Predictors of hepatocellular carcinoma in HCV cirrhotic patients treated with direct acting antivirals

Advanced liver disease outcomes after hepatitis C eradication by human immunodeficiency virus infection in PITER cohort

“…Low platelets level was associated to a decompensating event at univariate analysis, though it doesn't result independently associated by stepwise regression analysis, most probably due to not sufficient sample size. In fact, low platelet levels have been previously reported as one of the main predictors of Child-Pugh score deterioration and HCC development in the overall PITER cohort [27] and in accordance with the results of a previous prospective study, signs of portal hypertension can help to stratify the risk of HCC [24].…”

“…However, careful follow-up is important not only in patients with virological failure or with known risk factors (i.e., decompensation of liver cirrhosis prior to antiviral treatment or a "cured" HCC), but also in patients with F4 fibrosis stage/liver cirrhosis prior to viral eradication. The cumulative incidence reported in this study is similar with previously reported incidence of newly diagnosed HCC at 1 year after exposure to DAA [9,[24][25][26]. In patients with advanced hepatitis C receiving DAA, the residual HCC risk might be lower than that of untreated patients and declines progressively with time after a sustained virological response [26].…”

“…After successful DAA treatment, preliminary data have shown an improvement in Child-Pugh class (observed in 85% of coinfected and in 65.9% of monoinfected patients, with no significant difference between the two groups), suggesting that viral eradication helps liver function recovery in the majority of patients with liver cirrhosis (data not shown). As previously reported, HCV cured after DAA therapy induce a reduction of the risk of HCC occurrence compared with non-responders; however, a residual risk still persists even after viral eradication [23][24][25][26]. In particular, regarding the HCC occurrence following viral eradication, the cumulative incidence was 2.2% in coinfected and 3.9% in monoinfected patients, significantly lower compared to the cumulative incidence of HCC (13.8%) reported in patients who experienced treatment failure in the PITER cohort [23].…”

Improvement in hepatitis C virus patients with advanced, compensated liver disease after sustained virological response to direct acting antivirals

“…We feel that drawing any definite conclusion on this topic on the basis of our data may be premature and that longer follow‐up of larger cohorts is needed to confirm or confute these findings, yet we feel that patients who show a lack of decrease in liver stiffness after viral clearance may deserve particular attention, as in our series 20% of patients with this behaviour developed HCC during 1‐year follow‐up, and there is evidence showing that portal hypertension is an independent predictor of HCC development . Moreover, our results are consistent with those very recently reported in a study with a similar follow‐up (ie, 65.6 weeks after the end of successful DAA treatment) showing no liver‐related events in 158 patients with F3 fibrosis, while 4.7% of the 317 patients with compensated cirrhosis had a liver‐related event that included both decompensation and development of HCC; likewise, a very large study carried out in our Country, similar data showing that the actual rate of HCC may be reduced by means of DAA treatment, though a residual risk still exists …”

“…43 Moreover, our results are consistent with those very recently reported in a study with a similar follow-up (ie, 65.6 weeks after the end of successful DAA treatment) showing no liver-related events in 158 patients with F3 fibrosis, while 4.7% of the 317 patients with compensated cirrhosis had a liver-related event that included both decompensation and development of HCC; likewise, a very large study carried out in our Country, similar data showing that the actual rate of HCC may be reduced by means of DAA treatment, though a residual risk still exists. 44,45 Previous studies assessing liver stiffness modifications after HCV eradication suggested that part of the improvement in liver stiffness values that are observed may be related to a decrease in liver necro-inflammatory activity, as heralded by decreased aminotransferases after viral clearance, rather than by an actual improvement in liver fibrosis. 16,17 This suggestion is plausible, given the longer time necessary for fibrosis remodelling and the short-term follow-up of the majority of the studies carried out on this topic, and is also supported by the results of studies carried out with paired liver biopsy showing that histological findings compatible with cirrhosis are still present in approximately 40% of patients in a median time of 67 months after SVR, although even in patients who were still histologically classified as cirrhotics at follow-up the area of fibrosis assessed by morphometry was significantly, and dramatically, reduced.…”