## 4 Discussion  
The first descriptions of the elastography technique come from the mid-1990s [29; 30]. Since then, in laboratories around the world, there has been a rapid development of this method, adding new quality to the imaging studies used so far. This technique, in a way that is easy to perform and interpret, allows one to define the \"hardness\" of the tissue. In a sense, it can be said that this method replaces a physical examination performed inside the human body, differentiating tissues that are healthy or pathologically changed according to their \"hardness\" [29]. This method is non-invasive and not time-consuming, as compared to a liver biopsy, and it is therefore easy to repeat frequently. There are some limitations in which the severity of liver inflammation and portal hypertension are the main influence on the results [31; 32; 33; 34]. Currently, the measurement of liver stiffness is recommended by many hepatologic scientific societies as a method to determine the severity of liver disease before and after HCV treatment [8; 26]. In our study, all patients had an elastographic examination performed at predetermined time points, showing a total reduction in stiffness in the vast majority of patients. This observation has already been made in earlier studies [35; 36; 37; 38; 39]. In our cohort, the range of changes in kPa was \(-4.2\) to \(41.8\) kPa between baseline and FU24, \(2.3\) kPa to \(29\) kPa between baseline and FU96, and \(-2.6\) to \(18.7\) between EOT and FU96. According to the results of some previous studies, we have demonstrated that patients undergoing effective HCV treatment lower their LS values during follow-up (in FU24 by \(1.1\) kPa) and long-term observation (in FU96 by \(2\) kPa) in relation to baseline. In the [PERSON] et al. study, patients treated with pegylated interferon (pegIFN) and RBV were followed, observing a mean LS drop by \(5.3\) (\(4.1\)-\(6.3\)) kPa in two-year follow-up [37]. However, in the [PERSON] et al. study, the median decrease compared to baseline at the end of follow-up was \(3.4\) kPa, vs. \(1.8\) kPa in the patients who did not achieve an SVR [38]. Due to the \(100\%\) effectiveness of treatment in our cohort, we were unable to determine such a relationship. In the ANRS CO13 HEPAVIH Cohort study, patients with HIV/HCV co-therapy remaining on two- or three-drug therapy (pegINF plus RBV with or without protease inhibitor) were investigated [39]. It was observed that achieving SVR is an independent predictor of obtaining an LS decrease. For LS evaluation, the transient elastography method was used in the studies described above and, according our knowledge, there are insufficient trials in which the SWE method was used in patients with antiviral treatment. In the [PERSON] et al. study, the results of \(210\) patients treated with daclatasvir and asunaprevir were analyzed, and it was found that the average LS decreased by \(1.4\) kPa between baseline and EOT and \(2.6\) kPa between baseline and FU24, which is consistent with our results [40]. It should be noted that the type of DAA regimen used made no difference. We also found that a significant decrease in LS occurred during both periods, antiviral therapy (between baseline and EOT \(p=0.008\)) and in the long-term follow-up (between EOT and FU96 \(p=0.0002\); between FU24 and FU96 \(p=0.005\)) as well. In the previously mentioned [PERSON] et al. study and the  
Figure 5: Correlation (Spearman’s rank correlation coefficient) between baseline HCVcAg levels and change in liver stiffness between baseline and FU96. HCVcAg—HCV core antigen; kPa—kilopascal; LS—liver stiffness; fmol—femtomoles. [PERSON] et al. study, no further decrease in LS was observed after treatment in long-term follow-up--no change between in LS between 1 and 2 years of follow-up [35; 37]. Conversely, in the [PERSON] et al. study, as mentioned above, an LS decrease was also observed 24 weeks after therapy completion [40]. In the [PERSON] et al.