What we have found in the era of direct-acting antiviral agents is that the compensated cirrhosis patients actually achieve SVR rates not too differently from those without cirrhosis. That is a major advance. Our previous interferon-based therapies were not well tolerated in cirrhosis and we could not really give them safely in decompensated cirrhosis. Now that we have entered the field of direct-acting antiviral agents for decompensated cirrhosis, what we have been able to demonstrate is that we get sustained response rates of 85%-90% which are not that different (5-10% less) than what we see in the compensated and non-cirrhotic population. The challenge to be faced by most countries is getting access to these medicines for decompensated individuals. It is not a matter of poor efficacy. The studies still need to be done in Asia and particularly China, but it is highly likely that we are not going to see regional differences in sustained response rates. Rather it is going to be ensuring that those with decompensated cirrhosis are recognized, particularly in countries like China, and then making sure they are evaluated to determine if they are candidates for therapy using ledipasvir/sofosbuvir with ribavirin or sofosbuvir /daclatasvir with ribavirin. These regimens can achieve excellent sustained response rates if there is access to the therapies.
For compensated cirrhosis patients with hepatitis C genotype 1, there are multiple treatment options. I would refer you to the AASLD/IDSA website or the EASL website where all of these therapies are discussed. All of these in the compensated patient lead to excellent SVR rates and clinicians who treat these individuals can be very confident they will be able to achieve excellent sustained response rates with all of these therapies. We should consider that those with hepatitis C and compensated cirrhosis are not different from those without cirrhosis. The regimens may need to be changed minimally with durations out to 24 weeks and ribavirin is often very useful in this patient population, but the expectation would be that SVR rates would not be different.
It is important to let the patient know that they have been cured of the virus but not of their liver disease. They still need to be closely followed to determine if they develop hepatocellular carcinoma, particularly in Asia where people may have hepatitis C and hepatitis B infection. Hepatitis B infection is a tremendous risk factor for HCC. All of these cirrhosis patients with hepatitis C will have to be entered into regular screening programs for HCC with ultrasound every six months. In addition, they are going to have to be regularly monitored for decompensation or disease progression. We need to make sure they don’t develop varices or ascites. What has been shown thus far amongst the increasing number of people who have been cured, is that the older you are the more at risk you are for developing hepatocellular carcinoma. So again, for physicians who treat these cirrhosis patients, they will be able to achieve SVR rates at far higher rates than they would have been able to do in the era of interferon-based therapies, but they have to let their patients know that even though they are given a well tolerated therapy and achieved SVR, their liver disease is not gone and they have to see their physician regularly to make sure their liver stays well-compensated.