Long‐term liver stiffness assessment in hepatitis C virus patients undergoing antiviral therapy: Results from a 5‐year cohort study

Facciorusso, Antonio; Prete, Valentina Del; Turco, Antonio; Buccino, Rosario Vincenzo; Nacchiero, Maurizio Cosimo; Muscatiello, Nicola

doi:10.1111/jgh.14008

Cited by 56 publications

(47 citation statements)

References 23 publications

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“…Although there is ample evidence that supports the beneficial effect of HCV eradication on fibrotic regression, the relentless recover may not be taken for granted across all pupations and studies. The regression slop has been suggested to be very slow by non-invasive modalities 15 , 16 . It has also been reported that cirrhosis patients experience only 5% of net fibrosis improvement after 10 years of follow-up 15 .…”

Section: Discussionmentioning

confidence: 99%

“…More quantitative analyses, including immunostaining for cell-specific markers or morphometric analysis, may provide a future solution 20 , 36 . As noninvasive tests are widely applied in the directly acting antivirals (DAAs) era, accuracy is challenging and doubtful in the post-curative status 16 , 38 . Liver biopsy remains the gold standard to assess liver fibrosis.…”

Section: Discussionmentioning

confidence: 99%

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Tolloid-like 1 genetic variants determine fibrosis regression in chronic hepatitis C patients with curative antivirals

Huang

Yeh

Lin

et al. 2018

Sci Rep

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Hepatitis C virus (HCV) eradication by antivirals promote fibrosis modification. Whether host genetics determined fibrosis regression in chronic hepatitis C (CHC) patients with sustained virological response (SVR) is to be determined. One hundred and fifty-six SVR patients with paired liver biopsy before and after antivirals were enrolled. Host genetic factors including single nucleotide polymorphism rs17047200 of tolloid-like 1(TLL-1) were analyzed for their association with fibrosis modification. The proportions of improved, unchanged and worsening fibrotic stags were 39.1% (n = 61), 39.1% (n = 61), and 21.8% (n = 34), respectively. The rate of annual fibrotic improvement was 0.16 ± 0.79. There was a significant trend of increased fibrotic improvement rate in patients from F01 to F4 (P < 0.001). However, the rate of improvement seemed more limited in cirrhotic patients among those with advanced liver disease. Patients with fibrotic improvement had a significantly higher proportion of TLL-1 rs17047200 AA genotype compared to those without (92.5% vs. 79.3%, p = 0.039). Logistic regression analysis revealed that the TLL-1 rs17047200 AA genotype was the only independent factor associated with fibrosis improvement (odds ratio/95% confidence intervals: 3.2/1.01–10.12, p = 0.047). Compared with TLL-1 rs17047200 non-AA carriers, a significantly higher proportion of fibrosis improvement in AA genotype carriers was observed among patients with F0-2 (33.3% vs. 0%, p = 0.005) but not with F34 (70% vs. 80%, p = 1). We concluded that TLL-1 genetic variants determined fibrotic improvement in CHC with curative antivirals, particularly in patients with mild liver disease.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Tolloid-like 1 genetic variants determine fibrosis regression in chronic hepatitis C patients with curative antivirals

Huang

Yeh

Lin

et al. 2018

Sci Rep

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“…It has 91% specificity and an 87% sensitivity for detecting cirrhosis [ 11 ]. A recent meta-analysis indicated that there is a greater reduction of the TE score after DAA therapy compared to IFN-based treatment, with some data indicating a 50% decline in the TE score 6 months after DAA therapy, followed by a slower decline over the subsequent 5 years [ 12 – 15 ]. It is thought that liver stiffness during chronic infection is a combination of hepatic inflammation and fibrosis, while after viral eradication the component of inflammation abates, followed by a slower phase of fibrosis regression.…”

Section: Introductionmentioning

confidence: 99%

Soluble Markers of Immune Activation Differentially Normalize and Selectively Associate with Improvement in AST, ALT, Albumin, and Transient Elastography During IFN-Free HCV Therapy

