Metabolic Factors and Their Influence on the Clinical Course and Response to HCV Treatment

Abstract

Nowadays, direct-acting antivirals (DAA) have been used for hepatitis C virus (HCV) treatment leading to cure in 90-95% of non-cirrhotic patients depending on genotype, treatment experience, and regimen used. It was observed rates of antiviral response above 90% in compensated cirrhotic patients that should be treated for long time and/or ribavirin may be required. Metabolic syndrome, obesity, and insulin resistance are increasing worldwide and further contribute to hepatic steatosis and have long been recognized as a cause of lipid deposition in the liver. These factors affect the rate of antiviral response to interferon-based therapy, but it seems not impact DAA treatment. The effect of HCV eradication on hepatic steatosis and progression to fibrosis, cirrhosis, and hepatocellular carcinoma warrants further study in the era of direct-acting antivirals. Other factors that could be related to increase liver damage are vitamin D and associated polymorphisms. Patients with low concentration of total vitamin D [25(OH)D] presented high degree of fibrosis and high values of total cholesterol and triglycerides. In this chapter, we review the challenges and metabolic pathology associated with HCV infection and, discuss the influence of some metabolic factors which can cause liver damage.

The Prevalence and Impact of Hepatic Steatosis on Response to Direct-Acting Antiviral Therapy in HIV–HCV Coinfection

“…Although DAAs have negated the presence of steatosis on SVR in those with HCV monoinfection [30], less is known about those with HIV-HCV coinfection. In this cohort, the SVR-12 rate was high, similar to that found in studies on participants with HCV monoinfection (90%-95%) [27,29], and not impacted by the presence of hepatic steatosis.…”

“…In the interferon era, hepatic steatosis negatively impacted SVR [25,26]. The development of DAAs has dramatically increased the ability to achieve SVR in chronic HCV [27][28][29][30]. Although DAAs have negated the presence of steatosis on SVR in those with HCV monoinfection [30], less is known about those with HIV-HCV coinfection.…”

“…The presence of steatosis resulted in lower sustained virologic response (SVR) during the interferon-alpha treatment era of HCV infection [25,26]. The development of direct-acting antiviral (DAA) medications revolutionized the treatment of HCV infection, including those with HIV, resulting in high SVR (90%-95%) [27,28]. Past negative predictive factors associated with non-response when treated with interferon therapies, such as the metabolic syndrome, insulin resistance, advanced fibrosis, black race, GT1, and HIV-HCV coinfection, do not appear to be risk factors for relapse in the DAA era [27][28][29].…”

“…The development of direct-acting antiviral (DAA) medications revolutionized the treatment of HCV infection, including those with HIV, resulting in high SVR (90%-95%) [27,28]. Past negative predictive factors associated with non-response when treated with interferon therapies, such as the metabolic syndrome, insulin resistance, advanced fibrosis, black race, GT1, and HIV-HCV coinfection, do not appear to be risk factors for relapse in the DAA era [27][28][29]. Because hepatic steatosis does not appear to be a risk factor for DAA treatment failure in those with HCV monoinfection [30], it is hypothesized that steatosis will not impact SVR in HIV-HCV coinfection.…”