Abstract
Concomitant inflammatory bowel disease (IBD) and hepatitis C virus (HCV) infection is a relevant comorbidity since IBD itself exposes to a high risk of liver damage. We aimed to evaluate liver stiffness (LS) in IBD-HCV after antiviral treatment. We enrolled IBD patients with HCV. All patients at baseline underwent LS measurement by elastography. Patients who were eligible for antiviral therapy received direct antiviral agents (DAAs) and sustained viral response was evaluated at the 12th week. A control group was selected within IBD patients without HCV. One year later, all IBD-HCV patients and controls repeated LS measurement. Twenty-four IBD-HCV patients and 24 IBD controls entered the study. Only twelve out of 24 received DAAs and all achieved sustained viral response (SVR). All IBD subjects were in remission at enrollment and maintained remission for one year. After one year, IBD patients who eradicated HCV passed from a liver stiffness of 8.5 ± 6.2 kPa to 7.1 ± 3.9, p = 0.13. IBD patients who did not eradicate HCV worsened liver stiffness: from 7.6 ± 4.4 to 8.6 ± 4.6, p = 0.01. In the IBD control group, stiffness decreased from 7.8 ± 4.4 to 6.0 ± 3.1, p < 0.001. In conclusion, HCV eradication is able to stop the evolution of liver fibrosis in IBD, while failure to treat may lead to its progression. A stable IBD remission may improve LS even in non-infected subjects.
Highlights
Inflammatory bowel disease (IBD) is a chronic inflammatory condition with autoimmune pathogenesis affecting the digestive tract
It has been postulated that concomitant IBD-chronic hepatitis C (CHC) is a relevant comorbidity since IBD itself exposes to high risk of liver damage due to drugs assumed to treat IBD, such as azathioprine, for the possible association with primary sclerosing cholangitis, and the increased risk of liver steatosis in IBD [7,8,9]
Some authors have underlined that the evolution of fibrosis in IBD patients may be faster
Summary
Inflammatory bowel disease (IBD) is a chronic inflammatory condition with autoimmune pathogenesis affecting the digestive tract. It has been postulated that concomitant IBD-CHC is a relevant comorbidity since IBD itself exposes to high risk of liver damage due to drugs assumed to treat IBD, such as azathioprine, for the possible association with primary sclerosing cholangitis, and the increased risk of liver steatosis in IBD [7,8,9]. For these reasons, some authors have underlined that the evolution of fibrosis in IBD patients may be faster. In the paper by Loras et al [10], it was shown that double immunosuppression increased the risk of virus reactivation and worsened was shown that double immunosuppression increased the risk of virus reactivation and worsened
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