- مبلغ: ۸۶,۰۰۰ تومان
- مبلغ: ۹۱,۰۰۰ تومان
Background: Hepatitis C virus (HCV) infection can lead to increased insulin resistance, but the dynamics of insulin resistance in HCV-infected patients receiving pegylated interferon plus ribavirin remain elusive. Methods: This prospective study enrolled HCV-infected patients who received pegylated interferon plus ribavirin. Patients were classified according to the attainment of sustained virological response (SVR). Insulin resistance was measured using homeostatic model assessmentinsulin resistance (HOMA-IR). The change in HOMA-IR at baseline, the end of treatment, and 24 weeks after the end of treatment was compared in patients who achieved SVR and those who did not. Results: A total of 65 patients participated in this study, of which 46 (71%) achieved SVR. Overall, The HOMA-IR changed significantly during antiviral therapy, with the median values [interquartile range (IQR)] of 3.7 (1.6e10.0) prior to the treatment, 1.5 (0.8e2.9) at the end, and 1.6 (0.9e3.1) at 24 weeks after completion of therapy. However, only patients who achieved SVR had significant off-therapy reduction of HOMA-IR, with median values of 1.3 (IQR, 0.7e2.6) at 24 weeks off therapy and 3.6 (IQR, 1.5e9.9) at baseline (p < 0.0001). In those without SVR, the HOMA-IR measured 24 weeks after treatment completion (median, 2.2; IQR, 1.9e4.7) did not differ from baseline values (median, 3.9; IQR, 2.2e10.0; p Z 0.5). Conclusion: Dual therapy with pegylated interferon plus ribavirin ameliorated IR in HCVinfected patients, but the off-therapy improvement of IR was limited to those who attained SVR.
This prospective study unraveled how insulin resistance would change during the antiviral treatment for HCV infection. We demonstrated a significant reduction of insulin resistance in infected patients after they finished the therapy with pegylated interferon plus ribavirin. However, off-therapy amelioration of insulin resistance was observed only in patients who achieved SVR, indicating that viral clearance is essential for the efficacy to be sustained. Collectively, these findings corroborate the causative role of HCV in impairing glucose homeostasis and implicate the clinical effectiveness of viral eradication in extrahepatic outcomes.