In the Journals

DAAs do not affect HCC risk, SVR reduces risk

Recently published data showed a link between sustained virologic response and a reduced risk for hepatocellular carcinoma among patients treated with direct-acting antivirals for hepatitis C.

“Data on HCC risk following DAA induced SVR are still sparse and conflicting,” Fasiha Kanwal, MD, MSHS, from the DeBakey Veterans Affairs Medical Center, Houston, Texas, and colleagues wrote. “We found that, among patients treated with DAA, virological cure of HCV resulted in a considerable reduction in the risk of HCC. However, the absolute risk of HCC was high in several patient groups who achieved cure, including [approximately] 40% of patients who had progressed to cirrhosis.”

To assess the risk and determinants for HCC in patients cured with DAAs, the researchers gathered data on 22,500 patients treated for HCV with DAAs from the Veterans Health Administration system, 19,518 of whom achieved SVR.

The 2,982 patients who did not achieve SVR were more likely to be Hispanic (5.3% vs. 3.5%; P < .0001) and have cirrhosis (42.6% vs. 38.4%; P < .0001), HCV genotype 3 (8.8% vs. 3.5%; P < .0001) and a history of alcohol (66.7% vs. 60.6%; P < .0001) or drug use (58.9% vs. 53.4%; P < .0001), compared with those who did achieve SVR.

Among those who achieved SVR, 183 developed HCC during 20,415 person-years of follow-up for an annual incidence of 0.9 per 100 person-years (95% CI, 0.77-1.03). This was considerably lower than the rate of 3.45 per 100 person-years among the 88 patients who did not achieve SVR and developed HCC during 2,547 person-years of follow-up (95% CI, 2.73-4.18).

Researchers observed a strong association between SVR and time until development of HCC (P < .0001), and a 76% decrease in the risk for HCC (HR = 0.24; 95% CI, 0.19-0.31).

On a multivariate model, other factors that affected the risk for HCC in this cohort included cirrhosis (HR = 4.73; 95% CI, 3.34-6.68) and alcohol use compared with those without alcohol use (HR = 1.56; 95% CI, 1.11-2.18). Compared with Caucasian patients, African-American patients had a lower risk for HCC (HR = 0.56; 95% CI, 0.39-0.81).

“Our data highlight the potential consequences of delaying treatment — either by lack of access or by patient/provider choice — on subsequent risk of HCC, and support treatment of all patients with HCV prior to their progression to advanced fibrosis and cirrhosis. Delaying treatment until patients progress to cirrhosis might be associated with substantial downstream costs incurred as part of life long HCC surveillance and/or management of HCC,” the researchers concluded. “We did not find any evidence to suggest that DAAs promote HCC either during or after treatment.” – by Talitha Bennett

Disclosure: The researchers report no relevant financial disclosures.

Recently published data showed a link between sustained virologic response and a reduced risk for hepatocellular carcinoma among patients treated with direct-acting antivirals for hepatitis C.

“Data on HCC risk following DAA induced SVR are still sparse and conflicting,” Fasiha Kanwal, MD, MSHS, from the DeBakey Veterans Affairs Medical Center, Houston, Texas, and colleagues wrote. “We found that, among patients treated with DAA, virological cure of HCV resulted in a considerable reduction in the risk of HCC. However, the absolute risk of HCC was high in several patient groups who achieved cure, including [approximately] 40% of patients who had progressed to cirrhosis.”

To assess the risk and determinants for HCC in patients cured with DAAs, the researchers gathered data on 22,500 patients treated for HCV with DAAs from the Veterans Health Administration system, 19,518 of whom achieved SVR.

The 2,982 patients who did not achieve SVR were more likely to be Hispanic (5.3% vs. 3.5%; P < .0001) and have cirrhosis (42.6% vs. 38.4%; P < .0001), HCV genotype 3 (8.8% vs. 3.5%; P < .0001) and a history of alcohol (66.7% vs. 60.6%; P < .0001) or drug use (58.9% vs. 53.4%; P < .0001), compared with those who did achieve SVR.

Among those who achieved SVR, 183 developed HCC during 20,415 person-years of follow-up for an annual incidence of 0.9 per 100 person-years (95% CI, 0.77-1.03). This was considerably lower than the rate of 3.45 per 100 person-years among the 88 patients who did not achieve SVR and developed HCC during 2,547 person-years of follow-up (95% CI, 2.73-4.18).

Researchers observed a strong association between SVR and time until development of HCC (P < .0001), and a 76% decrease in the risk for HCC (HR = 0.24; 95% CI, 0.19-0.31).

On a multivariate model, other factors that affected the risk for HCC in this cohort included cirrhosis (HR = 4.73; 95% CI, 3.34-6.68) and alcohol use compared with those without alcohol use (HR = 1.56; 95% CI, 1.11-2.18). Compared with Caucasian patients, African-American patients had a lower risk for HCC (HR = 0.56; 95% CI, 0.39-0.81).

“Our data highlight the potential consequences of delaying treatment — either by lack of access or by patient/provider choice — on subsequent risk of HCC, and support treatment of all patients with HCV prior to their progression to advanced fibrosis and cirrhosis. Delaying treatment until patients progress to cirrhosis might be associated with substantial downstream costs incurred as part of life long HCC surveillance and/or management of HCC,” the researchers concluded. “We did not find any evidence to suggest that DAAs promote HCC either during or after treatment.” – by Talitha Bennett

Disclosure: The researchers report no relevant financial disclosures.