AI Article Synopsis
- The study aimed to evaluate the impact of interferon therapy on glucose metabolism in patients with chronic hepatitis C virus (HCV).
- Seventy-two patients were classified into sustained responders (48) and nonsustained responders (24), with various indices of glucose metabolism analyzed before and after treatment.
- Results showed that sustained responders experienced improved insulin metrics and decreased levels of certain inflammatory markers, whereas nonsustained responders exhibited no significant changes.
Article Abstract
Background/aims: To investigate whether eradication of hepatitis C virus (HCV) by interferon (IFN) therapy influences systemic glucose metabolism.
Methods: Seventy-two patients with chronic hepatitis C were enrolled in this study. Patients received IFN therapy and were classified into two groups: sustained responders (n=48) and nonsustained responders (n=24). We analysed systemic glucose metabolism in terms of the following indices: homeostasis model assessment for insulin resistance (HOMA-IR) and beta-cell function (HOMA-beta), insulinogenic index (II), composite insulin sensitivity index (ISI composite) and the area under the curve of plasma glucose (PG-AUC) and serum insulin (SI-AUC) in oral glucose tolerance tests. In 28 sustained responders and 16 nonsustained responders, serum levels of soluble tumour necrosis factor receptor 2 (sTNFR2) were measured. Indices were determined before and 6 months after therapy.
Results: In the sustained responders, HOMA-beta (P=0.0004) and SI-AUC (P=0.002) were significantly decreased and the ISI composite was increased (P=0.009), although there were no significant changes in HOMA-IR, II or PG-AUC. Serum sTNFR2 levels decreased significantly after therapy in sustained responders (P=0.001). In the nonsustained responders, there were no changes in any index.
Conclusions: Eradication of HCV by IFN therapy could improve whole-body insulin resistance and insulin hypersecretion with reduced serum TNF-alpha levels.
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| http://dx.doi.org/10.1111/j.1478-3231.2009.01993.x | DOI Listing |
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