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 beta-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 0xglucose 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 [10(4)/ (square root) (mean insulinxmean glucosexglucose 0xinsulin 0)] was lower in diabetic patients than in those with normal glucose tolerance (P<0.05). The insulinogenic index [Deltainsulin 30-0/Deltaglucose 30-0] and DeltaC-peptide 30 [DeltaC-peptide 30-0/Deltaglucose 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 beta-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 CHCpatients. METHODS: A total of 131 patients with CHC were enrolled in this study. Insulin resistance and beta-cell function were determined after 75 g oral glucose tolerance tests. RESULTS:Glucose intolerance was detected in 27.5% (36/131) of CHCpatients; 10 had DM and 26 impaired glucose tolerance. HOMA-R [insulin 0xglucose 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 [10(4)/ (square root) (mean insulinxmean glucosexglucose 0xinsulin 0)] was lower in diabeticpatients than in those with normal glucose tolerance (P<0.05). The insulinogenic index [Deltainsulin 30-0/Deltaglucose 30-0] and DeltaC-peptide 30 [DeltaC-peptide 30-0/Deltaglucose 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 beta-cell dysfunction contribute to glucose intolerance in CHCpatients.
Authors: M Vázquez-Vandyck; S Roman; J L Vázquez; L Huacuja; G Khalsa; R Troyo-Sanromán; A Panduro Journal: World J Gastroenterol Date: 2007-12-14 Impact factor: 5.742
Authors: Aymin Delgado-Borrego; Sergio H Jordan; Betania Negre; David Healey; Wenyu Lin; Yoshitaka Kamegaya; Marielle Christofi; David A Ludwig; Anna S F Lok; Raymond T Chung Journal: Clin Gastroenterol Hepatol Date: 2010-02-12 Impact factor: 11.382