Patients with hepatitis C who take tricyclic antidepressants (TCAs) have decreased fibrosis progression and a lower risk of developing cirrhosis, according to results published in the Journal of Viral Hepatology.
These results indicate a potential new application for TCAs.
The study included data from the Electronically Retrieved Cohort of Hepatitis C Virus Infected Veterans. Participants were categorized by their use of TCAs, selective serotonin reuptake inhibitors (SSRIs), or no antidepressants.
Hepatitis C virus (HCV)-related liver fibrosis improves significantly in the majority of patients with pre-treatment advanced fibrosis or cirrhosis after treatment resulting in a sustained virological response, Swedish investigators report in the Journal of Viral Hepatitis.
However, advanced fibrosis persisted in a quarter of patients and worsened in a small subset of patients, showing the need for regular monitoring after successful HCV therapy. Pre-treatment cirrhosis, older age and high body mass index were risk factors for the persistence of advanced cirrhosis.
“Our study shows that the vast majority of our 269 patients with pre-treatment advanced fibrosis or cirrhosis improved their fibrosis during long-term follow-up after SVR,” comment the researchers. “A minority, however, continued to have advanced fibrosis even after more than 5-10 years follow-up. In this subset of patients, a point of no return for advanced liver fibrosis might have been reached, where improvement is not possible.”
Direct-acting antiviral therapy was safe and highly effective in patients coinfected with HIV and hepatitis C, according to a recently published study. Factors that negatively affected sustained virologic response rates included HIV-related immunosuppression, HCV RNA load, severity of liver disease and suboptimal DAA-based regimens.
“Concern has been raised about the generalizability of inclusion criteria from clinical trials of different DAAs to the highly heterogeneous population of HIV/HCV-coinfected patients,” Juan Berenguer, MD, PhD, from the Hospital General Universitario Gregorio Marañón, Spain, and colleagues wrote. “We evaluated the response to treatment in a large prospective registry of HIV/HCV-coinfected persons receiving DAA-based HCV therapy in the region of Madrid (Spain) and analyzed factors associated with treatment failure.”
Berenguer and colleagues prospectively followed 2,396 patients with HIV/HCV-coinfection during treatment. Median patient age was 51 years, 78.2% were men, 63.9% were treatment-naive, 803 had compensated cirrhosis and 156 had decompensated cirrhosis. Patients had HCV genotype 1a (40.9%), 1b (15.1%), 3 (15%) or 4 (22.4%).
Infection with hepatitis B virus (HBV) or hepatitis C virus (HCV) can lead to cirrhosis as well as liver cancer. A Hepatology study from Taiwan has found that statins may provide benefits to patients with HBV- or HCV-related cirrhosis.
When the liver fails to compensate for the functional overload resulting from disease, a situation called decompensation occurs. Decompensation significantly lowers the survival rate among patients with cirrhosis, and very few effective drugs are available. This latest study assessed information on 1350 cirrhotic patients identified from a representative group of Taiwan National Health Insurance beneficiaries from 2000 to 2013. Statin use was linked with a decreased the risk of decompensation in a dose-dependent manner.
Statins reduce the risk of decompensation in patients with liver cirrhosis due to hepatitis B virus (HBV) and hepatitis C virus (HCV) infections, according to a study published in Hepatology.1
Decompensated liver cirrhosis can lead to hepatic encephalopathy, ascites with spontaneous bacterial peritonitis and variceal bleeding, and is associated with increased mortality. Treating cirrhosis early on may help prevent or delay decompensation.
Statins have been shown to reduce portal hypertension related to liver cirrhosis in animal models. Limited clinical data suggest that statin use may lower rates of decompensation in patients with liver cirrhosis related to nonalcoholic steatohepatitis (NASH), HCV, or chronic HBV infection.1 However, these studies were performed in specific populations, such as male veterans with HCV-related cirrhosis, or had small sample sizes.2,3
The risk for hepatocellular carcinoma was low among patients with cirrhosis, with a 10-year incidence of 4% or lower, according to the results of a U.K. population-based cohort study.
While low overall, investigators found the incidence of HCC was highest among patients with cirrhosis due to chronic viral hepatitis compared with other etiologies.
“This very low incidence of HCC occurrence in people with cirrhosis caused by alcohol or of unknown origin suggests that surveillance for HCC among these groups is likely to benefit patients little,” Joe West, PhD, of the division of epidemiology and public health at the University of Nottingham in the U.K., said in a press release. “As surveillance incurs substantial cost, it is therefore unlikely to represent value for money for the NHS. There may well be other ways of spending this money that would benefit patients far more.”
Complications of advanced liver disease including cirrhosis and hepatic decompensation have risen over the past decade among people with chronic hepatitis C, according to study findings presented at the 2016 AASLD Liver Meeting in November. However, in recent years the increase has slowed, especially among those at highest risk – black people and people aged 60 and over.
Over years or decades, chronic hepatitis C virus (HCV) infection can lead to severe liver damage including cirrhosis (build-up of scar tissue), hepatocellular carcinoma (HCC, a type of liver cancer) and hepatic decompensation (when the liver can no longer perform its vital functions).
Successful hepatitis C treatment can slow or halt liver disease progression, but people who are treated too late, after they have already developed cirrhosis, remain at risk for HCC and end-stage liver disease.