1 in 10 patients with advanced liver disease develops liver-related event after HCV cure
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The risk for hepatic decompensation and hepatocellular carcinoma remained constant after hepatitis C virus cure among patients with advanced chronic liver disease, underscoring the need for post-HCV risk stratification in the long term.
“Currently, more than 1 million individuals are being treated every year for hepatitis C virus; therefore, we need proper risk stratification to decrease resource utilization,” Georg Semmler, MD, of the division of gastroenterology and hepatology at the Medical University of Vienna, said at EASL Congress. “Compensated advanced chronic liver disease, also commonly known as compensated cirrhosis, is the target population for risk stratification tools because these patients are at risk to develop complications such as hepatic decompensation or hepatocellular carcinoma.”
He continued: “The risk for HCC and hepatic decompensation is decreasing after HVC cure, but it’s not zero.”
In a multicenter, retrospective analysis, Semmler and colleagues investigated the incidence of HCC and hepatic decompensation during long-term follow-up after HCV cure, the prognostic value of risk stratification algorithms during this follow-up and factors associated with hepatic decompensation.
Researchers evaluated 2,335 patients (mean age, 60.2 years; 59.4% men; 21.1% with obesity; 21.2% with diabetes) with compensated advanced chronic liver disease (cACLD) prior to HCV cure. After a median follow-up of 6 years, 3.6% of patients experienced hepatic decompensation at an incidence rate of 0.74 per 100 patient-years, and 7.8% developed HCC at an incidence rate of 1.6 per 100 person-years.
“If you look also in the long term, then you see a strictly linear increase of the risk both for hepatic decompensation and for HCC, with 3.2% of the cohort experiencing hepatic decompensation at 6 years compared with 8.3% that experienced HCC,” Semmler noted. “This also means that one in 10 cACLD patients develops a liver-related event despite etiological cure within these 5 to 6 years.”
Further, the cumulative incidence of hepatic decompensation at 6 years was 0.4% in the low-risk group vs. 14.3% in the high-risk group. Factors associated with risk for hepatic decompensation were liver stiffness (HR = 1.038; 95% CI, 1.021-1.056), platelet count (HR = 0.989; 95% CI, 0.982-0.997), albumin (HR = 0.888; 95% CI, 0.837-0.942) and gamma-glutamyl transferase (HR = 1.1333; 95% CI, 1.052-1.219).
Using risk stratification parameters of age 59 years or older, a liver stiffness measure of at least 19 kPa and albumin less than 42 g/L, the cumulative incidence of HCC was 6.2% in the low-risk group vs. 15.6% in the high-risk group.
“The risk for hepatic decompensation but also HCC is linear during long-term follow-up, corresponding to an incidence rate of 1.6% per year for HCC and 0.7% for hepatic decompensation,” Semmler concluded. “We can use a one-time assessment after etiological cure focusing on liver stiffness and platelet count for decompensation and also albumin, potentially alpha-fetoprotein and alcohol for HCC.”
He added, “Metabolic comorbidities do not impact hepatic decompensation within this timeframe that we were able to observe, rather the disease severity is driving long-term outcome.”