论文部分内容阅读
Background/Aims Diabetes mellitus (DM) is frequently observed in patients with chronic hepatitis caused by hepatitis C virus infection (CHC). The present study was designed to determine the pathogenic factors responsible for glucose intolerance in CHC patients. Methods A total of 131 patients with CHC were enrolled in this study. Insulin resistance and β-cell function were determined after 75 g oral glucose tolerance tests. Results Glucose intolerance was detected in 27.5% (36/131) of CHC patients; 10 had DM and 26 impaired glucose tolerance. HOMA-R insulin 0× glucose 0/22.5 was greater in patients with both impaired glucose tolerance and DM than in those with normal glucose tolerance (P< 0.01). Matsuda index 104/√ (mean insulin× mean glucose× glucose0× insulin 0) was lower in diabetic patients than in those with normal glucose tolerance (P< 0.05). The insulinogenic indexΔ insulin 30-0/Δ glucose 30-0 and Δ C-peptide 30 Δ C-peptide30-0/Δ glucose 30-0 were significantly lower even in patients with impaired glucose tolerance than in patients with normal glucose tolerance (P< 0.01). Conclusions Both insulin resistance and β-cell dysfunction contribute to glucose intolerance in CHC patients.
Background / Aims Diabetes mellitus (DM) is frequently observed in patients with chronic hepatitis caused by hepatitis C virus infection (CHC). The present study was designed to determine the pathogenic factors responsible for glucose intolerance in CHC patients. Methods A total of 131 patients Results with Glucose intolerance was detected in 27.5% (36/131) of CHC patients; 10 had DM and 26 impaired glucose tolerance with CHC were enrolled in this study. HOMA-R insulin 0 × glucose 0 / 22.5 was greater in patients with both impaired glucose tolerance and DM than those with normal glucose tolerance (P <0.01). Matsuda index 104 / √ (mean insulin × mean glucose × glucose × × insulin 0) was lower in diabetic patients than those with normal glucose tolerance (P <0.05). The insulinogenic index Δ insulin 30-0 / Δ glucose 30-0 and Δ C-peptide 30 Δ C-peptide 30-0 / Δ glucose 30- 0 were significantly lower even in patients with impaired glucose tolerance than in patients with normal glucose tolerance (P <0.01). Conclusions Both insulin resistance and β-cell dysfunction contribute to glucose intolerance in CHC patients.