report of an Egyptian case series. Hepatoma Res 2017;3:178-81.Egypt had been vexed by the highest load of chronic hepatitis C in the world. It represents a vast market of the new direct-acting anti-viral drugs (DAAs); effectively treating chronic hepatitis C virus (HCV) infection. Eradication of HCV in Egypt has been challenged by the observed increased diagnosis of hepatocellular carcinoma (HCC) in relation to DAAs therapy. This is the first Egyptian report annotating to a series of sixteen chronic HCV infected cases without a diagnosis of HCC before DAAs therapy and unexpected development of HCC during or after completion of DAAs therapy. Key words:Chronic hepatitis C, direct-acting anti-viral drugs, hepatocellular carcinoma, Egypt ABSTRACTArticle history:

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“…In a recent study it has been found that hepatic venous pressure gradient (HVPG) decreaseed after interferon-free treatment in patients with HCV-related cirrhosis, but in patients with a pretreatment HVPG of 10-15 mmHg, clinically significant portal hypertension was only decreased in 43% [21] . In our study, 4 out of 4 patients who developed clinical decompensation had a previous history of ascitis or were diagnosed with hepatocellular carcinoma during the follow-up, suggesting a more advanced disease.…”

Section: Discussionmentioning

confidence: 99%

Clinical outcomes of direct-acting antiviral therapy in patients with compensated hepatitis C virus-related cirrhosis

Berge¹,

Arencibía²,

Oton³

et al. 2017

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Aim:The aim was to assess the clinical impact of direct-acting antiviral treatment in patients with compensated hepatitis C virus-related cirrhosis after one year of follow-up. Methods: An observational retrospective study was conducted on 129 consecutive patients with compensated cirrhosis treated in 2015, analyzing the evolution of liver function and the development of hepatocellular carcinoma and clinical decompensations. Results: The median follow-up time was 16 months. Most patients were males (73%), the mean age was 58.1 years and the most frequent genotype was 1b (52.2%). All participants were Child-Pugh A class at the start of the treatment and the median model for end-stage liver disease (MELD) score was 7. Four patients (4.4%) suffered a decompensation: three episodes of ascites and one acute on chronic liver failure. The incidence of de novo hepatocellular carcinoma during the follow-up was 3.6%. Seven patients (7.8%) improved MELD score more than one point and in 11 patients (12.2%) it worsened more than one point. There was a significant improvement in the mean platelets count [P < 0.001, 95% confidence interval (CI) : -26,360, -12,096] and in the mean albumin levels (P < 0.001, 95% CI: -322, -130) after treatment. Conclusion: Direct-acting antiviral treatment is not associated in the short term with a decrease in the development of hepatic decompensation or hepatocellular carcinoma compared to what it was reported for untreated compensated cirrhotic patients. There is an improvement in pre and post-treatment platelet counts and albumin levels showing a probable improvement of the hepatic function. Key words:Direct-acting antiviral therapy, compensated cirrhosis, hepatocellular carcinoma, clinical decompensation ABSTRACTArticle history:

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

Cited by 272 publications

References 34 publications

Real-Life Use of 3 Direct-Acting Antiviral Regimen in a Large Cohort of Patients with Genotype-1b HCV Compensated Cirrhosis

Real-Life Use of 3 Direct-Acting Antiviral Regimen in a Large Cohort of Patients with Genotype-1b HCV Compensated Cirrhosis

Hepatocellular carcinoma following direct anti-viral for hepatitis C treatment: a report of an Egyptian case series

Clinical outcomes of direct-acting antiviral therapy in patients with compensated hepatitis C virus-related cirrhosis

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