Kostadinova

Shive

Zebrowski

et al. 2018

PAI

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Background:During chronic hepatitis C virus (HCV) infection, Aspartate Aminotransferase (AST) and Alanine Aminotransferase (ALT) levels mark active liver inflammation and tissue damage, while albumin reflects synthetic liver function and nutritional status. Transient Elastography (TE) is a clinical measure of liver stiffness that facilitates evaluation of liver damage stage. While a portion of the TE score is attributable to liver fibrosis and relatively irreversible damage, another component of the TE score is attributable to liver inflammation or edema. Markers of inflammation during chronic HCV infection include soluble markers of immune activation, which are also associated with morbid outcome (including cardiovascular disease and liver-disease progression). Whether soluble markers of immune activation or changes in their level during HCV therapy relate to normalization of AST, ALT, Albumin, or TE score, is not clear.Methods:We evaluated soluble markers of immune activation (plasma sCD14, IL-6, sCD163, autotaxin [ATX], and Mac2BP) and TE score, and their relationship in 20 HCV-infected patients before, during, and after HCV-directed IFN-free direct-acting antiviral (DAA) therapy. We evaluated normalization of parameters and the relationship between each over a 6-month window.Results:Before therapy, serum AST levels positively correlated with plasma levels of sCD14, sCD163, and Mac2BP, while ALT levels positively correlated with Mac2BP. Serum albumin level negatively correlated with plasma IL-6 and ATX levels. IFN-free therapy uniformly resulted in sustained virological response at 12 and 24 weeks after therapy completion. After initiation of therapy AST and ALT normalized, while levels of ATX, Mac2BP, sCD163, and TE score partially normalized over 6 months. Additionally, change in AST level and APRI score correlated with change in sCD163, IL-6, and Mac2BP levels, and change in ALT correlated with change in IL-6 and Mac2BP levels. Improvement in TE score correlated with a decrease in the level of sCD14 at week 4, and almost statistically significant with decrease in sCD14 at weeks 20-24 after initiation of IFN-free HCV therapy.Conclusions:Soluble markers of immune activation normalize or partially normalize at different rates after initiation of curative HCV DAA therapy, and TE scores improve, with wide variability in the degree of absolute improvement in liver stiffness from patient to patient. Decline magnitude of sCD14 was associated with improvement in TE score, while magnitude of improvement in AST correlated with reduction in sCD163 levels. These data provide support for a model where monocyte/Kupffer cell activation may account for a portion of the liver inflammation and edema, which is at least partially reversible following initiation of HCV DAA therapy.

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“…The results were spectacular with respect to the presence of liver cirrhosis: it disappeared in half of the patients after 6 months and it was still present in just under 5% of them after 4 years of the end of therapy. Instead, if patients did not respond to treatment, the liver stiffness value declined slightly at its end (from 19.2 kPa to 18.1 kPa), after which it returned to the baseline value after half a year and then increased along time to 23.7 kPa at 5 years [48].…”

Section: Liver Stiffness -A Way To Monitor the Evolution Of Patients mentioning

confidence: 98%

Liver stiffness in chronic hepatitis C virus infection

Mihăilă

2019

Romanian Journal of Internal Medicine

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Introduction. The severity of liver fibrosis can be assessed noninvasively today by liver stiffness measurements. Vibration-controlled transient elastography, shear wave elastography or magnetic resonance elastography are techniques increasingly used for this purpose. Methods. This article presents the recent advances in the use of new techniques for liver fibrosis assessment in chronic hepatitis C: the correlation between liver stiffness values and liver fibrosis estimated by liver biopsies, the prognosis role of liver stiffness values, their usefulness in monitoring the treatment response, in assessing the severity of portal hypertension and in estimating the presence of esophageal varices. Scientific articles from January 2017 to January 2018 were searched in PubMed and PubMed Central databases, using the terms “liver stiffness” and “hepatitis C”. Results. The median liver stiffness values measured with different techniques are not identical, so that FibroScan thresholds cannot be used on any other elastographic machine. The higher the liver’s stiffness measurement, the higher the liver-related events in patients with chronic hepatitis C. A liver stiffness measurement over 17 kPa could be an independent predictor for the presence of esophageal varices as well as a spleen with a longitudinal span ≥ 15 cm for patients with a value of liver stiffness < 17 kPa. A progressive and persistent decrease in liver stiffness is dependent on sustained virological response achievement. The lack of liver stiffness decrease has been associated with relapsers and a low value of liver stiffness at baseline. Conclusion. Liver stiffness provides clues about the severity and evolution of liver disease.

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Long‐term liver stiffness assessment in hepatitis C virus patients undergoing antiviral therapy: Results from a 5‐year cohort study

Abstract: Stiffness declines significantly after achieving response, and the magnitude of decline is greater in the first year after treatment, while it tends to plateau from 1 year onwards.

Cited by 56 publications

References 23 publications

Tolloid-like 1 genetic variants determine fibrosis regression in chronic hepatitis C patients with curative antivirals

Tolloid-like 1 genetic variants determine fibrosis regression in chronic hepatitis C patients with curative antivirals

Soluble Markers of Immune Activation Differentially Normalize and Selectively Associate with Improvement in AST, ALT, Albumin, and Transient Elastography During IFN-Free HCV Therapy

Liver stiffness in chronic hepatitis C virus infection

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