In:
Antiviral Therapy, SAGE Publications, Vol. 13, No. 8 ( 2008-11), p. 969-976
Kurzfassung:
Interferon (IFN)-γ inducible protein 10 (IP-10) is increased in hepatitis C virus (HCV) monoinfection, correlates with hepatic inflammation and predicts non-response (NR) to antiviral therapy. We aimed to clarify the role of IP-10 in HIV-HCV coinfection. Methods Serum IP-10 levels of 30 HIV-HCV- coinfected patients treated with pegylated (PEG)-IFN-α2a (180 μg/week) and ribavirin (800-1,200 mg/day) were measured at baseline and 24 h after first IFN dose. The predictive value of IP-10 was compared with established markers of treatment outcome by applying a multivariate logistic regression model. Results Patients with NR (476 ±156 pg/ml) or virological relapse (508 ±298 pg/ml) had significantly higher baseline IP-10 levels compared with patients who had a sustained virological response (SVR; 293 ±97 pg/ml, P=0.001). The IFN-induced increase of IP-10 was significantly stronger in patients with an SVR ( P=0.017). IP-10 levels were associated with HCV viral load, alanine aminotransferase (ALT) levels, hepatic inflammatory activity and fibrosis stage. Advanced fibrosis, high HCV viral load, hepatovenous pressure gradient and pretreatment IP-10 〉 400 pg/ml predicted NR to antiviral therapy. In the multivariate analysis, IP-10 was identified as the strongest baseline predictor of SVR with a specificity and sensitivity of 83.4% and 92.9%, respectively. Conclusions Pretreatment IP-10 levels correlated with HCV viral load, ALT levels, hepatic inflammation and fibrosis. An IP-10 cutoff level of 400 pg/ml might serve as a useful predictive marker for anti-HCV therapy in HIV–HCV-coinfected patients because it could discriminate patients with expected NR or HCV relapse after therapy from patients with an SVR before starting antiviral treatment.
Materialart:
Online-Ressource
ISSN:
1359-6535
,
2040-2058
DOI:
10.1177/135965350801300815
Sprache:
Englisch
Verlag:
SAGE Publications
Publikationsdatum:
2008
ZDB Id:
2118396-X
SSG:
15,3
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