Direct-acting antiviral treatment cured HCV in most patients with prior hepatocellular carcinoma and in almost all patients who received a liver transplant as treatment for HCC, according to a recently published study.
“DAAs have increased the efficacy of HCV therapy for many patients once considered difficult to treat, including those with prior HCC, with or without liver transplantation,” Lauren A. Beste, MD, MSc, of the General Medicine Service, Veteran Affairs Puget Sound Health Care System, and colleagues wrote. “While the odds of SVR in non-transplanted HCC patients was significantly lower compared to non-HCC, treatment success remains within reach for most HCC patients.”
The researchers accessed the Veteran Affairs Data Warehouse records between Jan. 1, 2014, and June 30, 2015. They identified 17,487 patients who received HCV treatment, including 624 who had prior HCC. Treatments used included Sovaldi (sofosbuvir, Gilead Sciences), Harvoni (ledipasvir/sofosbuvir, Gilead Sciences) and Viekira Pak (paritaprevir/ritonavir/ombitasvir plus dasabuvir, AbbVie).
Of those with prior HCC, the researchers reviewed separately 142 who had LT prior to antiviral therapy. Eight patients with HCC who received LT after HCV treatment were included in the HCC group.
Overall sustained virologic response rates were 91.9% (95% CI, 90.6-91.5) in patients without HCC, 74.4% (95% CI, 70-78.3) in patients with HCC and 94% (95% CI, 88.3-97) in LT patients with HCC.
Patients with prior HCC were less likely to achieve SVR compared with patients without HCC at an adjusted odds ratio of 0.38 (95% CI, 0.26-0.45) after adjusting for genotype, cirrhosis and other characteristics. In non-transplanted patients with HCC, genotype 3 was the only independent predictor of failure to achieve SVR at an adjusted OR of 0.19 (95% CI, 0.1-0.41).
“It is unclear why patients with HCC had such lower SVR rates compared to patients without HCC. The association between HCC and treatment failure persisted after adjustment for cirrhosis, markers of liver dysfunction, and genotype,” the researchers wrote. “Therefore, these factors cannot explain the lower SVR in patients with HCC, and lead us to suspect that HCC, itself, could be causally linked to antiviral treatment failure. ... Additionally, HCC arises in the setting of chronic inflammation, distorted liver architecture, and alterations in the cytokine and chemokine environment. We speculate that altered hepatic immune processes may predispose both to HCC and to poorer antiviral treatment outcomes.”
Comparing patients with and without cirrhosis, SVR rates were substantially lower in both cirrhotic patients without HCC (87.9% [95%CI, 86.1-88.8] vs. 92.4% [95% CI, 91.8-92.8]) and in those with HCC (73.0% [95% CI, 68.2-77.3] vs. 82.5% [95% CI, 70.8-90.2]).
The best SVR results were seen in patients with HCV genotype 1: 93.1% (95% CI, 92.6-93.5) for patients without HCC, 79.1% (95% CI, 74.4-83.1) for patients with HCC and 96.4% (95% CI, 90.1-98.7) for the liver transplantation patients. The lowest SVR rates were seen in patients with genotype 3: 75.9% (95% CI, 73.3-78.5) for patients without HCC, 47% (95% CI, 33.5-61.1) for patients with HCC and 88.9% (95% CI, 61-97.6) for the LT patients.
“Whether to offer HCV treatment pre-transplant versus deferring to the post-transplant setting remains an area of clinical uncertainty. Our findings suggest that HCC patients currently listed for transplantation, or those with a high probability of getting transplanted quickly, might benefit from postponing antiviral treatment until after transplant in order to maximize the chances of SVR. However, our findings also show that non-transplanted HCC patients, representing the majority of the HCC population, can still achieve SVR in most cases,” the researchers wrote. – by Talitha Bennett
: The researchers report no relevant financial disclosures.