الفهرس 
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Abstract
Infection with hepatitis C virus (HCV) is present in more than 184 million people worldwide and is responsible for the development of chronic hepatitis, cirrhosis and hepatocellular carcinoma, besides being the leading indication for liver transplantation in Western countries (Marcellin et al., 2018).
Until 2014, interferon-based treatment was the standard of care for HCV therapy. This treatment was not free from complications, especially in patients with advanced fibrosis and cirrhosis, in whom low rates of sustained virologic response (SVR) were observed (Fernandez-Rodriguez et al., 2010). However, the introduction of new direct-acting antiviral agents (DAAs) in the current treatment for HCV patients have changed this paradigm, achieving high SVR rates with minimal side effects, even in patients with cirrhosis (EASL, 2015).
The assessment of liver fibrosis by non-invasive methods is replacing invasive liver biopsy due to patient wariness and the low but ever-present morbidity of biopsies. Today, despite the historical dogma of the biopsy being the gold standard, the use of noninvasive liver fibrosis detection vastly outnumbers biopsies in chronic liver diseases (Mauss et al., 2017).
Mac-2bp was identified as a hyperfucosylated protein in the conditioned medium of cancer cell lines. Recently, it was demonstrated that serum Mac-2bp levels are also associated with liver fibrosis as an independent factor from a multivariate analysis (Kamada et al., 2013a).
In the current study, our aim was to study the impact of sustained virologic response (SVR) to direct acting antiviral therapies (DAAs) on liver stiffness using the serum level of Mac-2 binding protein (Mac-2bp) in patients with chronic HCV receiving DAAs according to National Committee for Combating Viral Hepatitis before treatment and after achieving SVR12, and assess how this biomarker correlates with another standard non-invasive methods of fibrosis assessment PAPAS index and Fibro scan.
Our study reported a significant improvement in liver stiffness measurement (LSM) with transient elastography (TE) after achieving sustained virologic response 12 weeks after treatment (SVR12), with significant decline in the studied validated score PAPAS index and the serologic noninvasive measurement Mac-2bp. Our results also, show that 42.3% of the cirrhotic patients (F4) became non-cirrhotic after achieving SVR. The remaining 57.7% patients who remain cirrhotic after SVR 12 they remain to have cirrhosis with lower Liver stiffness measurement (LSM) value than pretreatment.
In our study as regard laboratory results we found that after achieving SVR12 platelet count significantly increased denoting significant improvement of liver fibrosis, ALT significantly decreased denoting decrease in necroinflammation and albumin levels showed significant increase denoting improvement of synthetic function of liver.
Our study clearly demonstrated that the Mac-2bp level in chronic hepatitis C patients increased with the progression of liver fibrosis stage.
As regard age and BMI of our patients there were no correlation between Mac-2bp and both of them.
We found that the area under the curve (AUC) of Mac-2bp for predicting different stages of fibrosis including F0-1, F2, F3 and F4 was significantly greater than those for the PAPAS index. These results suggest that measurement of serum Mac-2bp values is the most accurate diagnostic tool for liver stiffness measurment among the surrogate marker investigated in this study.
In our study, we found that Mac-2bp had a higher diagnostic performance and characteristics than PAPAS index in differentiating cirrhotic patients (F4) from non-cirrhotics (F0-3) at baseline and after achieving SVR12.
Regarding differentiation between patients with advanced fibrosis (F3-4) from non-advanced fibrosis (F0-2) the AUC for Mac-2bp level after achieving SVR12 was superior to that for PAPAS index.
Mac-2bp also showed a higher diagnostic performance and characteristics than PAPAS index in differentiating patients with significant fibrosis (F2-4) from non-significant fibrosis (F0-1) at baseline and after achieving SVR12.